Embed Size (px)
Citation preview
Clemson UniversityTigerPrints
All Dissertations Dissertations
5-2010
OCCURRENCE AND FORMATION OFDISINFECTION BY-PRODUCTS IN INDOORSWIMMING POOLS WATERAmer KananClemson University, [email protected]
Follow this and additional works at: https://tigerprints.clemson.edu/all_dissertations
Part of the Environmental Engineering Commons
This Dissertation is brought to you for free and open access by the Dissertations at TigerPrints. It has been accepted for inclusion in All Dissertations byan authorized administrator of TigerPrints. For more information, please contact [email protected].
Recommended CitationKanan, Amer, "OCCURRENCE AND FORMATION OF DISINFECTION BY-PRODUCTS IN INDOOR SWIMMING POOLSWATER" (2010). All Dissertations. 532.https://tigerprints.clemson.edu/all_dissertations/532
OCCURRENCE AND FORMATION OF DISINFECTION BY-PRODUCTS IN
INDOOR SWIMMING POOLS WATER
A Dissertation
Presented to
the Graduate School of
Clemson University
In Partial Fulfillment
of the Requirements for the Degree
Doctor of Philosophy
Environmental Engineering and Earth sciences
by
Amer A. Kanan
May 2010
Accepted by:
Tanju Karanfil, Committee Chair
Cindy Lee
David Freedman
Elizabeth Carraway
ii
ABSTRACT
Chlorination is used to prevent the spread of waterborne infectious diseases from
swimming pools. This required disinfection practice also results in the formation of
undesirable disinfection by-products (DBPs) from the reactions of chlorine with the
organic matter (released by swimmers or present in the filling water of the pool) and
bromide. Some of these DBPs have important adverse public health effects; as a result
their concentrations in drinking waters are regulated. Unfortunately, DBPs formation and
control in swimming pools have not been studied and investigated to the same extent as
their formation and control in drinking water.
The main objective of this research was to improve our understanding of the
occurrence and formation of DBP classes: trihalomethanes (THMs) [Trichloromethane
(TCM), bromodichloromethane (BDCM), dibromochloromethane (DBCM), and
tribromomethane (TBM)], haloacetic acids (HAAs) [chloroacetic acid (CAA),
bromoacetic acid (BAA), dichloroacetic acid (DCAA), bromochloroacetic acid (BCAA),
trichloroacetic acid (TCAA), bromodichloroacetic acid (BDCAA), dibromoacetic acid
(DBAA), dibromochloroacetic acid (DBCAA), and tribromoacetic acid (TBAA), and
halonitromethanes (HNMs) [chloronitromethane (CNM), dichloronitromethane (DCNM),
trichloronitromethane (TCNM), bromonitromethane (BNM), bromochloronitromethane
(BCNM), bromodichoronitromethane (BDCNM), dibromonitromethane (DBNM),
dibromochloronitromethane (DBCNM), and tribromonitromethane (TBNM)] under
swimming pool operation conditions as practiced in the US and estimate their potential
adverse health impacts on swimmers and lifeguards. During the occurrence study
iii
conducted during this research, the occurrence of N-nitrosodimethylamine (NDMA) and
haloacetonitriles (HANs) [chloroacetonitrile (CAN), trichloroacetonitrile (TCAN),
dichloroacetonitrile (DCAN), bromoacetonitrile (BAN), bromochloroacetonitrile
(BCAN), and dibromoacetonitrile (DBAN)] were also investigated. Specifically, the
objectives of the research were: (1) to examine the occurrence of the five DBPs (THMs,
HAAs, HNMs, NDMA, and HANs) in indoor swimming pools in the US, (2) to conduct
a multi-pathway risk assessment on THMs (TCM, BDCM, DBCM) and two HAAs
(DCAA and TCAA) of swimming pool water, (3) to determine the role and contribution
of the two main precursors (i.e., filling water natural organic matter (NOM) vs. body
fluids (BF) from swimmers) to the formation of THMs, HAAs), and HNMs in swimming
pools, (4) to investigate the impacts of swimming pool operational parameters: free
available chlorine (FAC), pH, bather load (TOC), water bromide content, and
temperature on the formation and speciation of THMs, HAAs, and HNMs, and (5) to
measure the formation of THMs and HAAs from the body fluids during turnover time,
―the period of time (usually hours) required to circulate the complete volume of water in
a pool through the recirculation system” of swimming pool water.
The occurrence of DBPs was investigated by collecting samples from 23 indoor
pools in South Carolina, Georgia, and North Carolina. Furthermore, the occurrence of
DBPs and their speciation in three indoor pools was examined periodically for nine
months. Generally the DBPs in the investigated pools were far higher than the drinking
water regulation values in the US or swimming pool regulations in other countries. THMs
ranged between 26 and 213 µg/L with an average of 80 µg/L. HANs range between 5 and
iv
53 µg/L with an average of 19 µg/L. HNMs ranged between 1.4 and 13.3 µg/L with an
average of 5.4 µg/L. The HAAs ranged between 173 and 9005 µg/L with an average of
1541 µg/L. The NDMA ranged between 2 and 83 ng/L with an average of 26.5 ng/L.
Differences in swimming pool operation conditions and chlorination methods affected the
amount, formation and speciation of the DBPs investigated in this study. The
electrochemically generation of chlorine increased the brominated species.
Both the water and calculated air concentrations of TCM, BDCM, DBCM,
DCAA, and TCAA were used to estimate the potential lifetime cancer risk and non-
cancer hazard index from swimming in the three indoor pools sampled along nine
months. Results showed elevated lifetime cancer and non-cancer risks (hazard) from
swimming in these pools. The lifetime cancer risk was higher than the acceptable risk
level of 10-6
by a factor of 10 to 10,000 in most cases. The hazard index exceeded the
acceptable maximum hazard index ratio of 1 and reached a maximum of 26 at times.
To examine the contribution of different precursors in swimming pools, three
DBPs (THMs, HAAs, and HNMs) formation potentials in swimming pool waters were
examined using five filling waters obtained from five drinking water treatment plant
effluents in South Carolina and three body fluid analogs (BFAs). The BFAs were
mixtures prepared in the laboratory to simulate body fluids (mainly major components of
urine and sweat) which are continuously excreted from swimmers into pool water.
Reactivity of filling waters NOM and BFAs to form THMs, HAAs, and HNMs was
tested under swimming pool conditions. The results showed that BFAs were more
reactive with chlorine and exerted high demands as compared to filling waters NOM.
v
BFAs exhibited higher formation potential of HAAs than THMs. An opposite trend was
observed for filling water NOM which formed more THM than HAA. There was no
appreciable difference in HNM formation from BFAs and filling water NOM. The effect
of temperature was greater on THM formation, while the effect of contact time affected
HAAs more. Experiments with filling waters collected at different times showed that
there was less variability in THM than HAA formation from the water treatment plant
effluents studied in this project.
The formation and speciation of THMs, HAAs and HNMs were also investigated
under various disinfection and operation conditions typically used in US swimming
pools. Increases in free available chlorine, pH, (bather load) TOC, water temperature, and
bromide levels in the water increased the overall formation of DBPs. However these
factors affected the different classes of DBPs at different magnitudes. Higher free
available chlorine increased HAAs more than THMs. The temperature effect was greater
on the formation of THMs than for HAAs whereas contact time increased HAAs more
than THMs. The presence of bromide shifted the DBPs toward brominated species and
increased overall THMs and HNMs more than HAAs.
The formation of THMs and HAAs from the body fluids during turnover time of
swimming pool water, especially at short reaction times, was also studied. The results
showed that DBP formations are fast reactions, and an appreciable percentage occurred in
the first 3-6 hours which is about the typical turnover time for water in swimming pools.
THM formation was faster than HAA formation. From 53 to 68% of 5-day THMs were
formed within the first 3-6 hours while 15 to 30% of 5-day HAAs were formed at the first
vi
6 hours. These fast formation rates imply that DBP control strategies in swimming pools
should mainly focus on DBPs precursors control at the source (i.e., swimmers). Some
additional benefit may also be obtained for DBPs control by controlling some of the
operational parameters (pH, free available chlorine, bather load -the number of
individuals using a pool in a 24 hour period- or dilution).
vii
DEDICATION
To my wife,
Huda
and my children,
Manar, Rana, Samar, Sameh, and Noor,
for their love, patience, understanding, encouragement and supporting my decision
returning to school for my PhD degree in Environmental Engineering.
viii
ACKNOWLEDGMENTS
Great thanks are extended to my advisor Dr. Tanju Karanfil for his expertise,
guidance, encouragement, and support. Furthermore, sincere gratitude is given to my
advising committee, Dr. Cindy Lee, Dr. Elizabeth Carraway, and Dr. David Freedman for
devoting time to serve on the research committee.
Greatly appreciated is Al-Quds University for giving the long leaving permission
for the last three years and supporting, as always, during that time. Many thanks go for
Ford Foundation International Fellowships Program for financial support.
Much appreciation is offered to my colleagues in the research group for their
cooperation in the laboratory and field. Special thanks are for Dr. Sule Kaplan for her
fruitful notes and discussions during the research period.
Special thanks go to swimming pool and treatment water utilities personnel and
staff members who provided assistance in sampling the pools water and the treated water.
ix
TABLE OF CONTENTS
Page
TITLE PAGE .................................................................................................................... i
ABSTRACT ..................................................................................................................... ii
DEDICATION ............................................................................................................... vii
ACKNOWLEDGMENTS ............................................................................................ viii
LIST OF TABLES ........................................................................................................ xiii
LIST OF FIGURES ....................................................................................................... xv
LIST OF ABBREVIATIONS ..................................................................................... xviii
CHAPTER
I. INTRODUCTION ......................................................................................... 1
II. BACKGROUND ........................................................................................... 9
Swimming Pool Operation and Management .......................................... 9
Chlorine and Chlorine Chemistry .......................................................... 14
Disinfection By-Products in Indoor Swimming Pools........................... 18
N-nitrosamines ....................................................................................... 24
Other Disinfection By-Products ............................................................. 27
The Precursors of Disinfection By-Products in Swimming Pools ......... 28
Epidemiological Studies and Health Effects of Disinfection
By-Products............................................................................................ 32
Summary of Main and Important Findings from the Literature ............ 35
Research Motivation .............................................................................. 37
III. OBJECTIVES, APPROACHES, AND EXPERIMENTAL DESIGN ........ 38
Objectives .............................................................................................. 38
Tasks and Approaches ........................................................................... 39
Task 1: Examine the Occurrence of THMs, HAAs, HNMs,
NDMA, and HANs in Indoor Swimming Pools
in South Carolina, Georgia, and North Carolina ....................... 39
x
Task 2: Conduct a Multi-Pathway Risk Assessment on THMs
(TCM, BDCM, and DBCM) and HAAs (DCAA and TCAA)
of Indoor Swimming Pool Water ............................................... 41
Task 3: Determine the Role and Contribution of the Two
Main Precursors (i.e., Filling Water NOM vs. Body
Fluids from Swimmers) to the Formation of THMs, HAAs,
and HNMs in Swimming pools................................................. 41
Task 4: Investigate the Impacts of Swimming Pool Operational
Parameters: Free Available Chlorine, pH, bather load (TOC),
Bromide Content, and Temperature on the Formation and
Speciation of THMs, HAAs, and HNMs .................................. 44
Task 5: Measure the Formation of THMs and, HAAs
from the Body Fluids During Turnover Time of Swimming
Pool Water, Especially at Short Reaction Times ...................... 46
IV. MATERIALS AND METHODS ................................................................. 49
Glassware, Reagent Water, Chemical Reagents, and
Stock Solutions ...................................................................................... 49
Treated Water Samples .......................................................................... 50
Body Fluid Analogs (BFAs) .................................................................. 52
Chlorination Experiments ...................................................................... 53
Analytical Methods ................................................................................ 54
HAAs analyses ....................................................................................... 54
THMs and HANs Analyses ................................................................... 57
HNMs Analyses ..................................................................................... 59
NDMA Analyses .................................................................................... 60
Total Organic Carbon and Nitrogen ...................................................... 62
UV Absorbance ...................................................................................... 62
pH ........................................................................................................... 63
Free Available Chlorine ......................................................................... 63
Bromide.................................................................................................. 64
V. DISINFECTION BY-PRODUCTS OCCURRENCE IN INDOOR
SWIMMING POOLS .................................................................................. 65
Introduction and Objectives ................................................................... 65
Approach ................................................................................................ 68
Materials and Methods ........................................................................... 68
Results and Discussion .......................................................................... 69
Swimming Pools Water Characterization .............................................. 69
Occurrence of DBPs in Swimming Pools .............................................. 70
Conclusions ............................................................................................ 93
xi
VI. EXPOSURE CHARACTERIZATION AND RISK ASSESSMENT ......... 94
Introduction and Objectives ................................................................... 94
Methods and Materials ......................................................................... 100
Results and Discussion ........................................................................ 107
Swimmers Lifetime Cancer Risk Characterization from DBPs of
Swimming Pools .................................................................................. 109
Swimmers Lifetime Non-Cancer Risk Characterization from
DBPs of Swimming Pools ................................................................... 111
Lifeguards Exposure and Health Risk Assessment ............................. 119
Conclusions .......................................................................................... 126
VII. THE CONTRIBUTION OF FILLING WATER NATURAL
ORGANIC MATTER AND BODY FLUIDS TO THE
FORMATION OF DIFFERENT CLASSES OF DISINFECTION
BY-PRODUCTS IN SWIMMING POOL................................................. 128
Introduction and Objectives ................................................................. 128
Approach .............................................................................................. 129
Materials and Methods ......................................................................... 129
Filling Water NOM .............................................................................. 129
Body Fluid Analogs (BFAs) ................................................................ 130
Chlorination ......................................................................................... 130
Analytical Procedures .......................................................................... 131
Results and Discussion ........................................................................ 131
Reactivity and Formation Potential of DBPs from BFAs .................... 131
Reactivity and Formation Potential of DBPs from Filling
Water NOMs ........................................................................................ 141
Conclusions .......................................................................................... 154
VIII. SWIMMING POOL OPERATION PARAMETERS EFFECT
ON DISINFECTION BY-PRODUCTS FORMATION ............................ 157
Introduction and Objectives ................................................................. 157
Approach .............................................................................................. 158
Materials and Methods ......................................................................... 159
Synthetic Swimming Pool Waters ....................................................... 159
Chlorination Experiments .................................................................... 160
Analytical Methods .............................................................................. 160
Results and Discussion ........................................................................ 161
Effect of Free Available Chlorine on DBP formation ......................... 161
Effect of pH on DBP Formation .......................................................... 166
Effect of TOC on DBP Formation ....................................................... 169
Effect of Bromide on DBP Formation ................................................. 172
xii
Effect of Temperature on DBP Formation ........................................... 179
HAAs and THMs Formation Relation ................................................. 181
Conclusions .......................................................................................... 182
IX. TRIHALOMETHANES AND HALOACETIC ACIDS FORMATION
DURING TURNOVER TIME OF SWIMMING POOL WATER…. ...... 185
Introduction and Objectives ................................................................. 185
Approach .............................................................................................. 186
Materials and Methods ......................................................................... 186
Results and Discussion ........................................................................ 187
THMs Formation as Function of Time ................................................ 187
HAAs Formation as Function of Time ................................................ 194
Conclusions .......................................................................................... 203
X. CONCLUSIONS AND RECOMMENDATIONS…………………. ...... .205
Conclusions .......................................................................................... 205
Recommendations for Pool Operators and Swimmers ........................ 208
Recommendations for Future Research ............................................... 209
APPENDICES ........................................................................................... 211
A: Swimming Activity Distribution..................................................... 212
B: Guidelines and Regulations of DBPs .............................................. 213
C: DBPs Species in Three Monitored Indoor Pools ............................ 214
D: Exposure Factors and Calculated Doses ......................................... 219
REFERENCES .......................................................................................... 233
xiii
LIST OF TABLES
Table Page
2.1 Trihalomethanes (THMs) reported in indoor swimming pools in
different countries ........................................................................................ 23
2.2 Haloacetic acids (HAAs) reported in indoor swimming pools in
different countries ........................................................................................ 24
2.3 Different DBPs reported in indoor swimming pools ................................... 28
4.1 Natural water samples characteristics used in the experiments ................... 51
4.2 Body fluid analogs components ................................................................... 52
4.3 Analytical methods and minimum reporting levels ..................................... 55
5.1 Swimming pool water characteristics .......................................................... 70
5.2 Trihalomethanes (THMs) occurrence in indoor swimming pools ............... 73
5.3 Haloacetonitriles (HANs) occurrence in indoor swimming pools ............... 74
5.4 Halonitromethanes (HNMs) occurrence in indoor swimming pools ........... 75
5.5 Haloacetic acids (HAAs) occurrence in indoor swimming pools ................ 78
5.6 N-Nitrosodimethylamine (NDMA) occurrence in indoor
Swimming pools .......................................................................................... 80
5.7 Characteristics of three indoor swimming pools
waters monitored during 9 months ...................................................... 82
5.8 Occurrence of THMs, HAAs, and HNMs in three indoor
swimming pools ........................................................................................... 84
5.9 Occurrence of haloacetonitriles (HANs) in three indoor
swimming pools ........................................................................................... 88
5.10 Trihalomethanes (THMs) measured in indoor pools in the US
and other countries ....................................................................................... 92
6.1 Reference dose (RfD) and potency factor (PF) of DBPs (IRIS, 2009;
RAIS, 2009; US EPA, 1991, 1999) ............................................................. 99
6.2 Recommended human body information (personal information)
for exposure estimation (US EPA, 2009b) ................................................ 102
6.3 Henry’s Law Constant and Dermal permeability (Kp) of some DBPs ...... 104
6.4 Average of DBP species concentration used in risk assessment ............... 108
6.5 Cancer risk and hazard index from DBPs measured in S16
swimming pool on swimmers .................................................................... 112
6.6 Cancer risk and hazard index from DBPs measured in S17L
swimming pool on swimmers .................................................................... 113
6.7 Cancer risk and hazard index from DBPs measured in S17T
swimming pool on swimmers .................................................................... 114
6.8 Lifeguard body information (personal information), working hours,
and frequencies assumed for exposure estimation (US EPA, 2009b) ....... 122
6.9 Cancer risk and hazard index from DBPs measured in S16
swimming pool on lifeguards..................................................................... 122
xiv
6.10 Cancer risk and hazard index from DBPs measured in S17L
swimming pool on lifeguards..................................................................... 123
6.11 Cancer risk and hazard index from DBPs measured in S17W
swimming pool on lifeguards..................................................................... 123
7.1 Disinfection By-Products formation from BFAs at pH 7, TOC 1mg/L,
and initial chlorine dose 50mg/L ............................................................... 133
7.2 Disinfection By-Products formation from 1 mg/L BFA
components at 22°C, pH 7, initial chlorine dose 50 mg/L,
and 5-days contact time ............................................................................. 135
7.3 Trihalomethane (THMs), haloacetic acids (HAAs), and
halonitromethanes (HNMs) formation potentials of treated drinking
water samples at 26°C, pH 7, and initial chlorine dose 50 mg/L .............. 143
7.4 Trihalomethane (THMs), haloacetic acids (HAAs), and
halonitromethanes (HNMs) formation potentials of treated drinking
water samples at 40°C, pH 7, and initial chlorine dose 50 mg/L .............. 144
8.1 Trihalomethanes (THMs) and haloacetic acids (HAAs) formed
from synthetic swimming pool water ....................................................... 162
8.2 Halonitromethanes (HNMs) formed from synthetic swimming
pool water at similar swimming pool operation parameters formed
from synthetic swimming pool water ........................................................ 165
8.3 Trihalomethane (THM) and haloacetic acid (HAA) yields
from different chlorine to total organic carbon ratio ................................. 170
9.1 Trihalomethanes (THMs) formation change during 5 days reaction
time from synthetic pool water produced from BFA(G) (5mg/L TOC)
and Myrtle Beach water source (MB) (1mg/L), BFA(G)-MB,
without and with bromide .......................................................................... 188
9.2 Trihalomethanes (THMs) formation change during 5 days
incubation from synthetic pool water produced from
BFA(G) (5mg/L TOC) only, without and with bromide ........................... 189
9.3 Trihalomethanes (THMs) formation change during 5 days
incubation from synthetic pool water produced from BFA(G)
(1mg/L TOC), without and with bromide .................................................. 190
9.4 HAAs formation during 5days chlorination from synthetic pool water
BFA(G)-MB produced from BFA(G) (5mg/L TOC) and Myrtle
Beach water (1mg/L) ................................................................................. 195
9.5 Haloacetic acids (HAAs) formation during 5days chlorination from
synthetic pool water produced from BFA(G) (5mg/L TOC) ..................... 196
9.6 Haloacetic acids (HAAs) formation during 5days chlorination from
synthetic pool water produced from BFA(G) (1mg/L TOC) .................... 197
xv
LIST OF FIGURES
Figure Page
2.1 A schematic diagram of swimming pool ..................................................... 11
3.1 Sampling and determination of water quality and disinfection
by-products in swimming pools ................................................................... 40
3.2 Experiments conducted for task 3 ................................................................ 44
3.3 Experiments conducted for task 4 ................................................................ 47
3.4 Experiments conducted to measure THMs and HAAs from the body
fluid precursors during turnover time of swimming pool water .................. 48
5.1 Box-whisker plot key (a), FAC (Free chlorine),
TOC (total organic carbon) and TN (total nitrogen)
of the 23 indoor swimming pools ................................................................ 71
5.2 Occurrence of trihalomethanes (THMs), haloacetonitriles (HANs) (a) and
halonitromethanes (HNMs) (b) in 23 indoor pools ...................................... 76
5.3 Occurrence of haloacetic acids (HAAs) in 23 indoor swimming pools ...... 79
5.4 Average DBPs measured in three indoor swimming pools during
9 months ....................................................................................................... 85
5.5 Average DBPs species measured in three swimming pools
during 9 months, THM species (a), HAA species (b),
HNM species (c) and HAN species (d)........................................................ 86
5.6 THM measured in three pools during 9 months .......................................... 89
5.7 HAA measured in three pools during 9 months........................................... 90
6.1 Lifetime cancer risk from TCM (a), BDCM (b), DBCM (c),
and DCAA (d) estimated for different swimmers groups in the three
swimming pools ......................................................................................... 116
6.2 Additive lifetime cancer risk from TCM, BDCM, DBCM,
and DCAA in three swimming pools estimated for different
swimmers groups ....................................................................................... 117
6.3 Hazard index from TCM (a), BDCM (b), DBCM (c),
DCAA (d), and TCAA (e) estimated for different swimmers
groups in three swimming pools ................................................................ 118
6.4 Additive hazard indices from TCM, BDCM,
DBCM, DCAA, and TCAA in three swimming pools
imposed on different swimmers groups ..................................................... 119
6.5 Lifetime cancer risk (a) and non-cancer hazard on
swimmers and lifeguards from swimming pools ....................................... 125
7.1 Chloroform formed after 5 and 10 days chlorination
of three BFAs (1mg/L TOC) at pH 7 and 26°C (a) and 40°C (b) .............. 134
7.2 HAAs formed after 5 and 10 days chlorination of three
BFAs (1mg/L TOC) at pH 7 at 26°C (a) and 40°C (b) .............................. 138
xvi
7.3 Chloropicrin formed after 5 and 10 days chlorination of three
BFAs (1mg/L TOC) at pH 7 and 26°C (a) and 40°C (b) ........................... 140
7.4 THMs formed from five water types (NOMs) sampled three times
during 2008-2009 at 1 mg/L TOC (except GV water), pH 7, initial
chlorine dose 50 mg/L, 5 days incubation at 26°C (a) and 40°C (b),
and 10 days incubation at 26°C (c) and 40°C (d) ...................................... 146
7.5 HAAs formed from five water types (NOMs) sampled three times
during 2008-2009 at 1 mg/L TOC (except GV water), pH 7,
initial chlorine dose 50 mg/L, 5 days incubation at 26°C
(a) and 40°C (b), and 10 days incubation at 26°C (c) and 40°C (d) .......... 147
7.6 HNMs formed from five water types (NOMs) sampled
three times during 2008-2009 at 1 mg/L TOC (except GV water),
pH 7, initial chlorine dose 50 mg/L, 5 days incubation
at 26°C (a) and 40°C (b), and 10 days incubation
at 26°C (c) and 40°C (d) ............................................................................ 148
7.7 THM species formed from BFAs and treated drinking waters in
November-08 samples (i.e, filling waters) during the FP tests
at 1 mg/L TOC (except GV water, 0.7 mg/L), 26°C, pH 7, initial
chlorine dose 50 mg/L, and 5 days contact time ........................................ 150
7.8 HAA species formed from BFAs and treated drinking waters in
November-08 samples (i.e., filling waters) during the FP tests
at 1 mg/L TOC (except GV water, 0.7 mg/L) 26°C, pH 7,
initial chlorine dose 50 mg/L, and 5 days contact time ............................. 150
7.9 THMs (a) and HAAs (b) yield from BFAs and five NOMs
(November 08 samples) after 5 and 10 days under the
same conditions .......................................................................................... 152
7.10 HAAs yield from five NOMs (March 09 samples)
after 5 and 10 days under the same chlorination conditions ...................... 153
7.11 THMs yield from five NOMs (March 09 samples) chlorination
after 10 days at 26°C and 40°C .................................................................. 153
7.12 HAAs yield from five NOMs (March 09 samples)
chlorination after 10 days at 26°C and 40°C ............................................. 154
8.1 Effect of free available chlorine (FAC) on THM (a),
HAA (b), and HNM (c) formation during chlorination of
two synthetic pool waters........................................................................... 163
8.2 Effect of pH on THM (a), HAA (b), and HNM (c) formation
during chlorination of two synthetic pool water types
at three different pH levels ......................................................................... 168
8.3 Effect of TOC on the formation of THMs (a), HAAs (b),
and HNM (c) from two synthetic pool water types under
the same conditions of swimming pool operation parameters
at TOC 6, 11, and 16 mg/L ........................................................................ 171
8.4 Effect of Br on the formation and speciation of THMs
from BFA-MB (a) and BFA-SJWD (b) synthetic pool water.................... 173
xvii
8.5 Effect of Br on the formation of HAAs and speciation
from BFA-MB (a) and BFA-SJWD (b) synthetic pool water.................... 174
8.6 Br incorporation (n) into THM (a) and HAA (b) at three
different Br levels spiked into two synthetic pool waters .......................... 176
8.7 Effect of Br on HNM formation and speciation during
chlorination of two synthetic pool waters, BFA-MB (a) and
BFA-SJWD (b) .......................................................................................... 178
8.8 Formation of THMs (a), HAAs (b) and HNMs (c) at 26 and
40°C from two synthetic pool waters ........................................................ 180
8.9 HAAs and THMs correlation ..................................................................... 182
9.1 THM formation percent during five days
without Br (a) and with Br (b) ................................................................... 192
9.2 HAA formation percent during five days without Br (a)
and with Br (b) ........................................................................................... 198
9.3 DHAA and THAA formation rate at 20 Cl2/mg TOC in
the absence of Br (a) and at 200 µg/L Br (b) ............................................. 200
9.4 DHAA and THAA formation rate at 100 Cl2/mg TOC in
the absence of Br (a) and at 200 µg/L Br (b) ............................................. 201
9.5 THM4 and HAA9 formation rates during 5-day
incubation from BFA(G) at TOC 5mg/L, pH7, and T= 26°C ................... 202
xviii
LIST OF ABBREVIATIONS
ADD Average Daily Dose
ADI Acceptable daily dose
BAA Bromoacetic acid
BAN Bromoacetonitrile
BCAA Bromochloroacetic acid
BCAN Bromochloroacetonitrile
BCNM Bromochloronitromethane
BDCAA Bromodichloroacetic acid
BDCM Bromdichloromethane
BDCNM Bromodichoronitromethane
BF Body Fluid
BFA Body Fluid Analog
BFA(B) Body fluid analog proposed by Borgmann-Strahsen (2003)
BFA(G) Body fluid analog proposed by Goeres et al. (2004)
BFA(J) Body fluid analog proposed by Judd and Bullock (2003)
BNM Bromonitromethane
Br- Bromide
C Concentration
CAA Chloroacetic acid
CAN Chloroacetonitrile
CC Child competitive swimmer
CDC Center of Disease Control
xix
CDI Concentration daily intake
CH Charleston drinking water treatment plant water source
CNC Child non-competitive swimmer
CNM Chloronitromethane
DBAA Dibromoacetic acid
DBAN Dibromoacetonitrile
DBCAA Dibromochloroacetic acid
DBCM Dibromochloromethane
DBCNM Dibromochloronitromethane
DBNM Dibromonitromethane
DBP Disinfection by-products
DCAA Dichloroacetic acid
DCAN Dichloroacetonitrile
DCNM Dichloronitromethane
DDW Distilled deionized water
DHEC Department of Health and Environmental Control
DOC Dissolved Organic Carbon
DON Dissolved Organic Nitrogen
DPD N, N–diethyl– p–phynylenediamine
DWTP Drinking water treatment plant
ECGC Electrochemically generated chlorine
EPA Environmental Protection Agency (US)
FAC Free available chlorine
FAS Ferrous ammonium sulfate
xx
FC Female Competitive swimmer
FLG Female lifeguard
FNC Female Non-competitive swimmer
FP Formation potential
GV Greenville drinking water treatment plant water source
HAA Haloacetic acid
HAA9 Sum of 9 HAA species (CAA, BAA, DCAA, BCAA, TCAA,
BDCAA, DBAA, DBCAA, and TBAA)
HAN Haloacetonitriles
HBE Human body excretion
HNM Halonitromethane
HI Hazard index
HQ Hazard quotient
IRIS Integrated risk information system
LADD Lifetime average daily dose
MB Myrtle Beach drinking water treatment plant water source
MC Mail Competitive swimmer
MCL Maximum contaminate level
MF Modifying factor
MHO Materials of human origin
MLG Male lifeguard
MNC Mail Non-competitive swimmer
MRL Minimum reporting level
ND Not detected
xxi
NDMA N-nitrosodimethylamine
NOAEL no-observed-adverse-effect
NOM Natural organic matter
NSPF National swimming pool foundation
PDR Potential dose rate
R Lifetime cancer risk
RAIS Risk assessment information system
RfD Reference dose
rpm Round per minute
Sf Safety factor
PF Potency factor: An upper-bound estimate of a chemical probability
of causing cancer over a lifetime age
SJWD Startex-Jackson-Wellford-Duncan drinking water treatment plant
water source
SP Spartanburg drinking water treatment plant water source
SUVA254 Specific ultra violet light absorbance at 254 nanometers
TBA Tribromoacetic acid
TBM Tribromomethane
TBNM Tribromonitromethane
TCAA Trichloroacetic acid
TCAN Trichloroacetonitrile
TCM Trichloromethane (chloroform)
TCNM Trichloronitromethane
THAA Total haloacetic acids
THANs Total haloacetonitriles
xxii
THM Trihalomethane
THM4 Sum of 4 THM species (TCM, BDCM, DBCM, and TBM)
THNM Total halonitromethanes
TLR Total life risk
TOC Total organic carbon
TON Total organic nitrogen
TOX Total organic halides
TTHM Total trihalomethanes
UF Uncertainty factor
UV Ultra violet light
UV254 Ultra violet light at 254 nanometers
WHO World health organization
1
CHAPTER ONE
INTRODUCTION
Swimming is the second most popular sport in the US for all ages and the most
popular children’s recreational activity (Griffiths, 2003; National Sporting Goods
Association, 2006; US Census Bureau, 2009). In the US, there are about 10,000,000
residential pools, and 1,000,000 public swimming pools visited by approximately
56,000,000 people (Appendix A) paying an estimated total of 386,000,000 visits every
year (Griffiths, 2003; Zwiener et al., 2007; SBI, 2007; US Census Bureau, 2009). Usually
people visit swimming pools for relaxation, fitness, and therapy. Users of swimming
pools include young children, elderly people, pregnant women, individuals with
immunological disorders and competitive swimmers. As swimming pools are built and
constructed for fitness and health purposes, it is essential to maintain a healthy
environment in a swimming pool, which depends on the pool construction (design and
engineering), operation, and maintaining safe water quality. Since swimming pools have
large volumes of water, it is not feasible to frequently replenish the water. As a result,
swimming pool water is continuously circulated, filtered and disinfected to maintain clear
and safe water quality. Chlorine is the most common disinfectant used in swimming
pools disinfection and other recreational water systems (Glauner et al., 2005; Li and
Blatchely III, 2007). A disinfectant residual is always maintained in swimming pools.
According to World Health Organization (WHO) guidelines (WHO, 2006), it is
recommended to maintain free chlorine concentrations up to 3 mg/L and 5 mg/L in
normal temperature pools and in hot tubs, respectively. The WHO guidelines also include
2
free chlorine concentration of 1 mg/L for swimming pool with good circulation and
dilution (Erdinger et al., 2005; WHO, 2006; Zwiener et al., 2007). The free chlorine
residual required to be maintained in the swimming pool water is variable across the
world and even among different states in the US. In Germany, the free chlorine
concentrations required by DIN19643 range from 0.3 to 0.6 mg/L in pool water, and from
0.7 to 1 mg/L in spas (hot tubs) (Erdinger et al., 2005; Uhl and Hartmann, 2005; Zwiener
et al., 2007). In the US, UK and Australia, the guidelines require much higher free
chlorine concentrations ranging from 1 to 5 mg/L (Uhl and Hartmann, 2005; SC DHEC,
2007). South Carolina Department of Health and Environmental Control (SC DHEC)
public swimming pool regulations 61-51, published on May 25, 2007, requires
maintaining free chlorine concentrations in the range of 1 to 5 mg/L (SC DHEC, 2007).
Although disinfection is critical for controlling the microbial activity in
swimming pools, it has also important unintended consequences. Disinfectant(s) react
with the organic matter in water producing disinfection by-products (DBPs). Since the
first discovery of trihalomethanes (THMs) in drinking water in the early 1970s, a
significant amount of research effort has been directed toward improving our
understanding of DBPs and, to date, more than 600 DBPs have been identified in
drinking waters (Boorman et al., 1999; Richardson et al., 2007). Despite this daunting
number, only 11 DBPs (four THMs, five haloacetic acids [HAAs], bromate, and chlorite)
are currently regulated (Appendix B) under the US EPA Disinfectants/DBP Rule
(D/DBPR) (Karanfil et al., 2008). The presence of DBPs in water and in air is a major
human health concern because some of these DBPs are carcinogenic; others are
3
mutagenic, while some others have reproductive and developmental effects and outcomes
(Richardson et al., 2007). As a result, some of these DBPs are currently regulated in
drinking waters around the world (WHO, 2000; Richardson, 2003; EPA, 2006; Karanfil
et al., 2008). The presence of DBPs in swimming pools is very problematic because
DBPs in a swimming pool can be ingested, inhaled or absorbed through the skin. In a
swimming event, about 50 mL/hour of water could be ingested by a child and around 25
mL/hour by an adult swimmer (Borneff, 1979; EPA, 1989; Kim, 1997; ACC, 2002;
Dufour et al., 2006). This ingested water volume may increase to 500 mL in a typical
swimming visit especially for children (Borneff, 1979). THMs levels determined in
human blood showed that their concentrations are higher in blood after showering and
bathing than from drinking water (Aggazzotti et al., 1998; Martin et al., 2001; Caro and
Gallego, 2007). Epidemiological studies have also demonstrated that more risk of DBPs
exposure is associated with dermal and inhalation from swimming, showering and
bathing than ingestion from drinking water (Caro and Gallego, 2007; Richardson et al.,
2007; Villanueva et al., 2007a; 2007b). Therefore, understanding the formation and
control of DBPs in swimming pools have important public health consequences
considering the widespread use of swimming pools in the US.
The formation of DBPs in swimming pools depends on the organic matter
characteristics and the operation conditions of the pools (e.g., type and amount of
disinfectant, pH, temperature, bromide level in water, and dilution factor -replacement of
part of swimming pool water with fresh water). There are two organic matter sources in
the swimming pools: (i) natural organic matter (NOM) coming from the distribution
4
system that provides the water to the swimming pool (i.e., filling water), and (ii) the body
excretions (i.e., bather load) added by swimmers. NOM consist of the organic matter
remaining in the water after treatment operations in the drinking water treatment plant.
Since water is disinfected and maintaining a residual disinfectant concentration is
required in the distribution systems in the US, some amount of DBPs are already formed
in water. Thus, DBPs exist already in the filling water. However, the DBPs formation
potential of NOM is not completely exhausted in the distribution system because
disinfection in drinking water treatment plants is performed in a balanced manner to
eliminate microbial activity, while minimizing the DBP formation in order to comply
with the drinking water regulations. Therefore, the NOM components continue to form
DBPs as a result of high disinfectant (chlorine) residuals maintained in swimming pools
and long contact (reaction) time also.
The bather load is a mixture of particles (like skin cells, hair, and
microorganisms) and soluble organic and inorganic excretions composed mainly of urine,
sweat, dirt, saliva, and lotions (synthetic chemicals such as sunscreen, cosmetics, soap
residues, etc.). The bather load is the sum of the initial load introduced at the first entry of
a swimmer in the pool and the subsequent load that the swimmer excretes during the
swimming event. Body fluids (BFs), urine and sweat, mainly consist of ammonia, urea,
creatinine, arginine, citric acid, uric acid, glucronic acid, and amino acids (Putnam, 1971;
Anipsitakis et al., 2008; Barbot and Moulin, 2008), and they serve as potential precursors
of DBPs. It is estimated that a bather releases a mixture of 25 to 80 mL urine and 200 to
1000 mL sweat in an average one hour swimming event (Gunkel and Jessen, 1988;
5
Erdinger et al., 1997; Judd and Bullock, 2003; WHO, 2006). The bather input of organic
material may reach several grams during a bathing time (Borneff, 1979; Batjer et al.,
1980; Eichelsdorfer et al., 1980; Althaus and Pacik, 1981; Thacker and Nitnaware 2003;
Zwiener, 2007; Zwiener et al., 2007). Each swimmer release nitrogenous compounds into
the pool water that reach about 850 mg N per hour swimming (Seux, 1988). From a
survey of one thousand US adults, 17 percent said that they urinate while swimming in
pool water (CNN, 2009). These inputs accumulate and increase in the swimming pool
with time since the operational practices are not typically correlated to the number of
swimmers using the pools (Zwiener et al., 2007). The dissolved organic carbon (DOC)
concentration is significantly increased by the number of swimmers using a pool. DOC
levels reported in eight different indoor swimming pools in London ranged between 3.3
and 12.9 mg/L (Chu and Nieuwenhuijsen, 2002). Thacker and Nitnaware (2003) reported
a range of 93.8 µg/L and 16 mg/L total organic carbon (TOC) in swimming pool waters,
and they related the high TOC content to the number of swimmers. The increase in DOC
or TOC also results in more formation of DBPs and total organic halides (TOX) in the
pools (Chu and Nieuwenhuijsen, 2002; Glauner et al., 2004).
Although various disinfectants can be used for disinfection in swimming pools,
chlorine is by far the most commonly used disinfectant because of its availability, low
cost, efficiency, and capability of providing continuous residual in contrast to other
disinfection methods (e.g., UV light) that do not have lasting disinfection effect (Judd and
Black, 2000; Thacker and Nitnaware, 2003; Glauner et al., 2005; Zwiener et al., 2007).
As a result, alternative disinfectants other than chlorine have not been widely used in
6
swimming pools (Erdinger et al., 2005; Zwiener et al., 2007). Chlorine is introduced to
the pool water in either gas (Cl2 gas), liquid (e.g., sodium hypochlorite) or solid (e.g.,
calcium hypochlorite dry tablets) forms. Regardless of the form, when chlorine is added
to water, it forms hypochlorous acid (HOCl) and hypochlorite ions (OClˉ). At some
swimming pools, chlorine is generated electrochemically in-situ from sodium chloride
that is added to water.
The presence of bromide in the swimming pool water is also important because it
plays the major role in the formation of brominated DBP species (Judd and Jeffrey,
1995). Free chlorine in water oxidizes bromide forming hypobromous acid that reacts
with the organic matter producing brominated or mixed brominated-chlorinated DBPs
which are considered to have more toxic effects than chlorinated species (Icihashi, et al.,
1999; Duirk and Valentine, 2007; Plewa et al., 2008a, 2008b).
The pH conditioners are added to the swimming pool waters to keep the pH
within a desired certain range all the time. The pH range of the swimming pool water has
an important effect on the efficiency of the disinfection process, DBP formation and
speciation, and the tolerance of fabrics used for swimming clothes and accessories. The
pH of the water also affects the formation of DBPs classes differently (Nikolaou et al.,
2004). The pH required by the DIN19643 in Germany is within the range 6.5 to 7.2,
while the WHO guidelines and the SC DEHC regulations are in the range of 7.2 to 7.8
(WHO, 2006; SC DHEC, 2007).
Epidemiologic studies have shown that some chlorinated and brominated DBPs
are suspected human carcinogens (capable of inducing cancer) and others are considered
7
mutagenic (can induce an alteration in the structure of DNA) in addition to their potential
reproductive and developmental adverse effects (Villanueva et al., 2007a; 2007b;
Richardson, et al., 2007). Recent studies of the risk of exposure to THMs have
demonstrated that much exposure and risk are related to showering, bathing and
swimming rather than drinking water (Whitaker et al., 2003; Nuckols et al., 2005;
Gordon et al., 2006; Villanueva et al., 2007a; 2007b). DBPs are suspected to be
carcinogenic and toxic to living cells (Bull et al., 1990; DeAngelo et al., 1991; Loos and
Barcelo, 2001). The DBP species that are regulated in drinking water are considered as
probable human carcinogens (B2 cancer classification).
Although the most advanced and stringent regulations for DBPs in drinking
waters around the world are imposed in the US, DBPs formed in swimming pools are not
yet regulated in the US, and there is no federal regulatory agency that has authority on
swimming pools and other similar water parks. The responsibility of regulating
swimming pools and overseeing their operations has been assigned to the departments of
health and environmental control in each state. This leads to a considerable variation
across the country in terms of requirements, enforcement, and compliance (CDC, 2008;
Pool Operation Management, 2009). In contrast, there are some regulations for DBPs in
swimming pools in European countries (e.g., Germany, Switzerland, and Denmark)
despite their weaker DBP regulations in drinking waters as compared to the U.S. In
Germany and Switzerland THMs levels should not exceed 20 µg/L as CHCl3 in
swimming pools and 50 g/L as CHCl3 in swimming pools in Denmark (Bisted, 2002;
Borgmann-Strahsen, 2003; Uhl, 2007). The National French Institute of Research and
8
Security recommends a maximum of 0.5 mg/m3
in the air around a swimming pool
(Barbot and Moulin, 2008).
The main objective of this research was to investigate the occurrence and
formation of three DBP classes (THMs, HAAs, and HNMs) under swimming pool
operation conditions as practiced in the US and estimate their potential adverse health
impacts on swimmers. Following are the specific research objectives: (1) to examine the
occurrence of five DBPs (THMs, HAAs, HNMs, NDMA, and HANs) in indoor
swimming pools in the US, (2) to conduct a multi-pathway risk assessment on THMs
(TCM, BDCM, DBCM) and HAAs (DCAA and TCAA) of swimming pool water, (3) to
determine the role and contribution of the two main precursors (i.e., filling water NOM
vs. body fluids (BF) from swimmers) to the formation of THMs, HAAs, and HNMs in
swimming pools, (4) to investigate the impacts of swimming pool operational parameters:
free available chlorine (FAC), pH, bather load (TOC), water bromide content, and
temperature on the formation and speciation of THMs, HAAs, and HNMs, and (5) to
determine the formation of THMs and HAAs from the body fluid precursors during
turnover time of swimming pool water, especially at short reaction times.
9
CHAPTER TWO
BACKGROUND
In this chapter swimming pool operational and management parameters will be
overviewed briefly. Then chlorine and chloramines chemistry in water will be discussed.
Subsequently our current knowledge of DBPs formation and occurrence and their
precursors in swimming pools will be introduced. At the end epidemiological studies and
health effects related to DBPs in swimming pools will be reviewed.
Swimming Pool Operation and Management
It is essential to maintain a healthy environment in a swimming pool; as a result,
water in swimming pools is circulated, treated, and disinfected continuously while some
adjustments are also made in the water temperature and pH (Figure 2.1). Since swimming
pools have large volumes, it is not feasible to frequently replace the water; as a result, it
is not uncommon to see the same water staying two to three years in swimming pools (the
same water is circulated and recycled for several years without any replacement). The
following list includes the most common management practices and treatment processes
frequently used in swimming pools:
1- Filtration: Filters are essential to preserve water clarity and to decrease the
disinfectant demand by eliminating the suspended particulates from water. An
important role of filtration is the removal of oocysts and cysts of Cryptosporidium
and Giardia and other protozoa. Filters, however, do not remove dissolved materials
from water. Sand filters, diatomic filters, cartridge filters, and ultrafine filters are the
10
most common configurations used in swimming pools (Hagen, 2003; Glauner et al.,
2005; WHO, 2006; SC DHEC, 2007; Zwiener et al., 2007). In the US, the most
common filters used by the swimming pool industry are sand filters (Griffiths, 2003).
2- Coagulation and flocculation: Coagulants are mainly used to flocculate suspended
materials and to improve their removal during filtration. This is important in
removing the oocysts and cysts of Giardia and other microorganisms and organic
precursors (WHO, 2006; Zwiener et al., 2007), provided that chlorine is not effective
against Cryptosporidium but can inactivate Giardia at high relatively concentrations
(Korich et al., 1990; AWWA, 1990; PWTAG, 1999; Black and Veatch Corporation,
2010). Coagulation-flocculation is not a common practice in swimming pool water
treatment in the US; however, in a few countries, such as Germany, it is a
requirement to comply with the swimming pool water regulations (e.g., DIN19643).
3- Disinfection: Disinfection is mainly to inactivate microorganisms to prevent any
possible water borne diseases. Chlorine is the most commonly used form of
disinfectant, since it is possible to maintain continuously a consistent level of
disinfectant in pool water. Regardless of the form (gas, liquid or solid) of application,
chlorine, when added to water, forms hypochlorous (HOCl) and hypochlorite ions
(OClˉ). HOCl and OClˉ constitute free available chlorine (FAC). Chlorine can also
react with ammonia to form chloramines as discussed in the following sections. The
required disinfectant residual levels in swimming pools vary widely around the world
ranging from as low as 0.3 mg/L to 5 mg/L as FAC (WHO, 2006; SC DHEC, 2007;
Zwiener et al., 2007).
11
Figure 2.1: A schematic diagram of swimming pool. NOM (natural organic
matter in filling water), HBE (human body excretions). Dashed line shows
intermittent uses.
4- pH Adjustment: The pH of swimming pool is maintained within a range that will (i)
be tolerable to and acceptable by bathers, and (ii) minimize any negative impact on
the pool pipes, construction, and swimmers fabrics. pH is also an important parameter
for disinfection effectiveness of chlorine (pKa of HOCl= 7.6). HOCl is the dominant
specie at pH values below pH 7, while OClˉ is the dominant specie at alkali pH
conditions. HOCl is a more powerful disinfectant than OClˉ (AWWA, 1990; White,
1999).
5- Dilution: Dilution of pool water is used to reduce the accumulation of materials
continuously added by the swimmers and to conserve water quality and clarity that
cannot be maintained by other methods or operational practices. Thirty liters per
Cl2
Coagulant (optional)
Wastewater
Backwash water
Filling water (NOM & Br-)
Volatile DBPs
Splash water
pH adjustment
Cl2
Drainage basin Heat exchangerFilter(s)
DBPsNOM
HBE
Br-
+
12
bather per day is used in England and Germany, while fifty liters per swimmer is
replaced in France (PWTAG, 1999; WHO, 2006; Tintometer GmbH, 2006; Barbot
and Moulin, 2008). Dilution is not a requirement in US; as a result it is not used by
the majority of the swimming pools.
6- Heating: The swimming pool water should be maintained at a constant temperature
depending on the pool type and usage. In general, the temperature of swimming pool
water ranges from 26°C in competitive pools to 40°C in therapeutic hot tubs and spas.
7- Circulation (turnover): In order to achieve comprehensive filtration, disinfection and
maintain water quality, an equivalent volume to the whole water body in a swimming
pool should be turned over (circulated) in a period of time. “Turnover Time means
the period of time (usually 6-8 hours) required to circulate the complete volume of
water in a pool through the recirculation system” (SC DHEC, 2007). Continuous
circulation in a swimming pool is necessary to maintain the required water quality
(WHO, 2006; Zwiener et al., 2007; SC DHEC, 2007). The WHO guidelines
recommend ―good‖ circulation and dilution. However, no specific guideline for what
is considered ―good‖ circulation or dilution has been developed. SC DEHC (2007)
regulations recommend that an acceptable circulation of the swimming pool water
should achieve a turnover of an equivalent volume of the swimming pool water
volume within several (4-6) hours depending on the swimming pool type and use.
8- Super-chlorination (shock treatment): An extra large chlorine dose that raise the FAC
for 8-10 mg/L for few hours is applied frequently when the pool is not being used by
swimmers (SC DEHC, 2007). This high chlorine dose is applied to oxidize the
13
organic compounds and prevent algae growth in the pool. Shock treatment is applied
either as a routine treatment operation or occasionally after vomiting or an accidental
fecal release (Chrostowski, 2004).
9- Filling water: The water used in filling swimming pools and for any make up for
water losses during operation should be obtained from a public drinking water system
(SC DEHC, 2007). It is recommended to avoid chloraminated water for filling
swimming pools (IAF, 2005). Chloraminated water has high (1-3 mg/L) inorganic
chloramines (monochloramine (NH2Cl) and dichloramine (NHCl2). Chlorine must be
added at five to ten times the chloramines concentration to reach the break point and
eliminate these chloramines (IAF, 2005). Chloramines irritating smell and other
suspected health effects (e.g., Asthma, irritant eye, nasal and throat symptoms)
(Massin et al., 1998; Thickett et al., 2002) make them undesirable in pool water.
Chloramines, particularly trichloramine (NCl3), are volatile (Holzwarth et al., 1984;
Blatchley et al., 1992). Inorganic chloramines are suspected to cause eye, nasal, throat
and respiratory tract irritation and affects lungs also (Carbonnelle et al., 2002;
Lagerkvist et al., 2004; Bernard et al., 2005). Respiratory illness and asthma are
thought to be result from exposure to these volatile chlorination byproducts (Thickett
et al., 2002; Bernard et al., 2003). These possible human health effects regarding the
atmospheric and air quality of indoor swimming pool are the reason behind avoiding
these compounds during swimming pool treatment.
All these operational and management practices are of great importance regarding
chlorination and hence the formation and accumulation of DBPs in swimming pools.
14
Acceptable disinfection with reduced DBP formation can be reached through proper
management and operational criteria and water treatment (Judd and Bullock, 2003;
Zwiener et al., 2007). However, the effect of operational parameters on DBPs levels and
their classification and speciation are still not well known (Judd and Black, 2000).
In the US, no federal regulatory agency has the authority on swimming pools and
water parks. The responsibility of regulating swimming pools and fulfillments of
requirements is assigned to each state. This leads to a considerable variation across the
country in terms of requirements, enforcement, and compliance (CDC, 2008; Pool
Operation Management, 2009). As a result, swimming pool regulations are significantly
weaker as compared to drinking water regulations, and little research has been conducted
to examine the impacts of swimming pool water quality on public health (WHO, 2006;
Zwiener et al., 2007).
Chlorine and Chloramines Chemistry
The majority of swimming pools in the US and around the world use chlorine as a
disinfectant (Griffiths, 2003; Anipsitakis et al., 2008). The advantage of chlorine stems
from its availability, ease of use, efficacy, and ability to maintain a long-lasting residual
for disinfection. Chlorine may be introduced in different forms to the swimming pool
water. There are three most common forms of chlorine that are usually used in
chlorination of swimming pools and developing free chlorine residual. These are chlorine
gas (Cl2(g)), sodium hypochlorite (NaOCl) which is available as a liquid, or calcium
hypochlorite (Ca(OCl)2) in the solid form. Regardless of the dosed form of chlorine, it
15
will react with water and produce hypochlorous acid (HOCl), and hypochlorite (OClˉ).
The mixture of both hypochlorous acid and hypochlorite is considered free chlorine
residual and referred to as free available chlorine (FAC). The proportion of the two
species (hypochlorous acid and hypochlorite) is pH dependent (Deborade and Gunten,
2008).
The chlorine gas reacts with water producing hypochlorous acid and hydrochloric
acid (White, 1999; Deborade and Gunten, 2008):
Cl2 + H2O ↔ HOCl + H+ + Cl
ˉ (2.1)
HOCl ↔ OClˉ + H
+ (2.2)
The hypochlorite salts of sodium and calcium dissociate in water producing the
hypochlorite ion
NaOCl ↔ Na+ + OCl
ˉ (2.3)
Ca(OCl)2 ↔ Ca2+
+ 2OClˉ (2.4)
The hypochlorite ions react with H+ depending on the pH, establishing the equilibrium
with hypochlorous acid
OClˉ + H
+ ↔ HOCl (2.5)
From the above equations of chlorine chemistry in water we can see that the gas form of
elemental chlorine tends to decrease the pH, while the sodium and calcium hypochlorites
tend to increase the pH. Thus in the management and operation of swimming pools it is
critical to adjust pH for maintaining the disinfection action efficiency. An acidic pH
conditioner is necessary when hypochlorite salts are dosed to the pool, while a basic pH
conditioner is required in the case of using chlorine in the gas form. The pK of
16
hypochlorous acid (pK=7.54) dictate the proportionality of hypochlorous and
hypochlorite that also control the disinfection efficiency (Deborade and Gunten, 2008).
HOCl is one thousand times more effective than OClˉ (AWWA, 1990; White, 1999;
AWWA, 2005). Equal proportions of HOCl and OClˉ are found at pH 7.54 but this
proportionality changes according to pH. At pH 6 or less, HOCl predominate, while OClˉ
predominates at pH 9 and greater (Clark and Sivaganesan, 2002). Since HOCl is a
stronger disinfectant than OClˉ, the optimum and most powerful disinfection action pH
range of swimming pool water should be kept between 6.5 and 7.5 (Suslow, 2001).
When chlorine is added to water it reacts rapidly with organic and inorganic
constituents.
HOCl + X → X-Cl(n) (2.6)
Oxidation, addition, elimination or substitution reactions are the major reaction types that
occur as a result of water chlorination between chlorine and organic and inorganic water
constituents (Lahl et al., 1981; Clark and Sivaganesan, 2002; Deborade and Gunten,
2008). Consequently, chlorine is consumed until the demand is satisfied. To achieve a
preset goal of residual free chlorine concentration (FAC) the chlorine demand of the
chlorinated water should be satisfied. The chlorine demand of particular water is
dependent on the water constituents, contact time, temperature, pH, and initial chlorine
dose (Clark and Sivaganesan, 2002). The formation of halogenated disinfection by-
products (DBPs) is a function of chlorination conditions, water constituents and quality,
and contact time (reaction time) also.
17
Chlorine can also oxidize bromide to bromine when it is available in the water
(Deborade and Gunten, 2008). The following oxidation-reduction reaction can describe
the production of hypobromous (HOBr) under the conditions of water chlorination in a
swimming pool
OClˉ +Brˉ + H2O → Clˉ + HOBr + OHˉ (2.7)
Thus similar to chlorination reactions, bromination reaction are taking place resulting in a
mixture of chlorinated, brominated, and bromochlorinated species of DBPs (Chu and
Nieuwenhuijsen, 2002; Kim et al., 2002; Glauner et al., 2005; WHO, 2006). The bromine
substitution reaction is more rapid than chlorine with organic compounds producing more
mutagenic and toxic brominated-DBPs (Westerhoff et al., 2004).
Another important class of chlorine reactions is its reaction with nitrogenous (e.g.
ammonia) substances. When chlorine reacts with ammonia in water chloramines are
formed. The formation of three different chloramines species can be summarized in the
following three sequential reactions (Hailin et al., 1990; Bryant et al. 1992; Black and
Veatch Corporation, 2010)
HOCl + NH3 ↔ NH2Cl (monochloramine) + H2O (2.8)
HOCl + NH2Cl ↔ NHCl2 (dichloramine) + H2O (2.9)
HOCl + NHCl2 ↔ NCl3 (trichloramine) + H2O (2.10)
The rate of these reactions is dependent on the water pH, temperature and the Cl2/N ratio.
At lower Cl2/N ratio monochloramine dominates, while dichloramine formation increases
by increasing Cl2/N ratios. Dichloramine is odorous and its formation should be avoided
during pool water chlorination. Further increase in the Cl2/N ratio ends with oxidizing
18
ammonia to nitrogen (N2) and chlorine is reduced to chloride which are the conditions
known as the ―breakpoint‖ after which free chlorine starts to increase in water with a
direct proportion to chlorine dose applied. After achieving the breakpoint in swimming
pool the odor caused by dichloramine is minimized. Regarding solubility of chloramines
in water and Henry’s law constant, trichloramine is the most likely to be found in the air
above swimming pool water whereas mono- and dichloramine can reach the air via water
droplets produced by the disturbance of the surface of the water rather than as an
insoluble gas (Holzwarth et al., 1984).
Disinfection By-Products in Indoor Swimming Pools
A long lasting disinfectant residual in a swimming pool is required and chlorine is
still the most wide used disinfectant to maintain acceptable swimming pool water
biological quality (Griffiths, 2003; Anipsitakis et al., 2008; NSPF, 2006). However, since
the discovery of THMs formation in chlorinated drinking water and their related health
risk, some studies have been conducted to investigate their formation in swimming pools
and partitioning between water and air. These investigations have included measurements
of THMs in swimming pools and in bench and pilot scales experiments using human
origin material (HOM), body fluid analogs (BFA), or microbial suspensions (Batjer et al.,
1980; Beech et al., 1980; Lahl et al., 1981; Judd and Black, 2000; Kim et al., 2002;
Erdinger et al., 2005).
Disinfection by-products (DBPs) are formed from the reactions of dissolved
organic matter (DOM) with oxidants and disinfectants. The majority of DBPs are
19
halogenated organics that are generally characterized as total organic halide (TOX)
(Reckhow, 2008). Swimming pools water is always disinfected for inactivation of
waterborne microbial pathogens. Chlorine in different forms is applied as the
disinfectant. Koski et al. (1966) conducted a study comparing the efficiency of three
disinfectants for swimming pool water disinfection. The results showed that chlorine was
more effective than bromine which was also more effective than iodine.
In the 1980s, the first studies of trihalomethanes and other chemical constituents
in indoor public swimming pools water and air were published. In these studies
chloroform and other halomethanes were measured in public indoor swimming pools in
Bermen, Germany, in 1979 and in the US in 1980 (Batjer et al., 1980; Beech et al., 1980;
Lahl et al., 1981). Maximum chloroform concentration was 1200 µg/L in pool water, and
384 µg/m3 in air (i.e., within 2 meters from the water surface) in Germany pools (Batjer
et al., 1980). Total trihalomethanes ranged between 96 and 1287 µg/L in different type of
swimming pools filled either with fresh or saline water in the US (Beech et al., 1980).
Also mutagenic activity of swimming pool water was investigated using
Salmonella/mammalian-microsome test; results indicated that a variety of mutagens in
the complex mixture of pool water is present (Honer et al., 1980). Batjer et al. (1980) and
Beech et al. (1980) concluded that the high concentrations of chlorination by products in
swimming pools water did not result from only the natural organic matter in the filling
waters (i.e., local drinking waters). Instead they related their formations to the swimmers
input of ―several grams of organic compounds‖ such as urine into the swimming pool
water. Another study also showed that the swimming pool trihalomethanes content was
20
much higher than the trihalomethanes in the drinking water source (Lahl et al., 1981).
This led to the conclusion that precursors for THMs formation in swimming pools water
were not only the natural organic matter in the drinking water that was used for filling the
swimming pools or the make-up of the lost water. Urine was suggested as the cause of
the high chlorinated THM species observed in swimming pools, and the overall THM
formation was correlated to the pool users. The researchers also concluded that pool
water quality could be improved by diluting the water of the pool frequently (Lahl et al.,
1981).
Whirlpool spas or hot tubs are swimming pools in which water temperature may
reach 40°C and halogen disinfection (chlorine or bromine) is continuously applied. The
occurrence of trihalomethanes in the water and air of these hot whirlpools was
investigated. When chlorine was used as disinfectant chloroform dominated, however,
bromoform was the dominant species when bromine was the disinfectant (Benoit and
Jackson, 1987). Chloroform maximum level was 750 µg/m3 and 674 µg/L in air and
water respectively, while bromoform maximum level was 1910 µg/m3 and 3600 µg/L in
air and water respectively (Benoit and Jackson, 1987). Sandel (1990) reported data of
about 114 residential pools in the US; in his report the chloroform maximum amount was
313 µg/L and the average is 67.1 µg/L. In Italy chloroform reported in swimming pools
water and air were 9-179 µg/L and 16-853 µg/m3, respectively, and within the range of
0.1-3 µg/L in the plasma of 127 swimmer volunteers (Aggazzotti et al., 1995; 1998). The
alveolar air content of swimmer volunteers was 14-312 µg/m3 (Aggazzotti et al., 1995;
1998). In another Italian study the levels THMs were 17.8-70.8 µg/L in water and 26-58
21
µg/m3 in air (Fantuzzi et al., 2001). In a swimming pool model two disinfectants were
used, hypobromous and hypochlorous acids, to disinfect human urine analog prepared
mainly from sodium chloride, urea, creatinine, citric acid, and ammonia. In this synthetic
swimming pool water disinfection, it was concluded that only the urine concentration and
disinfectant type had a significant effect on THMs total amount and species formed (Judd
and Jeffrey, 1995). In Ireland, THMs determined in swimming pools were 105-134 µg/L
in which chloroform was about 86 percent (Stack et al., 2000). A study on THMs in
water from swimming pools in London found that the mean value of TTHMs was 132.4
µg/L of which the chloroform mean value was 113.3 µg/L (Chu and Nieuwenhuijsen,
2002). Material of human origin (such as hair, saliva, skin and urine) and a body lotion
were chlorinated separately and together as a mixture in two water sources (surface and
ground water) (Kim et al., 2002). In both waters five different DBPs (chloroform,
bromodichloromethane, chloral hydrate, dichloroacetonitrile, and trichloropropane) were
detected (chloroform was the major product) and increased in different amounts
compared to the control water (Kim et al., 2002). Creatinine, urea, and other nitrogenous
compounds including amino acids, which are present in both urine and perspiration of
humans were used as model compounds to study the production and occurrence of
inorganic chlorination byproducts (chloramines) in swimming pools (Tachikawa et al.,
2005; Li and Blatchley III, 2007). Recently UV combined with chlorine was investigated
in indoor swimming pool water disinfection in France. Results showed acceptable
bacteriological levels in compliance with the French requirements, but chloroform and
bromodichloromethane were increased considerably, whereas bromoform and
22
dibromochloromethane decreased. These results were explained by the effect of UV on
increasing chlorine activity in reacting and forming more haloforms (Cassan et al., 2006).
Three THM species, three inorganic chloramines, and other volatile by products were
measured in eleven indoor swimming pool water samples (Weaver et al., 2009). About
92% of the samples measured had THMs more than 20 µg/L and THMs measured in
45.3% of the samples exceeded the MCL (80 µg/L) in drinking water regulations
(Weaver et al., 2009).
HAAs occurrence in swimming pools waters has not been investigated as much as
THMs, although HAAs are usually formed in parallel with the formation of THMs they
are mostly at lower levels compared to THMs but in some waters HAAs exceeded the
THMs levels (Chellam 2000; Zhang and Minear, 2002; WHO, 2006). In drinking water,
levels of some HAAs were found to be at the same level as THMs (Guy et al., 1997). In
order to study human exposure to DCAA and TCAA from chlorinated water during
household use and swimming, Kim (1997) measured DCAA and TCAA in nine samples
from three indoor pools during 1995-1996. DCAA and TCAA measured by Kim (1997)
were in the range 52-647 µg/L and 57-871 µg/L, respectively. In Spain HAAs were
reported in the range of 1300 - 3200 µg/L (Loos and Barcelo, 2001) and from 307 µg/L
to 330 µg/L (Sarrion, 2000). In another study of indoor swimming pools water in Italy,
HAAs were found to exist in the range of 81-215 µg/L (Fantuzzi et al., 2007).
THMs and HAAs are the main and the only regulated organic DBPs in drinking
water. Although less investigated and monitored in pools, THMs and HAAs seem to
occur at higher levels in swimming pools. The information and factors affecting their
23
occurrence under swimming pool chlorination conditions is limited, especially in the US.
THMs and HAAs occurrence data reported in the literature for swimming pools from a
wide variety of countries were compiled during this study (Table 2.1 and 2.2). Data about
occurrence of DBPs in indoor swimming pools is lacking compared to other countries.
Table 2.1: Trihalomethanes (THMs) reported in indoor swimming pools in different
countries
Country THMs
µg/L
TCM
µg/L
BDCM
µg/L
DBCM
µg/L
TBM
µg/L Reference
Italy 19-94 Aggazzotti et al., 1993
9-179 Aggazzotti et al., 1995
25-43 1.8-2.8 0.5-10 0.1 Aggazzotti et al., 1998
17.8-70.8 Fantuzzi et al., 2001
USA 113-430 Beech et al., 1980;
3-580 0.1-105 0.1-48 0.1-183 Armstrong and Golden, 1986
Germany 1200 Batjer et al., 1980
2.4-29.8 Eichelsdorfer and Jandik., 1981
43-980 0.1-150 0.1-140 0.1-88 Lahl et al., 1981
0.5-23.6 1.9-16.5 0.1-3.4 0.1-3.3 Ewers et al., 1987
40.6-117.5 4.2-5.4 0.78-2.6 Puchert et al., 1989
80.7 8.9 1.5 0.1 Puchert, 1994
3-27.8 0.69-5.64 0-6.51 0.02-0.83 Cammann & Hubner, 1995
7.1-24.8 Erdinger et al., 2004
Denmark 145-151 Kaas and Rudiengaard, 1987
Hungary 2-62.3 1-11.4 Borsanyi, 1998
UK 45-212 2.5-23 0.67-7 0.67-2 Chu and Nieuwenhuiijsen, 2002
Ireland 105-134 Stack et al., 2000
Poland 35.9-99.7 2.3-14.7 0.2-0.8 0.2-203.2 Biziuk et al., 1993
TTHM (total trihalomethanes), TCM (chloroform), BDCM (bromdichloromethane), DBCM
(dibromochloromethane), and TBM (tribromomethane)
24
Table 2.2: Haloacetic acids (HAAs) reported in indoor swimming pools in different
countries
Country THAAs
µg/L
CAA
µg/L
BAA
µg/L
DCAA
µg/L
DBAA
µg/L
TCAA
µg/L Reference
Germany 2.6-81 0.5-3.3 1.5-192 0.2-7.7 3.5-199 Stottmeister and
Naglitsch, 1996 25-136 Mannschott et al., 1995
2.3-100
Spain 307-330 Sarrion et al., 2000
1300-3200 Loos and Barcelo, 2001
Italy 81-215 Fantuzzi et al., 2007
THAA (total HAA), CAA (chloroacetic acid), BAA (bromoacetic acid), DCAA (dichloroacetic
acid), DBAA (dibromoacetic acid), TCAA (trichloroacetic acid), DBAA (dibromoacetic acid)
N-nitrosamines
Nitrosamines are a group of non-halogenated DBPs. The presence of mutagenic
and carcinogenic N-nitrosamines in chlorinated or chloraminated water has attracted
attention for the last ten years. Nitrosodimethylamine (NDMA) was initially identified in
Ontario, Canada, in drinking water in 1980s and 1990s. Then NDMA was identified at
ng/L concentrations in chlorinated and/or drinking waters, and at higher levels in
chlorinated wastewaters. In a survey of 145 Ontario drinking water plants, NDMA
concentration in the treated water was in the range of 5 to 9 ng/L (Jobb et al., 1994).
Results from California Department of Health Services survey in 2001 showed that
NDMA ranged between 5 and 10 ng/L or more depending on treatment process (CDHS,
2002). High levels of NDMA (3µg/L) were detected in groundwater from an aquifer that
received effluents from wastewater recharge (Mitch et al., 2003). Sources of NDMA
were thought to be anthropogenic contaminants, such as rocket fuels, plasticizers,
25
polymers, batteries and other industrial sources and microbiological transformation of N-
precursors or partial oxidation of hydrazines (Gunnison et al., 2000; Richardson, 2003).
Mainly N-nitrosodimethylamine (NDMA) was found in finished water which could be
attributed to the use of chlorine or chloramine for the disinfection of drinking water or
wastewater (Mitch et al., 2003; Sedlak et al., 2005; Pehlivanoglu-Mantas et al., 2006). It
was proposed that dichloramine which is produced, besides monochloramine, from
chlorine and ammonia reacts with specific organics in water yielding NDMA (Schreiber
and Mitch, 2006). Another proposed pathway was that breakpoint chlorination conditions
likely involves reactive nitrosating intermediates formed from hypochlorite and nitrite
(Choi and Valentine, 2003; Schreiber and Mitch, 2007). NDMA is an emerging water
contaminant that is of interest to the environmental community because of its miscibility
with water, as well as its carcinogenicity and toxicity. NDMA is an unintended byproduct
of water treatment that uses mainly chloramines for disinfection (Mitch et al., 2003;
Bradley et al., 2005). These nitrosamines compounds were found especially in
chloraminated drinking water and were also found in chlorinated swimming pools water
(Walse and Mitch, 2008). Nitrosamines can form as a result of chloramine or chlorine
used during water treatment but more after chloramination (Najm and Trussell, 2001;
Wilczak et al., 2003; Charrois, 2007). Previously it was suggested that NDMA can be
formed by the reaction of dimethyl amine with monochloramine (Choi and Valentine,
2002; Mitch and Sedlak, 2002). Chlorination or chloramination of model compounds
such as diuron, a herbicide that contains a dimethylamine functional group formed
NDMA (Chen and Young, 2008). High concentrations of NDMA were formed from
26
dimethyamine, trimethylamine, benzalkonium chloride (a quaternary amine) and its
breakdown product dimethylbenzylamine (Mitch et al., 2009). The formation of other
nitrosamines such as N-nitrosopyrrolidine (NDPA), N-nitrosopiperidine (NPIP), N-
nitrosmethylethylamine (NMEA), N-nitrosodiethylamine (NDEA), N-
nitrosodibutylamine (NDBA), and N-nitrosodiprpylamine (NDPA), from chlorination or
chloramination of water has also been shown (Zhao et al., 2008).
NDMA is classified as a B2 carcinogen –reasonably anticipated to be a human
carcinogen (ATSDR, 1999; IRIS, 2009). Nitrosamines are a group of the most toxic and
carcinogenic chemicals. Their carcinogenic effect was observed at very low
concentration (ng/L) levels. EPA classifies these compounds as ―probable human
carcinogens‖ and determined their 1 in one million cancer risk level in drinking water is
as low as 0.7 ng/L (EPA, 1997; Andrzejewski et al., 2005; IRIS, 2009). Exposure to high
levels of NDMA may cause liver damage in humans. Symptoms of overexposure include
headache, fever, nausea, jaundice, vomiting, and dizziness (ATSDR, 1999; HSDB, 2007).
EPA has included six of these nitrosamines in the proposed unregulated contaminant
monitoring rule (EPA, 2005). Since 2003, Ontario has established a drinking water
quality standard of 9 ng/L for NDMA (Government of Ontario, 2009), while California
has set a notification level of 10 ng/L for NDMA (CDHS, 2009). A guide value of 12
ng/L for NDMA has been in effect in the Netherlands since 2004. In Germany a guide
value of 10 ng/L for NDMA and N-nitrosmorpholine (NOMR) is recommended (Planas
et al., 2008), and recently guidelines have been published for nitrosamines in the UK with
27
the water utilities required to take action to reduce concentrations of nitrosamines when
the concentration is greater than 10 ng/L (DWI, 2008).
Only one recent study measured nitrosamines in swimming pools, hot tubs, and
aquaria (Walse and Mitch, 2008). In this study nitrosamines were found at higher levels
in pools than in drinking water though indoor pools had more than outdoor pools. Higher
nitrosamines in pools were attributed to nitrogenous components of body fluids that are
introduced continuously by swimmers and also to the intensive and continuous
chloramines formation under swimming pools treatment conditions. NDMA was the most
abundant nitrosamine in swimming pools water and was 500-fold greater than in drinking
water. Other nitrosamines were detected also but at lower levels compared to NDMA.
In 2004, the EPA established a method (EPA method 521) for nitrosamines
measurement in water (US EPA, 2004). Nitrosamines that are included in the EPA
method for their determination in finished water are N-nitrosodimethylamine (NDMA),
N-nitrosomethylethylamine (NMEA), N-nitrosodiethylamine (NDEA), N-nitrosodi-n-
propylamine (NDPA), N-nitrosodi-n-butylamine (NDBA), N-nitrosopyrollidine (NPYR),
and N-nitrosopiperidine (NPIP).
Other Disinfection By-Products
Other DBPs were identified in limited research conducted in swimming pools.
These include chloral hydrate, chlorate, chloropicrin, cyanogen chloride, haloacetonitriles
(dichloroacetonitrile, bromoacetonitrile, bromochloracetonitrile, trichloroacetonitrile,
tribromoacetontirile), haloketones (1,1,1–trichloropropanone, 1,1-dichloropropanone,
28
1,3-dichloropropanone,) dichloropropanoic acid, dichloromethylamine, N-
nitrosodimethylamine, N-nitrosodibutylamine, N-nitrosopiperidine, trichloramine (Kim et
al., 2002; WHO, 2006; Zwiener et al., 2007; Li and Blatchley III, 2007; Walse and Mitch,
2008).
Table 2.3: Different DBPs reported in indoor swimming pools
Country DCAN DBAN TCAN TCNM
Chloral
hydrate NDMA
Reference
µg/L µg/L µg/L µg/L µg/L ng/L
Germany 6.7-18.2
>1
Puchert, 1994
0.1- 148 >1-24 >1-11 >1-1.6
Stottmeister, 1998, 1999
>1-2.6
Scholer and Schopp, 1984
>1-104
Mannschott et al., 1995
US >1-87
Weaver et al., 2009
21-44 Walse and Mitch, 2008
DCAN (dichloroacetonitrile), DBAN (dibromoacetonitrile), TCNM (trichloronitromethane),
NDMA (N-nitrosodimethylamine).
The Precursors of Disinfection By-Products in Swimming Pools
There are two main sources that can serve as precursors of DBPs in pool water: (i)
filling water NOM (and bromide) already present in the filling water that comes from the
distribution systems, and (ii) human body excretions (HBE) that are added to the pool
water by swimmers. These two types of mixtures have very different characteristics, and
it is hypothesized that they will exhibit different reactivity toward DBP formation and
speciation.
NOM consists of the organic matter remaining in water after treatment operations
at the drinking water treatment plant. NOM is a heterogeneous mixture of various organic
29
molecules originating from allochthonous (i.e., soil and terrestrial vegetation) and
autochthonous sources (i.e., biota in a water body). The treatment processes in
conventional drinking water treatment plants typically remove high molecular weight and
hydrophobic components of NOM. Therefore, the NOM remaining in water after
treatment usually consists of low molecular and hydrophilic NOM fractions. Since water
is disinfected at the effluent of water treatment plants and maintenance of a residual
disinfectant concentration is required in the distribution systems in the US, some amount
of DBPs are already formed in water and exist in the filling water of swimming pools.
However, the DBP formation potential of filling water NOM is not completely exhausted
in the distribution system because chlorine is applied only at sufficient amounts in order
to comply with the US EPA’s microbial and DBP regulations. Given the fact that much
higher free chlorine residuals are continuously maintained for longer contact times
(several days due to circulation and very low or negligible dilution) in swimming pools,
NOM components will continue to form DBPs in the swimming pool environment.
The human body excretions is composed of mainly urine, sweat, dirt, saliva, body
cells (skin cells, hair), and lotions (synthetic chemicals such as sunscreen, cosmetics,
soap residues, etc.). Specifically urine and sweat constituents such as ammonia, urea,
creatinine and arginine, citric acid, uric acid, gluconic acid, various amino acids, and
sodium chloride are the major components that are released to the water of a swimming
pool (Putnam, 1971; Barbot and Moulin, 2008; Anipstakis et al., 2008). It is estimated
that a bather releases a mixture of 50 mL urine and 200 mL sweat in an average
swimming event (Judd and Bullock, 2003; WHO, 2006). These inputs accumulate and
30
increase in swimming pools with time since the operational practices of pools, such as the
frequency of water replacement, are not typically correlated with the number of
swimmers using the pools (Zwiener et al., 2007). In indoor swimming pools the dissolved
organic carbon (DOC) significantly increased with the number of swimmers (Chu and
Nieuwenhuijsen, 2002; Thacker and Nitnaware 2003). The increase in DOC also results
in an increase of THMs and total organic halides (TOX) formed from chlorination of pool
water (Thacker and Nitnaware, 2003; Glauner et al., 2004). Kim and his colleagues
chlorinated materials of human origin (i.e., hair, saliva, skin and urine) separately and
together as a mixture in two water sources (surface and ground water). The formation of
five different DBPs (chloroform, bromodichloromethane, chloral hydrate,
dichloroacetonitrile, and trichloropropane) from these materials was shown in addition to
the amounts formed from the background water used in the experiments (Kim et al.,
2002).
Investigation of organic halides formation potential as a result of water
chlorination at swimming pool conditions using algal extracellular products showed the
production of both purgeable (mainly chloroform) and nonpurgeable organic halides
(Wachter and Andelman, 1984). Amino acids and peptides are present in the source water
of swimming pool and are also introduced by the pool users (Trehy et al., 1986; Hureiki
et al., 1994; Hong et al., 2008). Chlorination of peptides and free amino acids produced a
variety of chlorination byproducts including chloroform. Different yields of chloroform
were shown to form from different amino acids depending on the amino acid side group
(Trehy et al., 1986; Hureiki et al., 1994; Hong et al., 2008). The chlorination of the 20
31
amino acids was repeated recently and both HAAs and THMs were reported (Hong et al.,
2008). Usually the HAAs produced from amino acids were more than THMs (Hong et
al., 2008).
A body fluid analog (BFA) to represent the body fluids that are introduced to
swimming pool water during swimming was developed and used in swimming pool
models to investigate different issues such as trihalomethane formation and accumulation
in swimming pools (Judd and Black, 2000; Judd and Bullock, 2003). BFA were also
introduced for the purpose of examining the efficiency of disinfection against biofilm
formation in swimming pools (Goeres et al., 2004) or to examine the different biocidal
efficacy of different disinfectants used or proposed for swimming pools (Borgmann-
Strahsen, 2003). These BFAs were developed depending on the different major
constituents of body fluids mainly urine and sweat that are estimated to be released into
swimming pool water in a ratio of 1:4 (Putnam, 1971; Judd and Black, 2000; Judd and
Bullock, 2003; Goeres et al., 2004; Borgmann-Strahsen, 2003; WHO, 2006). The three
BFAs that have been used and described in the primary literature recently are
summarized in Chapter Four (Table 4.2) in this dissertation. These BFAs are synthesized
to simulate the release of 50 mL urine and 200 mL sweat in an average swim event of one
person (Judd and Black, 2000; Judd and Bullock, 2003; Borgmann-Strahsen, 2003;
Goeres et al., 2004; WHO, 2006).
The ambient bromide concentrations in fresh waters used for water supply in the
U.S. can reach as high as 200-1000 µg/L at some locations according to previous surveys
of US drinking source waters (Amy et al., 1994). Therefore, bromide in filling water can
32
serve as an important inorganic DBP precursor. Free chlorine oxidizes bromide to
hypobromous acid that reacts with the organic DBP precursors in the water producing
brominated or mixed bromo-chloro DBPs, which have been shown to have more toxic
effects than the chlorinated species (Icihashi et al., 1999; Plewa et al., 2008a, 2008b). It
was shown that the presence of bromide in the filling water plays a major role in
producing the brominated THM species in swimming pools waters (Judd and Jeffrey,
1995). Therefore, it is important to understand the role of bromide in DBP speciation at
the typical operation conditions of the swimming pools.
Epidemiological Studies and Health Effects of Disinfection By-Products
Recently more attention is given to possible health impacts associated with
practicing swimming or working or attending swimming pool facility (lifeguard, trainers,
and technical operators). Chemical hazards associated with swimming pool are not
limited to the water but also includes the air in an indoor swimming pool. Volatile
organic and inorganic chlorination by-products can accumulate in the air above the water
of the swimming pool. After Rook (1974) discovered DBPs in chlorinated water, DBPs
became a public health issue. These DBPs were investigated for their health effects soon
after that. Of these DBPs chloroform, bromodichloromethane and bromoform were
categorized by US EPA in group B2 (i.e. probable carcinogenic for human being). The
fourth trihalomethane, dibromochloromethane is considered a possible carcinogenic and
categorized in group C. After that trichloroacetic acid (TCAA) and dichloroacetic acid
(DCAA) were placed in group B2 and C, respectively (Xu et al., 2002). DBPs have been
33
indicated to increase risk of bladder and colon cancer (Cantor, 1997; Villanueva et al.,
2004). Reproductive and developmental effects such as low weights at birth, intrauterine
growth retardation, and abortion were correlated with THMs exposure also (Waller,
1998; Nieuwenhuijsen et al., 2000; Graves et al., 2001; Bove et al., 2002; Richardson et
al., 2002; Savitz et al., 2005).
Following their categorizing as probable and possible carcinogens and concern for
other adverse health effects, DBPs exposure routes and risk assessments were researched
and are still under investigation. In addition to the ingestion route of exposure, inhalation
and dermal exposure to DBPs is another possible route during swimming, bathing, and
showering also (Aggazzotti et al., 1990; Kim, 1997; Lindstrom et al., 1997; Gordon et al.,
1998). Two THMs exposure routes, dermal and inhalation were shown to be dominant
especially when showering, bathing, swimming, or attending indoor swimming pools
(Villanueva et al., 2007a; 2007b). It was shown that risk of bladder cancer is more
associated to exposure to chlorinated water during showering, bathing, and swimming
than exposure via drinking (Villanueva et al., 2006, 2007a; 2007b). Specific activities
cause the THMs level to increase in blood. These activities are showering, bathing and
manual washing of dishes (Ashley et al., 2005). In indoor swimming pools exposure
assessment study, it was concluded that a positive correlation between air chloroform
content and blood levels of chloroform in both swimmers’ and other attendants’ blood is
present. Using scuba tanks by swimmers to compare inhalation and dermal pathway
showed that inhalation is a more important up-take pathway of THMs compared to
dermal up-take while swimming (Erdinger et al., 2004). Dermal pathways of THM
34
uptake during swimming result in 24 percent of the total intake of chloroform (Levesque
et al., 1994). Erdinger and coworkers concluded that one third of total body intake of
chloroform is through dermal pathway, and the rest is taken up by inhalation (Erdinger et
al., 2004). Chloroform exposure from swimming had been shown to be of more relevance
than ingestion (Whitaker et al., 2003). Higher bladder cancer risk was found for
showering, bathing, and swimming than for drinking water (Villanueva et al., 2006).
HAAs are ionic and more soluble in water. Their exposure is more probable
through ingestion but skin permeability of HAAs is not excluded and some studies
suggested that dermal exposure to DCAA and TCAA is possible (Kim, 1997) and
contributed to increased exposure more than drinking water alone. Also during
swimming, water aerosols can be a source of HAAs exposure during inhalation while
swimming or attending a swimming pool facility. HAAs are expected and already
reported to be at high concentration in swimming pool water. Ingesting even a small
volume of water during swimming will result in high exposure doses compared to
drinking water that has much lower levels of HAAs compared to swimming pools.
The permeability of the skin for these DBPs was investigated in vitro using
human breast skin cells (Xu et al., 2002). Permeation coefficients (Kp) of THMs and
some HAAs species from this study were determined. THMs permeability was found to
be more than HAAs as ionized compounds. Chloroform dose of exposure through dermal
route during showering (10 minutes) is equivalent to the ingestion dose from drinking 2 L
of chlorinated tap water (Jo et al., 1990). Using modeling, the chloroform dermal dose
from bathing at 40°C for half an hour was estimated to be equivalent to 68 percent of the
35
dose from ingesting 1.4 L of tap water (Corley et al., 2000). Finally it was shown that
more than one mutagen are present in pool water extracts by using the
Salmonella/mammalian-microsome test [a test to screen substances for their ability to act
as mutagens in Salmonella typhimurium (Ames et al., 1975)] (Honer et al., 1980).
Summary of Main and Important Findings from the Literature
In all swimming pool operational guidelines and regulation requirements, a
disinfectant should be used in swimming pool water. Chlorine has been found to
be the most effective disinfectant in pool water. Chlorine in its different forms is
the most commonly used disinfectant in swimming pools.
High chlorine dose (shock treatment) is required upon some accidental events
such as fecal release or vomiting while swimming. Suggestions for regular super-
chlorination to ensure disinfecting more resistant parasites (i.e. Cryptosporidium
and Giardia) have been made.
Swimming pool operational guidelines and regulations widely vary among
different countries in the world. In the US each state has its own regulation and
requirements specified for swimming pool construction and daily operation.
The free available chlorine required for swimming pool water in the US is one of
the highest compared to other countries in the world.
DBPs formation and control in swimming pools have not been investigated and
studied to the same extent as they have been in drinking water. Less concern is
given in the US compared to other countries for DBPs formation and control in
36
swimming pools. Some countries have already regulated THMs in swimming
pool water; others have also provided advisory air content of chloroform in the air
above the water of swimming pools.
Among DBPs, THMs are the most frequently measured in swimming pool waters
and to less extent in air. Other DBPs formation and determination are much less
determined and reported in the literature. Data available about THM formation in
swimming pools in the US are lacking and only a few older studies have been
reported. However, one recent study (which was published during this research)
reported THMs in addition to other volatile DBPs in swimming pools in the US.
Three main exposure routes to DBPs while swimming have been suggested and in
very limited occasions investigated. Few studies tried to find human skin dermal
permeability constants of DBPs, especially for DBPs other than THMs.
Epidemiological studies indicated that swimming pools could be a major public
exposure to DBPs that may contribute more to risk than drinking water sources.
Health effects such as bladder cancer have been shown to correlate with
swimming activity.
Body fluid analogs have been suggested and prepared consisting of the major
human urine and sweat components to use in different studies related to
swimming pools such as biofilm formation and also to compare biocide effects of
different disinfectants in swimming pools.
During swimming a considerable amount of swimming pool water is ingested.
This ingested water volume is dependent on swimmer age and type (i.e.
37
competitive vs. non-competitive). Children especially are thought to swallow
large amounts of water that can reach 500 mL during a swimming event.
Research Motivation
THMs are the most investigated DBPs in swimming pools. DBPs in pool water
are not limited to THMs. All DBPs that have been identified in drinking water are
possible DBPs in the swimming pools, even at higher magnitude folders, because of the
treatment and free available chlorine differences between drinking and swimming water.
Information about the presence of HAAs and HNMs in pool water is limited and more
investigation of their occurrence, classification, and speciation is required and may be
useful for the improvement of the environmental health conditions of swimming.
Especially in the US data about DBPs in swimming pools is limited. Information
concerning DBPs formation and classification under the swimming pool treatment
conditions can be used to improve the operational measures and standards of pools to
maintain acceptable environmental health conditions in the pools water and atmosphere.
38
CHAPTER THREE
OBJECTIVES, APPROACHES, AND EXPERIMENTAL DESIGN
Objectives
Despite significant efforts devoted to investigating and regulating DBPs in
drinking water in the US, the formation of DBPs in swimming pools is poorly
understood, and there is no systematic strategy to control their formation and speciation.
In this research project, the main objective of this research was to improve our
understanding of the formation of three DBP classes (THM4, HAA9, and HNM9) under
swimming pool operation conditions practiced in the US and estimate their potential
adverse health impacts on swimmers. During the occurrence study conducted during this
research, the formation of NDMA and HANs was also investigated. Specifically, research
was carried out in the following areas:
(1) to examine the occurrence of THMs, HAAs, HNMs, NDMA, and HANs in
indoor swimming pools in South Carolina, Georgia, and North Carolina.
(2) to conduct a multi-pathway risk assessment on THMs (TCM, BDCM, and
DBCM) and HAAs (DCAA and TCAA) of swimming pool water,
(3) to determine the role and contribution of the two main precursors (i.e., NOM
from the distribution system vs. body fluids from swimmers) to the formation of
trihalomethanes (THMs), haloacetic acid (HAAs), and halonitromethanes (HNMs) in
swimming pools,
39
(4) to investigate the impacts of swimming pool operational parameters: chlorine
residual (FAC), pH, bather load (TOC), water bromide content, and temperature on the
formation and speciation of THMs, HAAs, and HNMs, and
(5) to measure the formation of THMs and HAAs from the body fluids during
turnover time of swimming pool water, especially at short reaction times.
Tasks and Approaches
Five tasks were performed in this research project to accomplish the objectives
listed above. The first task involved examining of DBPs occurrence in 23 indoor
swimming pools in South Carolina, Georgia, and North Carolina and monitoring 3 indoor
pools during 9 months. The second task was devoted to estimate the lifetime health risk
and hazard related to DBPs in indoor swimming pool water and air. The other three tasks
involved laboratory scale experiments using BFAs and filling water NOMs from different
drinking water treatment plants under different conditions, to be described in detail in the
following sections.
Task 1: Examine the Occurrence of THMs, HAAs, HNMs, NDMA, and HANs in
Indoor Swimming Pools in South Carolina, Georgia, and North Carolina.
The occurrence and formation of DBPs in swimming pools in the US have not
been well documented especially for HAAs and HNMs. In this current research task,
DBPs in indoor public swimming pools were investigated in 23 indoor pools and
monitored to examine the actual occurrence and speciation of DBPs and the accumulation
40
of DBP precursors under US operational conditions. Five DBPs (THMs, HANs, HAAs,
NDMA, and HNMs) were investigated simultaneously for the first time in indoor public
swimming pool waters from the US. In addition several parameters (TOC, TN, free
available chlorine, pH, and temperature) were also monitored for the pools. In addition to
these 23 another three public indoor pools located at South Carolina were sampled during
this study for 9 months. Water samples of these pools were characterized and four DBPs
were determined in the samples. The pools sampling, the investigated parameters, and the
measured DBPs in task 1 are shown in Figure 3.1
Figure 3.1: Sampling and determination of water quality and disinfection by-
products in swimming pools
Sampling 3 indoor pools in South
Carolina for long period of time
Swimming pool water
Sampling 23 indoor pools in South
Carolina, Georgia, and North
Carolina
1- Determination of FAC, pH, TOC, TN, and Temp.
2- Determination of THMs, HAAs, HNMs, HANs, and NDMA
41
Task 2: Conduct a Multi-Pathway Risk Assessment on THMs (TCM, BDCM, and
DBCM) and HAAs (DCAA and TCAA) of Indoor Swimming Pool Water
For this task, SWIMODEL version 3 published by EPA was used. The model was
developed by Versar, Inc. upon the request of the EPA. The computerized model utilizes
EPA exposure equations that were originally applied for pesticides and antimicrobials.
These exposure equations estimate exposure tailored to swimmers exposed to chemicals
from swimming in indoor pools. Although default values for body weights, surface area,
and physicochemical data for some chemicals is included in the model, the user can input
(change) these information when there is need to do so. The user can also insert other
chemicals and their data values if interested. After adding the chemical information, the
water concentration is required as input for the model, which will estimate the air
concentration, and exposure from different routes (oral, inhalation, and dermal). Since the
measurement of DBPs in the air above the water of swimming pools has some difficulties
and limitations, Henry’s Law was used to estimate their equilibrium concentration in air
using the SWIMODEL. Measured THM and HAA concentrations in indoor swimming
pool waters and the calculated air phase concentrations were used for conducting lifetime
cancer risk and non-cancer hazard according to US EPA guidelines.
Task 3: Determine the Role and Contribution of the Two Main Precursors (i.e.,
Filling Water NOM vs. Body Fluids from Swimmers) to the Formation THMs,
HAAs, and HNMs in Swimming Pools.
There are two types of DBPs precursors in swimming pools:
42
a. Precursors already present in the filling water (NOM and bromide) that come
from the distribution systems.
b. Human body excretes, which are composed of mainly urine and sweat (together
they are referred to as body fluids).
These two types of mixtures have different characteristics, and it was
hypothesized that they will exhibit different reactivity toward DBP formation and
speciation. In this task, the main goal was to identify the reactivity of filling water NOM
and human body fluid in the formation of THMs, HAAs, and HNMs. Because human
body fluids constitute the significant fraction of human body excretions released by
swimmers, they were examined carefully in this task. However, it is not feasible to
collect large amounts of human body excretes from people and preserve them to conduct
a large experimental matrix. Therefore, three different body fluid analogs (BFAs) that
have been proposed in the literature to simulate swimmers’ body fluids were used in this
study (Putnam, 1971; Judd and Black, 2000; Borgmann-Strahsen, 2003; Judd and
Bullock, 2003; Goeres et al., 2004; WHO, 2006). These BFAs were synthesized to
simulate the release of 50 mL urine and 200 mL sweat during an average swim event for
one person (Judd and Black, 2000; Judd and Bullock, 2003; Borgmann-Strahsen, 2003;
Goeres et al., 2004; WHO, 2006). They have been used to investigate the following
factors in swimming pools: (i) the formation and accumulation of THMs (Judd and
Black, 2000; Judd and Bullock, 2003) (ii) the efficiency of disinfection against biofilm
formation (Goeres et al., 2004), and (iii) biocidal efficacy of different disinfectants
(Borgmann-Strahsen, 2003). Synthetic BFAs produced in the lab resemble the actual
43
body fluids that are introduced to the water of swimming pools. Constituents of the BFAs
used in this study are shown in Table 4.2 in the Chapter Four of this thesis. To date, no
study has compared the formation and speciation of DBPs from the selected BFAs side-
by-side despite some differences in their compositions and the differences in the
formation of DBPs from NOM in the pool filling waters and BFAs. Such comparisons
were made for the first time in this study.
Treated water samples after conventional treatment processes before any
disinfectant addition (to measure formation potentials) were collected from five drinking
water treatment plants in South Carolina using different influent water sources. These
waters cover a wide range of TOC and bromide levels that represent many water utilities
across the U.S. (Bisted, 2002) and they also represent the filling waters that are used for
swimming pools. Samples of treated waters were collected three times during 2008 and
2009 to examine the changes in the reactivity of DBPs precursors in the treated drinking
waters with time.
DBPs formation potential (FP) tests were conducted using treated drinking water
NOM samples and BFAs to compare the reactivity of these precursors in forming DBPs
under swimming pool conditions. The FP test protocol, developed for drinking water
samples, was conducted at excess chlorine concentrations for a long period of time (five
or ten days) with the main goal of determining the overall DBP reactivity of precursors in
a sample. Since temperature is an important factor for some recreational waters (e.g., hot
tubs and therapeutic pools), FP experiments were conducted at two different
temperatures, 26 or 40 ºC. Experiments were conducted in head space free amber bottles.
44
Experiments for task 3 are shown in Figure 3.2.
Figure 3.2: Experiments conducted for task 3
Task 4: Investigate the Impacts of Swimming Pool Operational Parameters: Free
Available Chlorine, pH, bather load (TOC), Bromide Content, and Temperature on
the Formation and Speciation of THMs, HAAs, and HNMs.
Free available chlorine, pH, water temperature, bromide content, and bather load
(TOC and TN) are the major parameters that can be managed and controlled during
swimming pool operation. These factors have also important effects on overall DBPs
formation and speciation. The main goal in this task was to examine the role of these
operational parameters on DBP formation and speciation.
1L of each BFA and each natural water types (3BFA + 5 treated water samples)
TOC: 1mg/L, pH 7, Chlorine dose: 50 mg/L
Contact time 5 or 10 days
Determination of THMs, HAAs, and HNMs
T 26 °C T 40 °C
45
For these experiments, two simulations of swimming pool water (synthetic
swimming pool water) were prepared. Treated waters of two utilities, one with high
SUVA254 (Myrtle Beach, MB) and one with low SUVA254 (Startex-Jackson-Wellford-
Duncan, SJWD) drinking water treatment plant water source waters, were used as the
filling waters. The filling (i.e., treated) waters were brought to the same initial TOC level
(1 mg/L), then the BFA(G) of Geores et al. (2004) was used to increase the TOC by
mixing with each filling water to prepare the two simulations of swimming pool water.
The BFA(G) was selected for this task because the other tested BFAs form high amount
of HAAs due to the free amino acids (histidine and aspartic acid) selected for their
formulations, as demonstrated in the third task. However, BFA(G) contains a protein that
is a source of amino acids and peptides that are expected to occur in swimming pool
water.
For the effect of chlorine residual (FAC), target concentrations of 1, 3, and 5
mg/L free available chlorine (FAC) were tested separately. The goal was to maintain
these residuals after five days of contact time. For the effect of pH, three pH conditions
(6, 7, and 8) were tested at a constant TOC and chlorine residual of 1 mg/L for the two
synthetic pool waters mentioned above. The effect of bather load was tested at three
levels (6, 11 and 16 mg/L TOC) by varying BFA concentration in each swimming water
simulation and maintaining the same background water (i.e., filling water) TOC (1
mg/L). These experiments were conducted at constant chlorine residual, pH, bromide,
and temperature conditions. The bromide concentrations in fresh waters in the US can be
as high as 200-1000 µg/L according to previous occurrence surveys (Amy et al., 1994;
46
Obolensky and Singer, 2005). The effect of bromide was tested by conducting
experiments at 100, 300, 600 µg/L for 1 mg/L of chlorine residual conditions at pH 7
using the two synthetic pool water simulations. All the experiments described in this
section were conducted at 26 ºC using a water bath. To examine the effect of temperature,
one set of experiments was repeated at 40ºC for the two simulations of synthetic
swimming pool water. Experiments conducted in this task are summarized in Figure 3.3.
Task 5: Measure the Formation of THMs and HAAs from the Body Fluids During
Turnover Time of Swimming Pool Water, Especially at Short Reaction Times.
The turnover period in swimming pools (the period of time (usually hours) required to
circulate the complete volume of water in a pool through the recirculation system),
typically ranging from four to eight hours (Griffiths, 2003; SC DEHC, 2007), is
important from a DBPs formation and control perspective. When fresh body fluids are
released by a swimmer, while swimming, this is the retention time in the pool for them to
react with chlorine before water goes through treatment processes outside of the pool
(Figure 2.1). It is important to understand the formation kinetics of DBPs, at swimming
pool conditions for developing possible DBPs control strategies in swimming pools.
Today, there is no information in the literature regarding the DBPs formation kinetics of
treated NOMs and body fluids under swimming pool conditions.
47
*: MBor SJWD drinking water
**: For 6, 11 and 16 mg/L solutions: 1 mg of TOC is from the filling water and the remaining TOC is from the BFA(G)
Figure 3.3: Experiments conducted for task 4
1L synthetic swimming pool water prepared using BFA(G) and filling water*
pH 6, 7, 8 FAC: 1, 3, 5 mg/L
Temperature: 26°C
Contact time: 5 days
TOC: 6 mg/L,
FAC: 1 mg/L, pH 7
TOC: 6 mg/L,
FAC: 1 mg/L, pH 7
TOC: 6 mg/L,
FAC: 1 mg/L
TOC: 6 mg/L,
pH 7
Br-: 100, 300, 600 µg/L
FAC: 1 mg/L,
pH 7
TOC: 6, 10, 15 mg/L
Temperature: 40°C
Determination of THMs, HAAs, and HNMs
48
Therefore, during this task, experiments were performed with BFA(G) at two TOC levels
and with NOM of treated water to determine the formation kinetics of THMs, HAAs and
HNMs. Kinetics experiments were performed at 26°C (swimming pool water
temperature), the same pH, and initial Cl2 dose at ambient bromide content and at 200
µg/L bromide concentration. Special attention was given to collect several DBPs samples
at 0.5, 1, 3, 5, 7, 10, 15, and 24 hours, then samples were also taken after 48, 72, 96, 120
hours. The main goal was to determine how fast THMs, HAAs, and HNMs are produced
in swimming pools, and what percent of the first day and fifth day DBP yields forms
during the first hours of contact in the swimming pool before water undergoes any further
treatment. Experiments conducted to measure DBPs during turnover time under
swimming pool conditions are shown in Figure 3.4.
Figure 3.4: Experiments conducted to measure THMs and HAAs from the body fluid
precursors during turnover time of swimming pool water
1L of synthetic pool water: 6 mg TOC/L (5mg/L BFA(G) + 1mg/L MB filling water
1L of BFA(G) in DDW (5mgTOC/L)
1L of BFA(G) in DDW (1mgTOC/L)
For all cases: pH=7, Chlorine C₀=100 mg/L, T=26 ˚C
Contact time: 0.5, 1, 3, 5, 7, 10, 15, 24, 48, 72, 96, 120 hours
Determination of THMs and HAAs
Br: ambient conc. Br: 200µg/L
49
CHAPTER FOUR
MATERIALS AND METHODS
An overall and detailed description of experimental materials and methods used in
this research are provided in this chapter. However, because different samples and
methods were used for different tasks and experimental matrices, there will be a short
section on the experimental materials and methods in the following chapters listing the
water samples used and the experimental matrix conducted for a particular objective.
The experiments conducted in this research mainly included the measurements of
five classes of DBPs (THMs, HANs, HAAs, HNMs, and N-Nitrosamines) in chlorinated
synthetic pool waters at variable TOC level, chlorine dose, bromide concentration,
temperature, pH, and reaction time (incubation time). DBPs were also analyzed in actual
swimming pool water samples. Frequently measured parameters during this project
included TOC, TN, UV245, FAC, pH, and bromide.
Glassware, Reagent Water, Chemical Reagents, and Stock Solutions
Glassware was scrupulously cleaned by tap water and a detergent, and then rinsed
with distilled water several times and finally with hydrochloric acid solution three times
before rinsing again with distilled deioinzed water (DDW). The glassware was dried at
least 80 ºC inside an oven to avoid any contamination and dust.
Reagent water used in the experiments was distilled deionized water (DDW)
produced by a Millipore water purification system (Millipore S.A. 67120 Molsheim-
50
France). The DDW was Type I water with residual DOC less than 0.1 mg/L and
resistivity of 18 MΩ-cm.
All chemicals used were American Chemical Society (ACS) reagent grade.
Solvents used in the extraction and standard preparation were high purity grades. All
stock solutions and buffers were prepared fresh at the use time; otherwise they were
stored in brown glass bottles at 4°C.
Treated Water Samples
At each sampling event, 20 L of water were collected from each of five drinking water
treatment plants [Greenville (GV), Startex-Jackson-Wellford-Duncan (SJWD),
Spartanburg (SP), Myrtle Beach (MB), and Charleston (CH)] in South Carolina after
conventional treatment processes (coagulation, flocculation, and sedimentation or
floatation). Table 4.1 shows the characteristics of each water sample on the date of
collection. These treatment plants were selected for the study because they have different
source water and NOM characteristics. Greenville source water is obtained from a
reservoir which has high aquagenic NOM (produced in the water column) which contains
more aliphatic moieties and low molecular compounds. The source water for Myrtle
Beach is located in a forest and wetland area that enriches the water with aromatic
compounds and lignin. Myrtle Beach water source has pedogenic (soil-derived) humic
substances which are characterized with high molecular weights and intense color. The
SJWD water source is the Middle Tyger River (Lyman Lake) and the North Tyger River
51
(Lake Cooley and North Tyger Reservoir). All the source water is treated at the SJWD
water plant. The Charleston Water System primarily draws raw water from the Edisto
River and the Bushy Park Reservoir, both of which are surface water sources. These
water sources also represent coastal and inland locations in the state.
Table 4.1: Natural water samples characteristics used in the experiments
Water
source
Sampling
Date
TOC
mg/L
TN
mg/L
UV254
cm-1
SUVA
L/mg-m
Br-
µg/L
SJWD
November-08 1.7 0.3 0.0300 1.74 31
March-09 1.4 0.3 0.0237 1.73 19
September-09 1.7 0.3 0.0287 1.71 19
SP
November-08 1.6 0.2 0.0181 1.11 <MRL
March-09 1.7 0.2 0.0209 1.25 <MRL
September-09 1.7 0.2 0.0204 1.17 <MRL
GV
November-08 0.7 0.1 0.0119 1.63 <MRL
March-09 0.8 0.1 0.0138 1.71 10
September-09 0.8 0.1 0.0075 0.96 <MRL
CH
November-08 2.5 0.3 0.0535 2.10 110
March-09 3.1 0.3 0.0586 1.88 79
September-09 3.1 0.3 0.0583 1.86 75
MB
November-08 6.7 0.3 0.1365 2.05 37
March-09 6.1 0.3 0.1212 1.98 29
September-09 5.4 0.3 0.1127 2.08 45
TOC (total organic carbon), TN (total nitrogen), SJWD (Startex-Jackson-Wellford-
Duncan), SP (Spartanburg), GV (Greenville), MB (Myrtle Beach), CH (Charleston),
MRL (minimum reporting level: 10 µg/L).
52
Water samples were filtered using 0.2 µm Supor® membrane filters immediately after
being brought into the laboratory, and stored in a cold dark room at 4°C until experiments
that were usually performed within few days of collection.
Body Fluid Analogs (BFAs)
Three body fluid analogs (BFAs) were produced and tested for DBPs formation
under swimming pool operation conditions. These BFAs (Table 4.2) were synthesized to
simulate the release of 50 mL urine and 200 mL sweat during an average swim for one
person (Judd and Black, 2000; Borgmann-Strahsen, 2003; Judd and Bullock, 2003;
Goeres et al., 2004; WHO, 2006).
Table 4.2: Body fluid analogs components
BFA(G)
BFA(J)
BFA(B)
Ingredient mg/L Ingredient mg/L Ingredient mg/L
urea 62.6 urea 14800 urea 23000
creatinine 4.3 creatinine 1800 creatinine 1250
uric acid 1.5 uric acid 490 glutamic acid 300
lactic acid (85%) 3.3 citric acid 640 aspartic acid 830
albumin 9.7 histidine 1210 glycine 450
glucuronic acid 1.2 hippuric acid 1710 histidine 200
ammonium chloride 7.0 ammonium chloride 2000 lysine 75
sodium chloride 22.1 sodium phosphate
(NaH2PO4) 4300
sodium sulfate 35.3
sodium bicarbonate 6.7
potassium phosphate
(KH2PO4) 11.4
potassium sulfate 10.1
53
The BFAs used to produce synthetic swimming pool water are prepared from the
dominant nitrogenous and carbonaceous compounds that are most available and dominant
in human sweat and urine that is continuously introduced to the pools water body. Urea,
creatinine, uric acid, free or combined amino acids (small peptides), and others are the
most abundant compounds in human body fluids that are assumed to have an impact on
the chlorine demand and possible DBPs formation in swimming pools (Hureiki, et al.,
1994; Li and Blatchelly III, 2007). Albumin protein, which is usually used as a model of
protein present in nature (Hureiki, et al., 1994), was used in BFA(G) with the purpose to
simulate the human body proteins and peptides and amino acids that are likely to occur in
swimming pool water.
Chlorination Experiments
Sodium hypochlorite (NaOCl) that has 5% available chlorine was used as a free
chlorine (Cl2) source. The stock chlorine solution was always standardized by the N,N-
diethyl-phenylenediamine (DPD) titrimetric method (Standard Methods, 1995). The
chlorination experiments were conducted in a series of 125-mL amber glass bottles
closed tightly with Teflon-faced septa screw caps. After mixing well, using a magnetic
rod and magnetic stirrer, the bottles were stored headspace free in a water bath for the
required time and at the experimental temperature. After the bottles were opened,
accurate sample volumes were obtained rapidly and transferred to extraction vials to
54
determine the three classes of DBPs (THMs, HAAs, and HNMs). Free available chlorine
(FAC) and pH were determined as soon as possible after the opening of the bottles.
Analytical Methods
A summary of parameters, analytical methods, and instruments used in the
different measurements is presented in Table 4.3. In general, methods used are either
following the Standard Methods or US EPA Methods with slight modification for some
of them. Thus analytical methods are described briefly here.
HAAs Analyses
All nine chlorinated, mixed chlorinated brominated and brominated HAAs were
analyzed. Standards of HAAs were purchased from Supelco. Serial standard
concentrations for calibration were prepared from the mixture of nine HAAs stock by
spiking into DDW. Extraction of standards from water by the extraction method used to
extract the HAAs from the samples was applied to account for the extraction efficiency
and recovery. The analytical method for HAAs determination and quantification
developed by Singer et al. (2002) and based on Standard Method 6251B was used with
some slight modifications. This method uses diazomethane derivatization. Screw-cap
glass vials (40 mL) with Teflon-faced septa were used for the extraction. A water sample
(20 mL) was transferred into the extraction vial using a glass pipette and electrical pipette
55
Table 4.3: Analytical methods and minimum reporting levels
Parameter Unit Measurement Method Instrument MRL or Accuracya
DOCb
mg/L SMc 5310B TOC-V CHS & TNM-1, Shimadzu Corp., Japan 0.1
Total Nitrogen mg/L High Temperature Combustion TOC-V CHS & TNM-1, Shimadzu Corp., Japan 0.1
UV Absorbanced cm-1 SM 5910 DU 640, Beckman Inst. Inc., USA 0.005
d
NO2ˉ, NO3
ˉ, Br
ˉ g/L US EPA Method 300 ED 40, Dionex Corp., USA NO2
ˉ: 20; NO3
ˉ: 15; Br
-: 10
pH SM 4500-H+ 420A, Orion Corp., USA 0.01
e
THMs and HANsf g/L US EPA Method 551.1 6890 GC-ECD, Agilent, USA 1
HAA9g g/L SM 6251 B
g 6890 GC- ECD, Agilent, USA 1
HNMh g/L US EPA Method 551.1 6850 GC-ECD, Agilent, USA 0.7
NDMA ng/L US EPA 521 Varian GC/MS/MS 2
FACi mg/L SM 4500-Cl F NA
k 0.1-0.15
a Minimum reporting levels were determined in the lab in previous works (Hu, 2009). Accuracy as reported by the manufacturer.
b Reagent grade potassium hydrogen phthalate used to prepare external standards. Precision ranged from 0.05 to 0.15 mg/L.
c SM: Standard Methods (Standard Methods,1995; AWWA, and WEF, 2004).
d At wavelengths of 254 nm using a 1- or 5-cm cell. Photo-metric accuracy (absorbance units).
e Accuracy (pH units).
f THMs: Trihalomethanes. Methyl-tert butyl ether (MTBE) solvent extraction and (GC) with an (ECD) analysis.
g HAA9: All nine haloacetic acid species. Diazomethane derivatization, MTBE solvent extraction and GC-ECD analysis.
h HNM: Halonitromethanes. Methyl-tert butyl ether (MtBE) solvent extraction and (GC) with (ECD) analysis.
i Free Available Chlorine.
k NA: Not applicable
56
aid. Then 2 mL of concentrated (98%) H2SO4 was added to the water in the extraction
vial to convert acetates to their corresponding acids.Then 4 mL of methyl-tertiary butyl
ether (MtBE, Sigma-Aldrich) 99.8% HPLC grade, that contained 200 µg/L 1,2-
dichloropropane as an internal standard, was added to the water sample in the extraction
vial. Sodium sulfate (Na2SO4) of reagent grade was added (10 g) to the extraction vial to
enhance the partitioning of the HAAs into the organic phase and also to minimize the
MtBE water solubility. Extraction vials were placed on a horizontal shaker to shake
vigorously for 15 minutes at 300 rpm. Then the extraction vials were allowed to settle
for at least 10 minutes to separate the two phases. After settling, 2 mL of the upper MtBE
layer were transferred to volumetric flasks (2 mL) for the derivatization process.
Diazomethane was used for the methylation of the separated HAAs. Diazomethane was
produced in MtBE from carbitol (diethylene glycol ethyl ether) and diazald (N-methyl-N-
nitroso-p-toluene sulfonamide) under alkaline conditions in a special glass diazomethane
generator. Before adding diazomethane to the 2 mL volumetric flask, magnesium sulfate
(100 mg) was used to dry the sample. Then 225 µL diazomethane was added to the 2 mL
volumetric flask and allowed to react for 30 minutes, converting the haloacetic acids to
their methyl esters which can be separated and quantified chromatographically. After the
methylation reaction time, the excess diazomethane was quenched by silica gel (100 mg).
Then the top layer of the 2 mL sample was transferred to a GC vial for subsequent
analyses with GC.
An Agilent 6890 GC equipped with an ECD, autosampler and HP Chemstation
software was used for the separation and measurement of HAAs. The column used was a
57
phenomenex ZB-1 column (equivalent to DB-1 column), ID 0.25 mm; film thickness, 1.0
µm; and 30 m length. The following temperature program was applied. The initial oven
temperature was 45°C, initial time 20 minutes, 5°C/minute up to 140°C held for 0
minutes, 15 °C/minute up to 165°C, and held for 0 min, and 40°C/minute up to 320°C
held 6 minutes. Total run time was 50.54 minutes. Injection and detector temperature
were 200°C and 300°C, respectively. Injection volume was 2 µL. High purity (99.998%)
nitrogen gas was used for the makeup gas, and ultra pure (99.999%) helium as the carrier
gas. Injection mode was splitless. Septum purge was 3.3 mL/minute; split vent was 47.8
mL/minute. Carrier and makeup gas flow was at 62.2 mL/minute, and carrier gas at 2.2
mL/minute.
THMs and HANs Analyses
A mixture of four THM standards were purchased from Supelco. Another six
HANs standards were purchased from Ultra Scientific. Serial standard concentrations for
calibration were prepared from the THM mixture stock and HANs stock by spiking into
TOC reagent water. Extraction of standards from water by the extraction method used to
extract the THMs and HANs from the samples was applied to account for the extraction
efficiency and recovery. US EPA method 551.1 for the liquid-liquid extraction and GC
measurement was employed with minor modifications to extract and quantify THMs and
HANs. Screw cap glass vials (40 mL) with Teflon-faced septa were used for the liquid-
liquid extraction. A water sample (20 mL) was transferred to the glass extraction vials
using a glass pipette and electrical pipette aid. To each 20 mL of water sample in the
58
extraction vial, 8 mL of methyl-tert butyl ether (MtBE, Sigma-Aldrich) 99.8% HPLC
grade, which contained 50 µg/L 1,2- dichloropropane as an internal standard, was added
gently. Then 8.5 g of reagent grade sodium sulfate (Na2SO4) was added to the extraction
vial to enhance the partitioning of the THMs into the organic phase and also to minimize
the MtBE water solubility. Extraction vials were closed tightly, laid horizontally on the
shaker table, and shaken at 300 rpm for 15 minutes. After shaking, the vials were allowed
to settle for at least 10 minutes. Two mL of the upper layer of MtBE were transferred via
a glass pipette into GC vials for subsequent GC analyses.
An Agilent 6890 GC with an electron capture detector (ECD), an autosampler and
HP Chemstation software was used for the determination and quantification of the
THMs. The column characteristics were ID, 0.25 mm; film thickness, 1 µm; and length,
30 m (Phenomenex ZB-1 column, cat# 7HG-G001-22, equivalent to DB-1 column).
The injection temperature was 250°C, and the detector temperature was 290°C.
The oven temperature program was as follows: initial temperature 35°C, initial time 22
minutes, 10°C/minute up to 125°C hold for 1 minute, 30°C/minute up to 300°C, and hold
for 4 minutes. Total run time was 41.83 minutes. Injection volume was 2 µL. Ultra-high
purity (99.999%) helium gas was used as a carrier gas. Nitrogen gas ultra-high purity
(99.998%) was the makeup gas. The injection mode was splitless. Septum purge was
approximately 3.3 mL/minute, and split vent approximately 47.8 mL/minute. The carrier
and makeup gas flow was equal to62.2 mL/min, and carrier gas approximately 2.2
mL/minute.
59
HNMs Analyses
HNM standards were obtained from Orchid Cellmark (New Westminster, Canada,
CNM 93.6%, DCNM 99+%, BCNM 91.9%, BDCNM 93.9%, DBNM 91.4%, DBCNM
94.1%, TBNM 99+%) and Sigma (TCNM 99+%, BNM 99+%). Stock solutions (106
µg/L) were prepared by adding 1 mg (measured by a micro-balance) of pure compound
to 1 mL of MTBE. Calibration standards were then produced from further dilutions of the
pure compounds. Halonitromethanes were measured using US EPA Method 551.1 with
minor modifications. A 10 mL sample was extracted using 10 mL of MtBE (Sigma-
Aldrich 99.8% HPLC grade). Three grams of sodium sulfate (Na2SO4) and 1 g of cupric
sulfate were added to the extraction vial for a salting out effect and enhancing
partitioning of the analytes into the organic phase. The extraction vials were then placed
horizontally on a shaker table and shaken at 300 rpm for 30 minutes. After shaking, the
samples within the extraction vials were placed in an ultrasonic bath for 10 minutes to
reduce the partitioning of the hydrophobic HNM species to the glass vial surface. After
that, the vials were allowed to settle for at least 10 minutes to allow phase separation.
Two mL of the upper layer of MtBE were transferred via a glass pipette into GC vials for
subsequent GC analyses.
The MtBE extract was analyzed on an Agilent 6850 gas chromatograph (GC)
equipped with a DB-5 (J&W Scientific 30m x 0.25mm) column. The GC was equipped
with a micro electron capture detector (-ECD). The GC temperature program used was
35 ºC for 6 minutes, 30 ºC /min to 190 ºC and hold for 1.5 min. A 2 μL injection volume
was used in splitless mode. The make-up and carrier gases used were ultra-high purity
60
helium at 2.3 mL/min and ultra-high purity nitrogen at 60 mL/min. The injector
temperature was set at 117 ºC in order to minimize the thermal decomposition of HNM
species (Chen et al., 2002), and the detector temperature was set at 297 ºC.
NDMA Analyses
N-nitrosodimethylamine (NDMA) was analyzed following EPA method 521. A
mixed standard of seven nitrosamines were purchased from Supelco. Two isotopically
labeled internal standards [N-nitrosodimethylamine-d6 (NDMA-d6) and N-nitrosodi-n-
propylamine-d14 (NDPA-d14)] were purchased from Restek. The EPA method is a solid
phase extraction procedure (SPE) using activated carbon for the determination of various
nitrosamines in water. In summary the analytes and internal standard were extracted from
a 500 mL water sample which was drawn through a solid-phase extraction cartridge
containing 2 grams of 80-120 mesh coconut activated carbon (charcoal). After passing
the whole water sample (0.5 L) through the cartridges at 10 mL per minute rate, the
cartridges were dried by suctioning air at full vacuum (20‖ Hg) for 10 minutes through
the cartridges. Then the analytes (N-Nitrosamines) were eluted from the solid-phase with
approximately 12 mL dichloromethane (MeCl2). Then extracts were dried by passing
them through an anhydrous sodium sulfate (6 g) column. Finally the extracts were
concentrated to 1 mL using a gentle ultra pure nitrogen gas stream and water bath at room
temperature. Extractions were collected in amber GC vials and analyzed using the
GC/MS/MS on the same day of extraction. Otherwise the samples were stored at -15°C
for less than 14 days. The sample components were identified after injection on a fused
61
silica capillary column (Column: RTX-5MS 30m, 0.25mmID with 0.25µm film
thickness) of a GC/MS/MS using an 8 µL injection volume and chemical ionization (CI)
with methanol. Injector program was as follows: injection temperature is 35°C holding
for 0.8 minute, and then increased to 260°C at 200°C/minute and hold for 2.08 minutes.
The column temperature program was as follows: 35°C for 5 minutes, increased to 70°C
at 5°C/min, then to 87°C at 3°C/min, then to 120°C at 5°C/min, and then to 250°C at
40/min holding for 2.48 minutes. Nitrosamines are sufficiently thermally stable and
volatile for direct analysis by gas chromatography. A set of calibration solutions were
prepared from a mixed stock of nitrosamines from Restek (Nitrosamine Calibration Mix)
and two internal standards. In this method isotopically labeled nitrosamines (NDMA-d6
and NDPA-d14) have been used as surrogate and internal standards. Typical calibration
curves were generated from at least six standard points covering the range of
nitrosamines in the samples. Average response factors of three injections of each standard
point calibration were used to obtain the calibration curve. The MRL of this method as
specified by EPA method is 2 ng/L. Pool water samples were collected in 1L amber glass
bottles. After collecting, samples were dechlorinated immediately by adding 100 mg
sodium thiosulfate to each 1L of water sample. Samples were transferred to the lab within
an ice box to maintain a temperature of less than 10°C. In the lab samples were stored at
4°C in the dark. Samples were always analyzed within two days or less of collection.
62
Total Organic Carbon and Nitrogen
Total organic carbon (TOC) and total nitrogen (TN) were measured using a
Shimadzu TOC-VCHS high temperature combustion analyzer equipped with an auto-
sampler. Samples for TOC and TN were preserved at 4°C in the refrigerator until analysis
within 24 hours of collection. The samples were automatically purged by the analyzer for
four minutes before analysis. TOC standards were prepared from 1000 mg C/L stock
solutions of potassium hydrogen phthalate, and calibration curves produced for TOC
ranging from 0.2-15 mg C/L. TN standards were prepared from 1000 mg N/L stock
solution of potassium nitrate, and calibration curves produced for TN ranged from 0.4-8
mg N/L. Samples with TOC and TN above the calibration range were diluted and
measured again.
UV Absorbance
UV absorbance was measured using a Cary 300 UV-Vis spectrophotometer
(Varian). Samples were placed in a quartz cuvette and measured at a wavelength of 254
nm. The spectrophotometer was zeroed by measuring the absorbance of DDW after
several rinses. The instrument was zeroed every 10 samples, and method performance
was monitored using total organic carbon standards made with potassium hydrogen
phthalate.
63
pH
The pH values for samples were measured using a SM 4500-H+ pH electrode
with an Orion 420A pH meter (Orion Corp., USA). The pH meter and electrode were
calibrated using standard pH 4, 7 and pH 10 buffer solutions before use.
Free Available Chlorine
Free available chlorine concentrations were measured using an N, N-diethyl-p-
phenylenediamine (DPD) method (Standard Method 4500 Cl). Chlorine samples were
diluted based on their expected residual chlorine concentration. The sample was then
poured into a beaker containing 5 mL of DPD indicator solution and 5 mL of phosphate
buffer. After mixing, the sample was titrated using a ferrous ammonium sulfate (FAS)
solution. The DPD solution was used for color formation, the phosphate buffer was used
for pH control, and the FAS titrant was used for color removal. The DPD indicator
solution and FAS solution were made according to Standard Method 4500 Cl. A standard
1:5 dilution was made for both the FAS solution and the sample. In this case, the volume
of titrant used was the chlorine concentration in the sample. Whenever dilution of the
sample was made, this was taken into account during the calculations for the
measurement.
64
Bromide
Bromide was measured using an ion chromatography system. A Dionex DX-600
equipped with a suppressor was used to determine the bromide content of the water
samples that were used in this study. The eluent was 9 mM Na2CO3. A Dionex HC9
column coupled with an AG-HC9 guard column was used to separate samples. The
injection volume was 250 µL. A calibration curve was obtained by a series of standard
concentrations (at a low range of 5-400µg/L) using NaBr (99.9% and more, from Sigma-
Aldrich).
65
CHAPTER FIVE
DISINFECTION BY PRODUCTS OCCURRENCE IN INDOOR SWIMMING POOLS
Introduction and Objectives
Swimming pool water quality is reduced during its use by swimmers.
Microorganisms and other organic constituents are released (Anipsitakis et al., 2008) into
the pool water from the skin, mouth, eyes, nostrils, ears, anus, and urethra of the
swimmers. Swimming pool water is required to be clear and biologically safe (CDC,
2008). Inactivation of microbial pathogens is mostly achieved by chlorine with the
chlorine added continuously to constantly maintain free available chlorine in public
swimming pools. The operational requirements in the US are variable among the
different states and enforced separately by each state health and environment department.
In general FAC should be maintained in the range of 1 to 5 mg/L in the pool water and
the water pH between 7.2-7.8 (NSPF, 2006). However, the free available chlorine
required to be maintained in swimming pool water varies across the world. For example,
it is required to be 1-2 by the United Kingdom, 0.3-0.6 by Germany and 0.6-1.2 mg/L by
Italy (WHO, 2006).
Chlorine is known to react with organic material that may be found in disinfected
(chlorinated) pool water producing a wide variety of disinfection by products (DBPs).
Organic material in swimming pool water includes natural organic matter (NOM) that is
already present in filling water coming from the public distribution system and the
organic matter that is introduced by swimmers mainly in the form of urine and sweat.
Organic matter addition to pool water is estimated to reach several grams (Borneff, 1979;
66
Batjer et al., 1980; Eichelsdorfer et al., 1980; Althaus and Pacik, 1981; Thacker and
Nitnaware 2003; Zwiener et al., 2007) by each swimmer in a swimming event. Thus TOC
of a swimming pool increases continuously demanding continuous chlorine addition to
keep the FAC within the acceptable range to ensure clear and biological safe water.
DBPs formed in water have different physiochemical properties that affect their
distribution and partitioning between pool water and the atmospheric environment of the
pool. Some of the DBPs are volatile and hydrophobic (e.g. THMs) which causes them to
be transferred to the air phase above the surface of the pool water. Other DBPs are
hydrophilic and highly soluble (e.g. HAAs) and preferentially stay in the water phase
accumulating by time. Both volatile and nonvolatile DBPs can be carried by tiny droplets
to the atmosphere of the pool (Hery et al., 1995).
There are multiple possible exposure pathways to DBPs during swimming. These
include ingestion, inhalation and dermal absorption (Aggazzotti et al., 1998; Whitaker et
al., 2003; Nuckols et al., 2005; Gordon et al., 2006; Villanueva et al., 2007a). In these
three exposure routes, swimming pool chemicals can enter the body depending on the
chemical concentration, contact time and body surface area (for dermal route), and
volume of water or air ingested or inhaled (inhalation rate) (Reiss et al., 2006). Exposure
to THMs related to swimming activity or attending a pool facility have been studied by
analyzing blood urine, and exhaled air of volunteers (Lindstrom et al., 1997; Aggazzotti
et al., 1998; Fantuzzi et al., 2001; Erdinger et al., 2004; Caro and Gallego, 2007). Some
countries have started to include THMs within the swimming pool regulations that
previously included mainly biological and physiochemical properties such as
67
temperature, pH, and free and combined chlorine (Bisted, 2002; Borgmann-Strahsen,
2003; Uhl, 2007; Barbot and Moulin, 2008). Although the US drinking water regulations
are some of the most stringent regarding the DBPs, there is no swimming pool water
DBPs legislations or guidelines to date.
Much of the DBPs research in the US is devoted to drinking water. Interest in
DBPs occurrence in indoor swimming pools is increasing. This interest is due to the risk
associated with DBPs exposure of swimmers from swimming activity or attendees who
work in a swimming facility such as lifeguards, workers, and reception employees. DBPs
in swimming pools can be ingested, inhaled, and absorbed through skin (Lindstrom et al.,
1997). Exposure to DBPs is associated with more risk of cancer and development and
reproductive outcomes (Aggazzotti et al., 1998; Villanueva et al., 2007b).
Bromide comes with the filling water and/or is introduced as impurities with the
sodium chloride for pools that use special systems to generate chlorine electrochemically
from sodium chloride salt on site. Overtime bromide accumulates in the pool water and is
oxidized by chlorine to HOBr, which can also react with organic precursors to produce
brominated and mixed chlorinated and brominated DBPs.
This part of the work was designed to measure three DBPs (THMs, HAAs, and
HNMs) in actual water samples from indoor swimming pools that either chlorinated by
adding chlorine to pool water continuously or generating it electrochemically from
sodium chloride. Twenty three indoor pools were sampled to measure the occurrence of
DBPs and their precursors in pool water. Of these pools, three were monitored for a long
period (9 months) to study how the DBPs and their precursors occurrence possibly
68
change with time. Two of these pools are operated at around 26°C and a third one was
operated at around 33.3°C.
Approach
Sampling and characterization of the pools water on site and determination of
selected DBPs in pools water samples. Figure 3.1 shows the sampling and lab work of
this chapter.
Materials and Methods
Swimming pools were sampled for the DBPs analyses with 125 mL amber glass
bottles with PPTE screw caps. Water samples were taken from about 30 cm below the
water surface of the pool. Ammonium chloride was used to quench the free chlorine in
the water samples before the bottles were closed with no headspace. For NDMA analysis,
a 1L sample was collected in an amber glass bottle and quenched by sodium thiosulfate
(80-100mg). Samples were transferred immediately to the lab using an ice box for DBPs
analyses. DBPs analyses were conducted either in the same day of sampling or the next
day. When stored, samples were kept in the refrigerator at 4°C overnight. DBPs
extraction and determination methods used are described and detailed in Chapter Four.
For the HAAs measurement the samples were diluted 1:20 before extraction and
determination, which was necessary to bring the HAAs level to the GC measurable
concentration and within the calibration range (1-150 µg/L) described in Chapter Four.
69
Results and Discussion
Swimming Pools Water Characterization
Twenty three indoor pools located in South Carolina, Georgia and North Carolina
were sampled in one survey event during the same week in February, 2010. Swimming
pools monitored here were all indoor public pools that can be accessed by a wide array of
people with different ages and health situations. All pools used chlorine as the
disinfectant. Some of the sampled pools used calcium hypochlorite directly where others
generate chlorine in situ electrochemically using sodium chloride to maintain a
predesigned free available chlorine level. Most of the pools were operated at low
temperature (≈ 26°C) but some were operated at higher temperature (≈ 34°C). In general,
the pools used the local water distribution system for filling and make up water. One of
the sampled pools used groundwater from a local well. Free available chlorine in the
pools was between 0.08 and 6 mg/L. These 23 pools are all public pools that either
belongs to a public recreation center, university, college, hotel, or therapeutic center. The
water samples of the 23 indoor pools were characterized in addition to their operational
parameters that have been obtained from the logbook of each pool (Table 5.1).
70
Table 5.1: Swimming pool water samples characteristics
Pool Temp.
pH FAC
Disinfectant Filter TOC TN
°C mg/L mg/L mg/L
S1 27 7.5 3 Cl2 Sand 4.3 1.4
S2C 18 7.4 3 Cl2 Sand 4.1 1.8
S2W 31 7.4 3 Cl2 Sand 11.3 4.7
S3S 29 7.4 1.4 Cl2 Microfilter 10.3 4.5
S3D 28 7.3 3.1 Cl2 Microfilter 5.5 2.8
S4C 27 7.4 4 Cl2* Sand 7.1 9.1
S4W 30 7.4 3 Cl2* Sand 6.5 3.2
S5 27 7.4 2 Cl2 Sand 3.0 1.2
S6L 29 7.6 2 Cl2* Sand 7.9 4.8
S6T 34 7.4 3 Cl2* Sand 7.7 2.5
S7 27 7.2 1 Cl2 Sand 7.8 4.3
S10 31 7.4 3 Cl2 Sand 8.4 5.2
S11L 28 7.2 2 Cl2 Sand 5.2 3.4
S11D 30 7.2 3 Cl2 Sand 5.3 3.6
S12L 27 7.5 2.7 Cl2 Sand 3.7 10.2
S12I 30 7.5 2.4 Cl2 Sand 4.3 7.4
S13 29 7.6 1 Cl2 Sand 3.9 1.2
S14 27 7.8 3 Cl2 Sand 13.8 12.3
S15L 27 7.7 2.8 Cl2* Sand 3.8 0.8
S15T 32 7.8 1.2 Cl2* Sand 7.5 1.2
S16 27 7.2 0.0 Cl2 Sand 7.5 2.2
S17L 28 7.6 3.5 Cl2* Sand 7.3 4.1
S17T 33 7.4 3.5 Cl2* Sand 23.6 4.4
Median 28 7.4 3
7.1 3.6
Maximum 34 7.8 4
23.6 12.3
Minimum 18 7.2 0
3 0.8
*Electrochemically generated chlorine; FAC (free available chlorine), TOC (total organic
carbon), TN (total nitrogen).
Occurrence of DBPs in Swimming Pools
A box and whisker plot form is used to show the different measured parameters
and DBPs in the surveyed swimming pools. The median, quartiles, minimum and
maximum values are shown. A key for reading the boxplot is shown Figure 5.1.
71
For the 23 indoor pools, the FAC, TOC and TN are shown in Figure 5.1.
a
Figure 5.1: Box-whisker plot key (a), FAC (Free chlorine), TOC (total organic
carbon) and TN (total nitrogen) of the 23 indoor swimming pools.
A great variation among the pools for the different water quality parameters was
observed. Few readings of the three parameters were outliers and occurred out the range
of the most measured values. The result shows how differently indoor swimming public
pools are managed and that no well defined standards are available to narrow the
variations among different pools also.
The pools sampled in this survey were operated mainly at two temperature ranges
27-29°C and 32-34°C. The pH average of the water was 7.5 and it ranged between 7.2
and 7.8. The measured TOC was between 3 and 13.8 mg/L and TN was between 0.8 and
Q3
Q1
Median
Minimum
value
Maximum
value
X Outlier point
0
5
10
15
20
25
30
FAC TOC TN
mg/L
b
72
12.3 mg/L. In four pools (S4C, S12L, S12I, and S14) TN exceeded TOC but in all other
pools the TOC was higher than the TN. All these 23 pools are using chlorine for
disinfection. In fourteen pools the chlorine was introduced in the solid form [Ca(ClO)2],
while is the remaining six chlorine was generated electrochemically in situ using sodium
chloride. The free available chlorine average in the tested pools was 2.5 mg/L and varied
between 0 and 4 mg/L. All the pools except two, which used microfiltration, used a sand
filter. Only one of the pools (S13) used ground water from a local well for filling water
whereas the other pools used the local drinking water distribution system for filling and
make up.
For this survey of indoor pools, five DBP classes were determined in each pool
water sample. Table 5.2 shows the species and total THM measured in these pools.
Median, maximum, and minimum THMs measured in the 23 pools investigated in this
survey were 62, 207 and 25 µg/L, respectively. Chloroform was the major THM
determined in all pools. Brominated THMs were at lower levels in most cases but were
relatively high in pools S6 and S13. S6 used ECGC which was shown to increase the
brominated species during this study. S13 was filled with groundwater from a local well
which can be a source of bromide that can be converted to HOBr, which then reacts to
form brominated species of DBPs. In 30% of the pools, the measured THM was higher
than 80 µg/L (MCL in US drinking water); while in 100% of the pools, the measured
THM was greater than 20 µg/L (the maximum allowed in some European countries
swimming pools).
73
Table 5.2: Trihalomethanes (THMs) occurrence in indoor swimming pools
Pool TCM BDCM DBCM TBM TTHM
µg/L µg/L µg/L µg/L µg/L
S1 41 1 <MRL ND 42
S2C 49 1 <MRL ND 51
S2W 119 3 <MRL ND 122
S3S 77 2 <MRL ND 80
S3D 62 1 <MRL ND 63
S4C 37 1 <MRL ND 38
S4W 49 3 <MRL ND 53
S5 26 1 <MRL ND 28
S6L 72 3 <MRL ND 76
S6T 72 12 4 1 90
S7 113 1 <MRL ND 114
S10 89 2 <MRL ND 91
S11L 29 2 <MRL ND 31
S11D 111 2 <MRL ND 113
S12L 25 1 <MRL ND 26
S12I 32 1 <MRL ND 34
S13 74 28 10 1 114
S14 47 3 <MRL ND 50
S15L 38 6 1 ND 45
S15T 121 5 1 ND 127
S16 61 2 <MRL ND 63
S17L 82 11 2 ND 95
S17T 207 6 <MRL ND 213
Median 62 2
63
Maximum 207 28 213
Minimum 25 1 26
TCM (chloroform), BDCM (bromdichloromethane), DBCM
(dibromochloromethane), and TBM (tribromomethane) TTHM (total
trihalomethanes), MRL (minimum reporting level), ND (not detected).
Total HANs and their species are shown in Table 5.3. The median, maximum and
minimum HANs were 16, 53, and 5 µg/L, respectively. The major and most frequent
haloacetonitrile measured was DCAN. In a few pools brominated acetonitriles were
detected at very low levels (1-3 µg/L) except in pool S13, which is filled with
74
groundwater, where the BCAN and DBAN were 13 and 5 µg/L, respectively. Also
sample S6 had 4 and 2 µg/L BCAN and DBAN, respectively. Unsurprisingly when
brominated THM species were high the brominated HANs species increased also. They
ranged between 1.4 and 13.3 µg/L with an average of 5 µg/L.
Table 5.3: Haloacetonitriles (HANs) occurrence in indoor swimming pools
Pool CAN TCAN DCAN BAN BCAN DBAN THANs
µg/L µg/L µg/L µg/L µg/L µg/L µg/L
S1 1 ND 8 ND ND ND 9
S2C ND ND 4 ND ND ND 5
S2W 1 ND 22 ND 1 ND 25
S3S 1 ND 27 ND 1 ND 30
S3D 1 ND 7 ND ND ND 8
S4C 1 ND 15 ND 1 ND 16
S4W 1 ND 21 ND 2 ND 24
S5 1 ND 14 ND 1 ND 15
S6L 1 ND 12 ND 1 ND 15
S6T 1 ND 13 ND 4 2 21
S7 1 ND 14 ND ND ND 15
S10 2 ND 16 ND ND 1 18
S11L 1 ND 11 ND ND ND 13
S11D 1 ND 7 ND ND 1 9
S12L 1 ND 15 ND ND ND 16
S12I 1 ND 17 ND ND ND 18
S13 1 ND 27 1 13 5 47
S14 1 ND 13 ND 1 ND 15
S15L 1 ND 7 ND 2 1 11
S15T 1 ND 4 ND ND ND 6
S16 1 ND 15 ND ND ND 16
S17L 1 ND 16 1 3 1 22
S17T 3 1 47 ND 2 ND 53
Median 16
Maximum 53
Minimum 5
CAN (chloroacetonitrile), TCAN (trichloroacetonitrile), DCAN (dichloroacetonitrile),
BAN (bromoacetonitrile), BCAN (bromochloroacetonitrile, DBAN
(dibromoacetonitrile), THANs (total haloacetonitriles), ND (not detected)
HNMs were at lower levels than THMs and HANs (Table 5.4).
75
Three HNM species (TCNM, BNM, and BCNM) were determined to be present
in the collected swimming pool samples.
Table 5.4: Halonitromethanes (HNMs) occurrence in indoor swimming pools
Pool TCNM BNM BCNM THNM
µg/L µg/L µg/L µg/L
S1 <MRL <MRL 2.4 2.9
S2C 0.8 <MRL 7.5 8.3
S2W <MRL <MRL 1.3 1.9
S3S 0.7 <MRL 6.3 7.0
S3D 0.9 <MRL 3.9 4.8
S4C <MRL <MRL 2.5 3.0
S4W <MRL <MRL 1.1 1.7
S5 <MRL <MRL 3.2 3.7
S6L 0.8 <MRL 2.6 3.6
S6T <MRL 2.2 3.8 6.5
S7 2 <MRL 3.4 5.4
S10 2.3 <MRL 11 13.3
S11L <MRL <MRL 3.6 4.1
S11D 0.9 <MRL 4.6 5.5
S12L 1 <MRL 4.3 5.4
S12I 1.1 <MRL 5.5 6.6
S13 <MRL 2.0 4.7 7.3
S14 0.9 <MRL 3.7 4.7
S15L <MRL 0.7 1.5 2.7
S15T <MRL <MRL 0.8 1.4
S16 0.8 <MRL 2.6 3.4
S17L 0.7 1.6 5.8 8.1
S17T 1.4 1 6.8 9.2
Median 3.7 4.8
Maximum 11 13.3
Minimum 0.8 1.4
TCNM (trichloronitromethane), BNM (bromonitromethane), BCNM
(bromochloronitromethane), THNM (total halonitromethane), MRL (minimum reporting
level).
76
Mostly the HNM species ranged between the MRL to 7.5 µg/L. To our knowledge, this is
the first time that HNMs rather than only TCNM have been determined and measured in
swimming pools water.
THMs, HANs and HNMs are shown in Figure 5.2 (a) and (b).
Figure 5.2: Occurrence of trihalomethanes (THMs), haloacetonitriles (HANs) (a)
and halonitromethanes (HNMs) (b) in 23 indoor pools.
0
50
100
150
200
250
THM HAN
µg/L
a
0
2
4
6
8
10
12
14
HNM
µg/L
b
77
HAAs were the highest measured class of DBPs in this survey (Table 5.5). The
median, maximum, and minimum HAAs were 960, 9005, and 172 µg/L, respectively.
TCAA and DCAA were the dominated species among the measured HAAs. In some
samples DCAA was lower than TCAA while in others it was higher. BCAA and BDCAA
appeared in all samples although at low levels compared to chlorinated HAAs. In some of
the samples DBAA and BAA appeared but at lower levels than BCAA and BDCAA.
Generally the brominated and mixed brominated and chlorinated haloacetic acids
showed high levels in the pools that use ECGC for disinfection and in the pool that used
groundwater for filling. The profile of HAAs in these pools is shown in Figure 5.3.
78
Table 5.5: Haloacetic acids (HAAs) occurrence in indoor swimming pools
Pool CAA BAA DCAA BCAA TCAA DBAA BDCAA DBCAA TBAA THAA
µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L
S1 ND <MRL 100 1 87 <MRL 8 1 ND 198
S2C ND <MRL 314 3 224 <MRL 13 1 ND 555
S2W ND 1 896 14 718 <MRL 36 <MRL ND 1665
S3S ND <MRL 712 5 1537 <MRL 21 <MRL ND 2276
S3D ND <MRL 937 7 776 <MRL 16 1 ND 1738
S4C ND <MRL 688 10 789 1 27 3 ND 1518
S4W ND 1 81 4 241 <MRL 60 5 ND 392
S5 ND <MRL 82 3 141 <MRL 22 2 ND 251
S6L ND 1 928 30 552 2 48 3 ND 1563
S6T ND 1 1033 36 351 4 36 7 ND 1468
S7 ND <MRL 1139 5 418 <MRL 22 <MRL ND 1585
S10 ND <MRL 1297 4 416 <MRL 13 <MRL ND 1731
S11L ND <MRL 123 2 76 <MRL 15 <MRL ND 216
S11D ND <MRL 360 3 149 <MRL 11 <MRL ND 523
S12L ND <MRL 162 1 95 <MRL 8 3 ND 269
S12I ND <MRL 242 2 216 <MRL 22 2 ND 484
S13 ND 1 73 13 100 2 55 15 ND 260
S14 ND <MRL 52 2 92 <MRL 25 2 ND 172
S15L ND 2 115 21 102 5 47 14 ND 306
S15T ND 2 690 31 183 6 45 2 ND 960
S16 ND <MRL 549 5 568 <MRL 20 1 ND 1143
S17L ND 5 504 106 288 25 110 32 ND 1070
S17T ND 4 6787 176 1925 16 93 4 ND 9005
Median 504 5 241 4.5 22 3 960
Maximum 6787 176 1925 25 110 32 9005
Minimum 52 1 76 <MRL 8 <MRL 172
CAA (chloroacetic acid), BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA
(bromochloroacetic acid), TCAA (trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA
(dibromoacetic acid), TBAA (tribromoacetic acid), THAA (total HAA), MRL (minimum
reporting level)
79
Figure 5.3: Occurrence of haloacetic acids (HAAs) in 23 indoor
swimming pools.
These exceptionally (compared to drinking water samples) high values of HAAs
are attributed to human body fluids that have been shown to have a high formation
potential of HAAs during this study (which will be discussed further in Chapter Seven).
Also HAAs are nonvolatile and soluble compounds and can accumulate in the pool water
unless the whole water is diluted. More change in concentration has been observed for
HAAs, compared to the other DBPs, among the pools investigated in this study. These
high HAAs concentrations can be greatly harmful especially considering the possibility
of ingesting considerable water volumes during swimming as will be explained in the
next chapter.
0
1000
2000
3000
4000
5000
6000
7000
8000
9000
10000
HAA
µg/L
80
N-nitrosodimethylamine (NDMA) was detected in the 23 indoor swimming pool
water samples (Table 5.6). NDMA ranged between 2 and 83 ng/L with a median of 17
ng/L.
Table 5.6: N-nitrosodimethylamine (NDMA) occurrence in indoor swimming pools
Pool NDMA
ng/L
S1 30
S2C 9
S2W 83
S3S 28
S3D 14
S4C 16
S4W 18
S5 28
S6L 9
S6T 60
S7 9
S10 3
S11L 12
S11D 17
S12L 2
S12I 6
S13 13
S14 18
S15L 15
S15T 76
S16 53
S17L 17
S17T 42
Median 17
Maximum 83
Minimum 2
81
Nitrosamines are a group of the most toxic and carcinogenic chemicals. Their
carcinogenic effect is manifested at very low concentration (ng/L) levels. EPA classifies
these compounds as ―probable human carcinogens‖ and determined their 10-6
cancer risk
level in drinking water to be as low as 0.7 ng/L (EPA, 1997; Andrzejewski et al., 2005;
IRIS, 2009). California has set a notification level of 10 ng/L of NDMA, while the
Ontario Government in Canada set a standard of 9 ng/L of NDMA in drinking water
(Government of Ontario, 2009). Exposure to high levels of NDMA from swimming may
cause serious adverse health effects.
Three indoor swimming pool waters were monitored over a nine month sampling
period. Table 5.7 shows the operational conditions and water quality of the three
monitored swimming pools during this time. The average FAC was 3 mg/L, which is
within the typical free chlorine level that is required by US swimming pool regulations
applied by the different states including South Carolina DEHC (2007). The TOC and TN
of pool water varied during the course of this study. The TOC ranged between 5.3 and
25.4 mg/L with an average of 10.6 mg/L. On the other hand TN varied over a more
narrow range, between 2 and 5 mg/L with an average of 3 mg/L. These parameters
changed and varied with time within the same pool and also among pools.
82
Table 5.7: Characteristics of three indoor swimming pools waters monitored during 9 months
Sampling
date
S16 S17L S17T
TOC mg/L
TN mg/L
FAC mg/L
Temp. °C
pH TOC mg/L
TN mg/L
FAC mg/L
Temp. °C
pH TOC mg/L
TN mg/L
FAC mg/L
Temp. °C
pH
22/05/2009 5.6 2.1 2.6 28 7.8 6.8 3.4 3 28 7.6 14.5 2.1 3 33 7.6
22/05/2009 5.8 2 2.4 28 7.8 6.6 3.4 3 28 7.6 14.6 2.2 3 33 7.6
22/05/2009 6.1 2 2.4 28 7.8 6.6 3.4 3 28 7.6 15 2.3 3 33 7.8
24/05/2009 5.7 2.1 3.5 28 7.2 6.3 3.5 3.5 28 7.6 15.1 2.2 2 33 7.6
24/05/2009 5.6 2.1 3.9 28 7.3 6.1 3.4 3.5 28 7.6 14.8 2.2 2 33 7.6
30/05/2009 6.2 2.1 4.6 28 6.7 6.5 3.5 3 28 7.6 15.5 2.3 4 33 7.6
02/06/2009 6.4 2.1 3.2 28 7.0 7 3.5 1.5 28 7.6 16.5 2.1 3 33 7.6
06/06/2009 6.3 2.1 0.7 26 7.0 7.4 3.6 4 28 7.6 16.9 2.3 4 33 7.6
09/06/2009 6.6 2.1 2.1 27 7.6 7.2 3.6 3 28 7.6 16.9 2.2 2 33 7.6
18/10/2009 5.3 2.0 2.3 28 7.5 6.6 4.3 3.5 27 7.2 21.7 3.07 3.5 34 7.8
25/10/2009 5.5 2.0 0.6 27 7.5 6.6 4.2 3 28 7.2 20.9 3.2 6 33 7.2
22/12/2009 NM NM NM NM NM 5.8 4.2 3 27 7.6 22.3 4.7 3.5 34 7.6
10/01/2010 6.9 2.4 1.6 27 7.7 6.3 4.3 4.5 26 7.5 25.2 4.98 3 34 7.6
17/01/2010 7.3 2.4 2.9 27 7.6 6.4 4.4 3.5 29 7.6 25.4 5 3.5 32 7.4
17/02/2010 7.5 2.2 0.08 27 7.2 7.3 4.1 3 27 7.6 23.6 4.4 3 33 7.5
TOC (total organic carbon), TN (total nitrogen), FAC (free available chlorine)
83
The results of the DBP classes determined in the water of the three monitored
swimming pools are shown in Table 5.8. Species of each DBP class are shown in
Appendix C. THMs concentrations in the water ranged from 29 to 259 µg/L with an
average of 108 µg/L. The highest THMs measured (259 µg/L) were in the warm pool
(S17T) monitored in this study (Figure 5.4), which also had the highest TOC
measurements. Chloroform was the major THM measured in the three pools (Figure 5.5).
BDCM was measured at higher levels (Figure 5.5) in the two pools that use sodium
chloride to generate chlorine electrochemically on site. The range of the measured
BDCM in the three pools was 0 to 29 µg/L. The atmospheric THM concentrations were
not measured directly in this study; however, it is well documented in the literature that a
strong correlation exists between water and atmospheric concentrations (Aggazotti et al.,
1995; 1998; Chu and Nieuwenhuijsen, 2002). Chlorination via electrochemical
generation of chlorine from sodium chloride resulted in increased brominated species.
84
Table 5.8: Occurrence of THMs, HAAs, and HNMs in three indoor swimming pools
Sampling
date
S16 S17L S17T
TTHM
µg/L
THAA
µg/L
THNM
µg/L
TTHM
µg/L
THAA
µg/L
THNM
µg/L
TTHM
µg/L
THAA
µg/L
THNM
µg/L
22/05/2009 60 2039 5.4 92 NM 9.7 163 NM 13.8
22/05/2009 57 2031 5.8 89 NM 9.7 160 NM 12.6
22/05/2009 57 2039 5.9 88 NM 10.1 162 3398 13.2
24/05/2009 54 1681 3.4 86 1531 8.7 171 2549 10.9
24/05/2009 52 1648 3.5 91 1437 8.5 161 2244 11.3
30/05/2009 53 1725 3.2 83 1392 7.8 199 2397 15.0
02/06/2009 56 1691 3.2 77 1377 6.6 192 2427 13.7
06/06/2009 48 1708 3.1 77 1434 7.5 137 2869 12.2
09/06/2009 40 1674 3.0 84 1470 9.0 160 2884 13.7
18/10/2009 81 1804 4.4 79 1174 5.8 259 9691 15.0
25/10/2009 38 1673 3.4 79 1196 6.4 249 9348 22.9
22/12/2009 NM NM NM 64 955 4.7 176 11695 8.6
10/01/2010 29 1479 5.0 72 793 8.1 182 7392 18.1
17/01/2010 54 1005 4.2 91 667 9.2 188 6291 16.7
17/02/2010 63 1143 3.4 95 1070 8.1 213 9005 9.2
TTHM (total trihalomethanes), THAA (total haloacetic acids), THNM (total halonitromethanes)
85
Figure 5.4: Average DBPs measured in three indoor swimming pools during 9 months. THM4 (sum of 4
trihalomethanes), HAA9 (sum of 9 haloacetic acids), HNM9 (sum of 9 halonitromethanes), HAN6 (sum of 6
haloacetonitriles). (error bars are the standard deviation)
0
50
100
150
200
250
THM4
µg/L
S16 S17L S17T
0
2000
4000
6000
8000
10000
HAA9
µg/L
S16 S17L S17T
0
5
10
15
20
HNM9
µg/L
S16 S17L S17T
0
10
20
30
40
50
60
70
HAN6
µg/L
S16 S17L S17T
86
Figure 5.5: Average DBP species measured in three swimming pools during 9 months, THM species (a), HAA species (b),
HNM species (c) and HAN species (d). TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and
TBM (tribromomethane)
0
40
80
120
160
200
S16 S17L S17T
µg/L
a
TBM
DBCM
BDCM
TCM
0
1000
2000
3000
4000
5000
6000
S16 S17L S17T
µg/L
b DBCAA
BDCAA
DBAA
TCAA
BCAA
DCAA
0
2
4
6
8
10
12
14
16
S16 S17L S17T
µg/L
c
DBNM
BCNM
BNM
TCNM
0
10
20
30
40
50
60
S16 S17L S17T
µg/L
d
TCAN
CAN
DBAN
BCAN
DCAN
87
This pool water concentration of THMs is expected to increase the lifetime
exposure to THMs that will increase the acute and chronic adverse health effects on a
wide range of the population considering the number of swimming pools and swimmers
and workers.
The HAAs in the three swimming pools were very high and ranged between 667
to 11695 µg/L with an average of 2820 µg/L (Table 5.8 and Figure 5.4). The dominant
HAAs were the DCAA and the TCAA. Brominated species of HAAs were measured also
with BDCAA as the major brominated HAA species. The maximum amount of BDCAA
was 151 µg/L and the minimum was 9 µg/L with an average of 57 µg/L. Dibrominated
species were at lower levels (less than 20 µg/L) (Table 5.8 and Figure 5.5).
The HNMs ranged from 3 to 23 µg/L with an average of 9 µg/L (Table 5.8 and
Figure 5.4). BCNM and BNM were the most abundant halonitromethane species found to
occur in the water of the swimming pools in this study. The BCNM range was 2 to 21
µg/L with an average of 6 µg/L. The BNM maximum amount was 6.5 µg/L with an
average of 2 µg/L. TCNM was the lowest HNM species in the swimming pool water
(Figure 5.5).
Haloacetonitriles were measured on three sampling occasions during the
monitoring. Their occurrence was also dependent on pool conditions. DCAN was the
major species measured in the three pools but other species were detected as shown in
Table 5.9 and Figure 5.4. Total haloacetonitriles ranged from 9 to 64 µg/L. Compared to
their drinking water occurrence, these are higher levels.
88
Table 5.9: Occurrence of haloacetonitriles (HANs) in three indoor swimming pools
Pool Sampling
date CAN TCAN DCAN BAN BCAN DBAN THANs
µg/L µg/L µg/L µg/L µg/L µg/L µg/L
10/1/2010 1 ND 10 ND ND ND 11
S16 17/1/2010 1 ND 8 ND ND ND 9
17/2/2010 1 ND 15 ND ND ND 16
10/1/2010 1 ND 6 ND 8 8 23
S17L 17/1/2010 1 ND 9 ND 4 3 17
17/2/2010 1 ND 16 1 3 1 22
10/1/2010 2 1 46 ND 11 5 64
S17T 17/1/2010 2 ND 38 ND 2 1 43
17/2/2010 3 1 47 ND 2 0 53
CAN (chloroacetonitrile), TCAN (trichloroacetonitrile), DCAN (dichloroacetonitrile),
BAN (bromoacetonitrile), BCAN (bromochloroacetonitrile, DBAN
(dibromoacetonitrile), THANs (total haloacetonitriles), ND (not detected)
During the monitoring period of the three pools a variation in the DBPs was
observed. The THM profile of the three pools is shown in Figure 5.6. The THM was
around the same level for each pool. On the other hand the HAA profile (Figure 5.7) of
each of the three pools shows a wider variation during the same monitoring period.
89
Figure: 5.6: Trihalomethanes (THMs) measured in three pools during 9 months
0
20
40
60
80
100
µg/L
S16
0
20
40
60
80
100
µg/L
S17L
0
50
100
150
200
250
300
µg/L
S17T
90
Figure 5.7: Haloacetic acids (HAAs) measured in three pools during 9 months
0
500
1000
1500
2000
2500
µg/L
S16
0
500
1000
1500
2000
µg/L
S17L
02000400060008000
100001200014000
µg/L
S17T
91
Having said that three DBPs exposure routes (inhalation, dermal, and ingestion) are
possible in swimming pools implies that these elevated and uncontrolled levels of DBPs
in US swimming pools increases the exposure doses that swimmers and other workers
and attendees can be exposed to. This higher exposure will increase the daily dose that
may result in an increased lifetime cancer risk and non-carcinogenic hazards. Recent
studies mainly performed in European countries reported lower concentrations of THMs
than we have measured in this study. Table 5.10 shows a comparison of THM
concentration levels measured in indoor swimming pools water in this study and values
measured in other countries. In Weaver et al. (2009), 45.3% of the swimming pools water
samples measured had THMs at greater than 80 µg/L which is the MCL for drinking
water in the US and similar high values have been found in this study also. Another
notable observation is the elevation of brominated species of THMs when chlorine is
generated electrochemically from sodium chloride, which was reported in both Lee et al.
(2009) for Korean indoor pools and in this study (US pools). Also higher water
temperature increased the reactivity of chlorine with DBP precursors. The higher
temperature also may increase the solubility of DBPs that will maintain higher
concentrations than in pools operated at lower water temperatures. More than 90% of the
measured THMs in this study and Weaver et al. (2009) were greater than 20 µg/L, which
is the maximum amount accepted by swimming pool regulations in some European
countries. HAAs have not been measured in swimming pools to the same extent as
THMs, however, a recent study on THMs and HAAs in indoor and outdoor pools in
Canada reported both THM and HAAs. THMs reported in Canadian indoor pools ranged
92
between 48.8 and 116.8 µg/L (most were less than 60 µg/L). On the other hand HAAs
reported in the same study were higher with a range of 348 to 510 µg/L (Simard, 2009).
Table 5.10: Trihalomethanes (THMs) measured in indoor pools in the US and other
countries
Country TCM
µg/L
BDCM
µg/L
DBCM
µg/L
TBM
µg/L Disinfectant
US (This study) 37-78 1-2 0 Cl2
63-239 3-25 0-7 Cl2*
Spain
(Marina et al., 2009) 13.7 Cl2
Korea
(Lee et al., 2009)
40.7 3 0.5 Cl2
28.5 2.4 0.2 O3/ Cl2
27.3 9.8 9.1 18.8 Cl2*
UK
(Chu and
Nieuwenhuijsen, 2002)
121.1 8.3 2.7 0.9 Cl2
Italy
(Fantuzzi et al., 2001) 33.2 4.2 1.9 0.4 Cl2
Germany
(Erdinger et al., 2004) 7.1-24.8 Cl2
Thailand
(Mallika et al., 2008) 9.5-36.97 8.9-18.01
5.19-
22.87 ND-6.65 Cl2
Taiwan
(Hsu et al., 2009) 43.5-74 Cl2
Poland
(Kozlowska et al., 2006) 10-41 0.7-5.7 0.37-1.6 Cl2
*Electrochemically generated chlorine using sodium chlorine. TCM (chloroform), BDCM
(bromdichloromethane), DBCM (dibromochloromethane), and TBM (tribromomethane), ND (not
detected)
93
Conclusions
The occurrence of DBPs in the investigated pools using chlorine as a disinfectant
was higher than amounts present in treated drinking water. Chloroform was the
major THM specie found in swimming pools studied. Among HAAs the major
two species were DCAA and TCAA. HANs, HNMs, and NDMA were at higher
levels in all pools compared to their occurrence in drinking water.
Variation in operational parameters and measured DBPs was noticed either in the
same swimming pool or between different pools.
The warm pools (32-34°C) produced generally more DBPs from all classes than
the pools operated at lower temperatures.
The electrochemically generated chlorine using sodium chloride resulted in more
brominated species occurrence in the swimming pools that use this method to
produce hypochlorite for chlorination.
The low volatility of HAAs causes their accumulation in the water and thus their
concentrations increased to a very high level over time. THMs are not
accumulating in the pool water since they are volatile and escape to the air over
the pool water.
94
CHAPTER SIX
EXPOSURE CHARACTERIZATION AND RISK ASSESSMENT
Introduction and Objectives
Although swimming is healthy and considered as a beneficial sport, it also can
cause an adverse health impact due to high exposures to the DBPs that are found in the
swimming pool water and also the air over the swimming water in indoor swimming
pools. The probable adverse health effect has recently caused more attention to research
of swimming pool water DBPs formation to improve the hygienic conditions and water
quality (Zwiener et al., 2007). Chloroform as the dominant volatile THM form in
chlorinated swimming pool fresh water was measured in human breath after exposure
from showering and bathing to investigate the dermal and inhalation pathway which were
shown to be significant intake routes (Xu and Weisel, 2005). In other studies, THMs in
blood and breath were measured after showering and bathing and reported at higher
levels than after ingestion of chlorinated drinking water (Miles et al., 2002; Egorov et al.,
2003; Nuckols et al., 2005). Physical stress (intensity of exercise) and swimming pool
water and air concentration were reported as important factors in increasing the uptake
(Lindstrom et al., 1997; Aggazzotti et al., 1998; Levesque et al., 2000). Swimmers are not
the only group that are exposed to DBPs from swimming pool water and air; employees
including lifeguards, trainees, reception workers, and maintenance workers or any
attendees are also exposed to DBPs in the swimming pool facility. Blood, urine, and
breath samples of swimming pools workers showed elevated levels of chloroform, which
was positively correlated to chloroform concentration in the ambient air in the swimming
95
pool area (Fantuzzi et al., 2001; Erdinger et al., 2004; Caro and Gallego, 2007).
Measurement of DBPs in air and breath samples is difficult and tedious, which may lead
to wide variability; moreover there is no well-defined sampling and measurement
procedure that can lead to confident measurements and minimize the variations that have
been observed in reported results in the literature (Caro and Gallego, 2008, Hsu et al.,
2009). An effect of swimming pool water agitation and number of swimmers in the pool
on the air chloroform concentration was observed (Lahl et al., 1981; Aggazzotti and
Predieri, 1986; Rogozen et al., 1988). In this study the ambient air content of DBPs in
swimming pools was determined indirectly from the aqueous DBPs concentration using
Henry’s law and US EPA SWIMODEL version 3.0 (US EPA, 2003a; 2003b).
DBPs in swimming pool water can result in acute or chronic health effects. An
evaluation of the adverse health effects of DBPs in swimming pool water and in air over
the pool water surface can be carried out by conducting a health risk assessment. Risk
assessment aims to indicate and evaluate quantitatively potential risks from exposure to a
contaminant, such as DBPs in swimming pool water. Risk assessment includes hazard
identification, dose response assessment, exposure assessment, and risk characterization
(NRC, 1983, 1994; US EPA, 2005). The four steps included in risk assessment are briefly
discussed and explained in this chapter as provided by the National Research Council
(1983, 1994) and US EPA (2005).
Hazard identification is the first step in risk assessment that determines the type
and degree of hazard that a contaminant could have on human health. Non-carcinogenic
health effect and hazard can be used to specify a dose that triggers an adverse health
96
effect. Carcinogenic risk identification can be tested by controlled animal studies or from
human epidemiological studies. The carcinogenic and non-carcinogenic health effects of
DBPs have been studied since their determination in chlorinated drinking water (Lee at
al., 2004). Evidence from animal studies and other epidemiological studies showed that
DBPs are associated with tumors in the liver, kidney, and intestine; in addition to their
carcinogenic effects on the bladder, rectum, and colon (Morris et al., 1992; King and
Marrett, 1996; Doyle et al., 1997; Cantor et al., 1998; Villanueva et al., 2004). Also
DBPs were shown to affect intrauterine growth and fetal growth retardation, low birth
weight, central nervous system defects, and spontaneous abortion (Kramer et al., 1992;
Bove et al., 1995; Gallagher et al. 1998; Waller et al., 1998). Epidemiological studies
showed positive possible association between DBPs exposure from chlorinated water and
cancer risk or incidence, especially cancer of the rectum, lung, bladder, skin, and kidney
(Page et al., 1976; Cantor et al., 1978, 1987, 1998; Yang et al., 1996, 1998, 2000;
Karagas, 2008). Consequently US EPA classified these hazardous DBPs into five
different groups of carcinogenicity: Group A, human carcinogen; Group B1 and B2,
probable human carcinogen; Group C, possible human carcinogen; Group D, not
classified as to human carcinogen; and Group E, evidence of non-carcinogenicity for
human.
Dose response assessment of DBPs is a characterization of dose-response effect
on the exposed population. A dose response study is to determine the dose magnitude
result with a specific adverse health effect. This numerical estimation is represented in a
dose-response curve. For carcinogenic effects a potency factor (PF) is the slope of dose-
97
response curve that gives the cancer risk per dose unit can be obtained (Benner, 2004; US
EPA, 2005). PF is an upper bound estimate of a chemical’s probability of causing cancer
over years of lifetime. For the non-carcinogenic effect a reference dose (RfD) is
determined (US EPA, 2005).
The NOAEL is defined as the highest dose or concentration of a contaminant that
does not show adverse health effect (WHO, 2004). In case the NOAEL is not determined,
the lowest-observed-adverse-effect level (LOAEL) which is the lowest observed dose or
concentration of a contaminant at which there is an adverse health effect, may be used
(WHO, 2004). The Acceptable daily intake (ADI) is the amount of a chemical to which a
person can be exposed on a daily basis over lifetime without adverse health effect. The
ADI is derived by dividing an experimentally determined no-observed-adverse-effect
level (NOAEL) by a safety factor (Sf) which is multiples of 10 representing a specific
area of uncertainty in the data (US EPA, 1993).
ADI (human dose) = NOAEL (experimental dose)/Sf (6.1)
The RfD is a benchmark dose derived from the NOAEL by consistent application of
generally order-of-magnitude uncertainty factors (UFs) and modifying factor (MF) which
is an additional uncertainty factor that is greater than zero and less than or equal to 10.
RfD = NOAEL / (UF x MF) (6.2)
The RfD is generally expressed in units of milligrams per kilogram of bodyweight per
day (mg/kg/day). Usually, doses less than the RfD are not likely to be associated with
98
adverse health risks. When the frequency and/or magnitude of the exposures exceeding
the RfD increase, the probability of adverse health effects in a human population
increases.
US EPA has developed an integrated risk information system (IRIS) that specifies
for each hazardous chemical specific RfD and PF (US EPA, 2009a). For regulated THM
and HAA species RfD and PF values are available in the IRIS database and Risk
Assessment Information System (RAIS) (Table 6.1).
Exposure assessment for a contaminant needs to specify its exposure routes and
exposure duration to estimate the amount (dose) that can reach the body and cause
detectable adverse health effects. The frequency and magnitude of exposure can be
reflected as an average daily exposure dose (ADD) , also known as chronic daily intake
(CDI), which can also be extrapolated to lifetime average dose (LADD). The exposure to
DBPs from swimming is dependent on age, sex, body weight, body surface area, and
other specific factors depending on the exposure pathway and route that is specified for a
DBP intake. These exposure variables and factors are available from US EPA in the
Exposure Factors Handbook: 2009 update (US EPA, 2009b).
Cancer potency reference value (i.e., Potency factor) of chloroform has been
withdrawn from the IRIS after it was reassessed. Upon reassessment it was determined
that quantitative dose-response assessment of chloroform is not supported and new
estimates of cancer potency were not derived yet. Specifically for chloroform oral
potency factor the reassessment used a nonlinear approach in contrast to linear dose-
response that was assumed before (Benner, 2004). The US EPA considers chloroform
99
likely to be carcinogenic to humans under high-exposure conditions that result in
cytotoxicity therefore the potency factor of chloroform and a dose of 0.01 mg/kg/day was
considered protective against cancer risk.
Table 6.1: Reference dose (RfD) and potency factor (PF) of DBPs (IRIS, 2009; RAIS,
2009; US EPA, 1991, 1999)
DBP Oral RfD*
(mg/kg/d)
PForal
(mg/kg/d)-1
PFdermal
(mg/kg/d)-1
PFinhalation
(mg/kg/d)-1
Chloroform (TCM) 1.00E-02 6.10E-03** 3.05E-02 8.05E-02
Bromodichloromethane (BDCM) 2.00E-02 6.20E-02 6.33E-02 ***
Dibromochloromethane (DBCM) 2.00E-02 8.40E-02 1.40E-01 ***
Bromoform (TBM) 2.00E-02 7.90E-03 1.32E-02 3.85E-03
Dichloroacetic acid (DCAA) 4.00E-03 5.00E-02 5.00E-02 1.40E-06
Trichloroacetic acid (TCAA) 3.00E-02
* No RfD is available for other two exposure routes
**Withdrawn from IRIS database.
*** PForal of BDCM and DBCM are used for inhalation exposure (Wang et al., 2007)
In swimming pools the three main exposure routes (ingestion, inhalation, and
dermal absorption) are considered (Aggazzotti et al., 1998) as well as the swimming
event duration and frequency with different specific personal and human body details.
Inhalation and dermal absorption of DBPs are considered as important routes of exposure
in recent studies (Whitaker et al., 2003; King et al., 2004; Nuckols et al., 2005; Gordon et
al., 2006).
Risk characterization is the final step in risk assessment that seeks a numerical
qualitative and quantitative risk level expression by the integration of the hazard
100
identification data, dose response data, and exposure information. Mathematical
calculations utilize the values specified for each hazardous contaminant such as CDI,
ADD, LADD, PF, and RfD result in quantitative risk characterization from DBPs in
swimming pools.
For carcinogens, lifetime cancer risk (R) is obtained by the equation
𝑅 = 𝐶𝐷𝐼 × 𝑆𝐹 (6.3)
Risk (R) in this equation is the probability of excess lifetime cancer. In general the US
EPA considers risk values more than 1 in a million (10-6
) unacceptable (US EPA, 2009a).
On the other hand, the non-carcinogenic hazard quotient (HQ) can be calculated as a
using the equation
HQ =𝐶𝐷𝐼
𝑅𝑓𝐷 (6.4)
The hazard index (HI) is the sum of two or more hazard quotients for multiple substances
and/or multiple exposure pathways. When the hazard index (HI) is greater than 1 then a
possible health effect is expected (US EPA, 2009a).
The objective of this chapter was to characterize and estimate the multipathway
risk assessment of carcinogenic and non-carcinogenic health effects of THMs (TCM,
BDCM, and DBCM) and HAAs (DCAA and TCAA) in indoor swimming pool water and
air.
Methods and Materials
Exposure to THMs and HAAs from swimming pools water depending on their
average water concentration can be estimated as an intake value that is related to a swim
101
event and swimming frequency. The three possible routes of exposure during swimming
(i.e. ingestion, inhalation, and dermal absorption) are used in calculating the intake during
a swim event expressed as mg/event. Average Daily Dose (ADD) and Lifetime Average
Daily Dose (LADD) expressed as mg/kg/day then can be calculated. This calculated dose
(ADD and LADD) magnitude does not account for any metabolism and/or excretion of
DBPs (US EPA, 2003a; 2003b). Swimmer Exposure Assessment Model (SWIMODEL)
and the guidelines for its use are available from US EPA (US EPA, 2003a; 2003b).
Estimations of water ingestion and air inhalation volumes are available in the Exposure
Factors Handbook: 2009 update (US EPA, 2009b). Water concentrations of THMs and
HAAs in swimming pool water can be used in determining the ingestion and dermal
absorption exposure doses. The permeability coefficient that is available for some DBPs
was used in estimating the dermal absorption of permeable DBPs. From the measured
water concentration (Cw), air concentrations (Cair) of volatile DBPs above the pool water
surface can be estimated using Henry’s law. The estimated air concentrations of volatile
DBPs can be used in determining inhalation exposure. Thus exposure from one
swimming event is the sum of the three doses from the three exposure routes. Swimming
duration event, ingested water volume rate during swimming, inhaled air volume, and
body weight and body surface area that have been specified by US EPA in the Exposure
Factors Handbook (US EPA, 1997; 2009b; Dufour et al., 2006) and by the American
Chemistry Council (ACC, 2002) were used to calculate the ADD, LADD, Potential Dose
Rate (PDR), and PDRnormalized. The personal and other swimming activity information is
summarized in Table 6.2.
102
Table 6.2: Recommended human body information (personal information) for exposure estimation (US EPA, 2009b)
Swimmer
group Swimmer
Body
weight
Body
surface
area
Swimming
frequency
Exposure
duration
Inhalation
rate
Ingestion
rate
Event
duration
kg m2 event/year years m
3/hr L/hr hr/event
Non
-
Com
petitiv
e
Adult male 78.1 1.94 120 30 1 0.025 1
Adult female 65.4 1.69 120 30 1 0.025 1
Child (11-14 years) 48.17 1.42 120 4 1 0.05 1
Com
petitiv
e
Adult male 78.1 1.94 238 22 3.2 0.0125 1
Adult female 65.4 1.69 238 22 3.2 0.0125 1
Child (11-14 years) 48.17 1.42 189 4 1.9 0.025 1
103
The main HAAs species measured in swimming pools in this study were DCAA
and TCAA. Both of these compounds have very low vapor pressures (<5.0E-06 mmHg).
Thus the major exposure routes of DCAA and TCAA is expected to be through water
ingestion during swimming. Dermal exposure of these compounds was not excluded
although it is also expected to be low as they occur in the ionic form in water. Some
studies have shown evidence of possible dermal absorption of these DBPs through skin
cells while showering and bathing in chlorinated water (Xu et al., 2002). A dermal
permeation coefficient (Kp) constant was estimated in vitro for HAAs in aqueous
solution across human skin cells (Xu et al., 2002). Measured Kp for HAAs was in a low
range (1-3 10-3
cm/hr) that indicates an insignificant dermal absorption compared to
ingestion intake. Still one can argue that very high swimming pool water HAA amounts
have been measured in the current study may cause appreciable dermal and inhalation
intake even at very low Kp and vapor pressure in addition to other intake pathways
especially ingestion.
THMs are nonpolar compounds that have low water solubility and high vapor
pressure values that make them volatile contaminants which move easily from water to
air. Chloroform, bromdichloromethane, dibromochloromethane, and bromoform vapor
pressures are 197.6, 50, 4.8, and 5.5 mm Hg respectively (US EPA, 2003a). The THM
human skin permeability coefficients from water measured are high compared to HAAs
(0.16-0.21cm/hr) (Xu et al., 2002). Exposure to THM during swimming could be more
significant through the three possible routes compared to HAAs that have much less
volatility and skin permeability (Table 6.3).
104
Table 6.3: Henry’s law constant and dermal permeability (Kp) of some DBPs
Disinfection By-Product
(DBP)
Henry’s Law
constant (25˚C)
(unitless)
Kp*
(cm/hr)
Trichloromethane 1.50E-01** 8.90E-03** , 6.83E-03***
Tribromomethane 2.19E-02** 2.60E-03** , 2.35E-03***
Bromodichloromethane 6.67E-02** 5.80E-03** , 4.02E-03***
Dibromochloromethane 3.21E-02** 3.90E-03**
Dichloroacetic acid 3.43E-07*** 1.21E-03***
Trichloroacetic acid 5.52E-07*** 1.45E-03***
*Kp (dermal permeability)
**US EPA, 2003a
***RAIS, 2009
The arithmetic average values of three THM species (chloroform,
bromodichloromethane, dibromochloromethane) measured through May, 2008 to
October, 2009, and two major HAA species (DCAA and TCAA) measured at the same
time were used to evaluate their health effect by conducting a multipathway health risk
assessment on swimmers and lifeguards. Swimmers were divided to six groups according
to age, sex, and swimming type (i.e. competitive or noncompetitive): (1) male
competitive swimmers (MC), (2) male noncompetitive swimmers (MNC), (3) female
competitive swimmers (FC), (4) female noncompetitive swimmers (FNC), (5) Child (11-
14 years) competitive swimmer (CC), and (6) Child (11-14 years) noncompetitive
swimmers (CNC). Lifeguards were either male lifeguard (MLG) or female lifeguard
(FLG).
105
The approach to human health risk assessment used for exposure to DBPs from
swimming in indoor swimming pools water is based on the US EPA guidelines (US EPA,
2005) and on the detailed description given by Lee et al. (2004) in doing a similar risk
assessment for DBPs in drinking water in Hong Kong. The source of exposure, exposure
pathways, swimmer’s body information, swimming durations and frequency for each
swimming group mentioned above, and the DBPs physiochemical properties and their
specific toxicological values (PF and RfD) were obtained from US EPA sources and
databases (US EPA, 2003a, 2003b; US EPA, 2005; IRIS, 2009) or from other available
sources (RAIS, 2009). The concentration of each DBP in water was used to determine its
concentration in air using Henry’s law with the proper unitless constant of each DBP.
Cancer risk from different routes was determined according to the contaminant
concentration available for each exposure route and its cancer potency factor (PF). The
hazard index for non-carcinogenic health effect was determined from lifetime average
dose (LADD) calculated and the reference dose (RfD) of each DBP. The LADD was
considered as the sum of LADD of each exposure route. The lifetime swimming exposure
duration for noncompetitive and competitive adult swimmers groups (male and female)
was considered 30 and 22 years, respectively, whereas the duration of swimming for
children of all categories was considered four years (Table 6.2). Exposure was converted
to a daily dose by considering aspirated air rate (inhalation), ingested water volume, body
weight, body surface area, and the entire lifetime of 70 years (Table 6.2). Swimming
event duration was considered one hour for all swimming groups in all calculations. This
conservative swimming event time limitation was used to avoid overestimation of cancer
106
risk or non-cancer hazard and to facilitate comparing different swimming groups and
ages. The Exposure Factors Handbook: 2009 update, gives longer times duration for
swimming events especially when the group considered is noncompetitive or children
(US EPA, 2009b). Also in a recent telephone survey of swimming coaches to develop
factors for estimating exposure while swimming, it was found that average swimming
duration is 9.1 hours/week for youth swimmers, 6.4 hours/week for adults, and 17
hours/week for collegiate teams (Reiss et al., 2006). Since all the calculations in this
study are based on one hour swimming event duration, an extrapolation of longer time
expended in swimming pool water can be easily obtained from the results of this risk
assessment if desired.
The general equation (equation 6.5) applied to estimate risk as the excess
probability of developing cancer over a lifetime from participating in known swimming
events through the three exposure pathways (ingestion, inhalation, and dermal
absorption) is
𝑇𝐿𝑅 = 𝐿𝐴𝐷𝐷𝑖 ∗ 𝑃𝐹𝑖 𝑛𝑚=1 (6.5)
Equation 6.6 considers all the exposure routes and their different variables and
parameters used in calculating cancer risk
𝑇𝐿𝑅 = Cw ∗EF∗ED
BW ∗AT PFo ∗ IR + PFd ∗ BA ∗ Kp ∗ ET + (PFh ∗ V ∗ AR ∗ ET)
𝑛
𝑚=1 (6.6)
107
Equation 6.7 considers all the exposure routes and their different variables and parameters
used in calculating the hazard index (HI)
𝐻𝐼 = Cw ∗EF∗ED
BW ∗AT IR/R𝑓Do + BA ∗ Kp ∗ ET)/RfDd + (V ∗ AR ∗ ET)/RfDh
𝑛
𝑚=1 (6.7)
TLR Total Lifetime cancer risk; PFo Potency Factor for oral exposure;
PFh Potency Factor for inhalation exposure; PFi Potency Factor;
PFd Potency factor for dermal exposure; EF Exposure frequency (days/year);
Cw Contaminant concentration in water; BW Body weight;
ED Exposure duration (year); AT Average time days;
IR Ingestion rate; KP Dermal permeability coefficient;
BA Body surface area; ET Exposure time (hours/day);
V Volatilization factor; AR Aspiration rate (m3/hour);
m Number of different chemicals; HI Hazard index;
RfDo Oral reference dose; RfDd Dermal reference dose;
RfDh Inhalation reference dose;
LADDi Lifetime average daily dose (mg/kg/day).
Results and Discussion
The average (arithmetic mean) concentration of THM and HAA species used in
this multipathway risk assessment study are presented in Table 6.4. These THMs and
HAAs were measured in three swimming pool water samples through a period of six
108
months during 2008-2009. The swimming pools have some differences in their daily
operational parameters such as chlorination method and water temperature as they were
described fully in Chapter Five.
Table 6.4: Average of DBP species concentration used in risk assessment
TCM BDCM DBCM DCAA TCAA
Swimming
Pool Cw Ca Cw Ca Cw Ca Cw Ca Cw Ca
µg/L µg/m
3 µg/L µg/m
3 µg/L µg/m
3 µg/L µg/m
3 µg/L µg/m
3
S16 53 7950 1 66.7 ND - 532 0.18 1237 0.68
S17L 68 10200 13 867.1 3 96.3 426 0.15 1373 0.76
S17T 170 25500 11 733.7 2 64.2 2030 0.7 4201 2.32
Cw (Concentration in water), Ca (Concentration in air)
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane),
DCAA (dichloroacetic acid), TCAA (trichloroacetic acid)
The air concentrations of DBPs in Table 6.4 are the result of Henry’s law
calculations using the SWIMODEL (US EPA, 2003a, 2003b) from each DBP water
concentration value and the Henry’s unitless constant for each DBP (Table 6.3) at 25 ˚C.
These air concentrations that were indirectly estimated here are with high agreement and
close to the latest air concentrations that are reported by Hsu et al. (2009) for indoor
swimming pools. TCM concentration averages measured in the agitated water and air
over it (20, 150, and 250 cm) in indoor swimming pool, using 6 L Summa canisters for
air sampling, were in the range 43.5-74 µg/L in water and 6500-13000 µg/m3 in air (Hsu
et al., 2009). Also Levesque and coworkers (1994) controlled the water chloroform
109
concentration in swimming pool water by increasing it from 159 µg/L to 553 µg/L, and
then measured the corresponding indoor air concentration over the water of the pool. The
mean air concentration measured was 597 ppb to 1630 ppb.
Chloroform concentration measured in air above the pool water surface at
different levels (20 – 150 cm) showed no significance differences (Erdinger et al., 2004).
Especially when anyone was swimming in the pool no significant variation was noticed
in chloroform air concentration at 20 to 250 cm (Hsu, 2009).
Swimmers Lifetime Cancer Risk Characterization from DBPs of Swimming Pools
Chronic health effect from exposure to DBPs during swimming from the three
possible pathways was evaluated during an average lifetime of 30 and 22 years of
swimming for noncompetitive and competitive adults and four years for children
(Appendix D). The multipathway lifetime cancer risk and hazard quotient for each of the
three THM species and two HAA species were estimated and compared to the 10-6
negligible risk level defined by US EPA. The lifetime human health risk cancer and
hazard index values for each swimming pool are summarized in Tables 6.5, 6.6, and 6.7.
Results are arranged to show health effect (lifetime cancer risk and hazard index) on
different groups of swimmers and also show the risk from each DBP regarding possible
exposure pathway. The lifetime cancer risks for all groups and categories of swimmers
from swimming in the studied swimming pools were higher than 10-6
, the negligible risk
level defined by US EPA. The results show that the major cancer risk for both male and
female swimmers is through the inhalation route. The inhalation route for THMs was the
110
major risk source followed by the dermal then the ingestion route. This dominance of the
inhalation route is in agreement with other studies that reported the respiratory pathway
as a major exposure source during showering and bathing (Erdinger et al., 2004).
Inhalation of chloroform exhibited the highest lifetime cancer risk. For DCAA the dermal
absorption exposure and ingestion route show the higher cancer risk than the inhalation
route. This is expected as DCAA is less volatile and its air concentration is low. Since the
minimum amount of water ingestion was always considered in these calculations, the
lifetime risk due to the ingestion route was the lowest. For the same reason DCAA cancer
risk was always less than THM cancer risk caused by swimming in the investigated
indoor pools. The risk from exposure to multiple hazardous contaminants has additive
effects (Hsu et al., 2001). US EPA when setting exposure standards use the additive
approach (Hallenbeck, 1993). Considering the additive effects of exposure to multiple
toxicants (Hsu et al., 2001), total lifetime risk from THMs and HAAs evaluated in the
studied swimming pools was over the US EPA negligible level of 10-6
by a factor of 100
to 10000 for all pools and swimmer groups. These high risks of cancer from swimming in
chlorinated water were also reported in similar levels in a risk assessment conducted for
exposure from swimming and tap water in Thailand (Mallika et al., 2008). Mallika and
coworkers estimated an acceptable cancer risk related to tap water while they estimated
an unacceptable cancer risk (7.99x10-4
-1.47x10-3
) from tap and swimming water together.
They concluded that 94% of the risk due to THMs exposure is from swimming. In a
recent health risk assessment associated with indoor swimming pools in South Korea,
lifetime cancer risk estimation from multipathway exposure showed that the greater risk
111
(7.8x10-4
-1.36x10-3
) is from inhalation exposure, whereas dermal and ingestion exposure
risks were less than 10-6
(Lee et al., 2009). Estimation of the total risk from THMs in
drinking water in Hong Kong (Lee et al., 2004) and Ankara (Tokmak et al., 2004) was at
or above the negligible risk level of 10-6
by a factor of 10. Ingestion is the major exposure
route reported by Lee et al. (2004) and Tokmak et al. (2004). Other studies reported that
inhalation is the major exposure route from drinking water during showering and risk was
also more than the negligible 10-6
level by a factor of 10 (Wang et al., 2007).
Swimmers Lifetime Non-Cancer Risk Characterization from DBPs of Swimming
Pools
Total hazard index of THMs and HAAs through the multipathway exposure of the
three swimming pools for different swimmers categories are shown in Tables 6.5, 6.6,
and 6.7. Exposure to chloroform shows a hazard index of non-carcinogenic risk greater
than one for all adult swimming groups in the three indoor pools evaluated in this risk
assessment study. The concentration of chloroform in the blood of swimmers with scuba
tanks was much less than swimmers without scuba tanks indicating that the respiratory
pathway is a major route of exposure during swimming (Erdinger et al., 2004). Very high
overall hazard indices for adult swimmers are shown due to swimming in indoor pools
disinfected by chlorine. Hazard indices are greater than one mostly and increase to reach
20 times the value of the acceptable hazard index of one.
112
Table 6.5: Cancer risk and hazard index from DBPs measured in S16 swimming pool on swimmers
Group Exposure
route
Cancer risk Hazard Index Additive
Cancer
Risk
Hazard
Index TCM BDCM DBCM DCAA TCM BDCM DBCM DCAA TCAA
MN
C
Oral 1.46E-08 2.80E-09
1.20E-06
Dermal 5.03E-07 1.28E-08
1.13E-06
Inhalation 1.15E-03 7.44E-06
1.65E-08
Total 1.15E-03 7.46E-06
2.34E-06 1.44E+00 6.05E-03
1.17E-02 4.00E-03 1.2E-03 1.46
MC
Oral 1.06E-08 2.03E-09
8.70E-07
Dermal 7.32E-07 1.87E-08
3.28E-05
Inhalation 5.38E-03 3.47E-05
1.53E-06
Total 5.38E-03 3.47E-05
3.52E-05 6.68E+00 2.80E-02
1.30E-02 4.60E-03 5.4E-03 6.73
FN
C
Oral 1.74E-08 3.34E-09
1.44E-06
Dermal 5.25E-07 1.34E-08
1.17E-06
Inhalation 1.38E-03 8.93E-06
1.97E-08
Total 1.38E-03 8.94E-06
2.62E-06 1.71E+00 7.20E-03
1.31E-02 4.43E-03 1.4E-03 1.73
FC
Oral 1.27E-08 2.43E-09
1.04E-06
Dermal 7.63E-07 1.94E-08
3.41E-05
Inhalation 6.42E-03 4.15E-05
1.83E-06 Total 6.42E-03 4.15E-05
3.70E-05 7.97E+00 3.35E-02
1.42E-02 5.00E-03 6.5E-03 8.02
CN
C
Oral 6.28E-09 1.21E-09
8.80E-07
Dermal 7.96E-08 2.03E-09
3.03E-07
Inhalation 2.50E-04 1.61E-06
6.05E-09
Total 2.50E-04 1.62E-06
1.19E-06 3.10E-01 1.31E-03
5.95E-03 1.14E-03 2.5E-04 0.32
CC
Oral 4.97E-09 9.55E-10
4.09E-07
Dermal 1.25E-07 3.20E-09
5.61E-06
Inhalation 7.47E-04 4.82E-06
2.13E-07
Total 7.47E-04 4.83E-06
6.23E-06 9.28E-01 3.90E-03
3.50E-03 1.18E-03 7.6E-04 0.94
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA (dichloroacetic acid), TCAA (trichloroacetic acid). MNC
(male noncompetitive swimmers), FNC (female noncompetitive swimmers), CNC (child, 11-14 years, non-competitive swimmers). MC (male
competitive swimmers), FC (female competitive swimmers), CC (child, 11-14 years, competitive swimmer)
113
Table 6.6: Cancer risk and hazard index from DBPs measured in S17L swimming pool on swimmers
Group Exposure
route
Cancer risk Hazard Index Additive
Cancer
Risk
Hazard
Index TCM BDCM DBCM DCAA TCM BDCM DBCM DCAA TCAA
MN
C
Oral 1.87E-08 3.63E-08 1.13E-08 9.60E-07
Dermal 6.47E-07 1.67E-07 5.73E-08 9.00E-07
Inhalation 1.48E-03 9.67E-05 1.46E-05 1.32E-08
Total 1.48E-03 9.69E-05 1.47E-05 1.87E-06 1.84E+00 7.85E-02 8.70E-03 9.38E-03 4.43E-03 1.6E-03 1.94
MC
Oral 1.36E-08 2.64E-08 8.27E-09 7.00E-07
Dermal 9.39E-07 2.43E-07 1.38E-08 1.31E-06
Inhalation 6.89E-03 4.51E-04 6.80E-05 6.15E-08
Total 6.89E-03 4.52E-04 6.80E-05 2.07E-06 8.57E+00 3.65E-01 4.05E-02 1.04E-02 5.10E-03 7.4E-03 8.99
FN
C
Oral 2.23E-08 4.34E-08 1.36E-08 1.15E-06
Dermal 6.71E-07 1.74E-07 5.96E-08 9.40E-07
Inhalation 1.77E-03 1.16E-04 1.74E-05 1.58E-08
Total 1.77E-03 1.16E-04 1.75E-05 2.10E-06 2.20E+00 9.35E-02 1.04E-02 1.05E-02 4.93E-03 1.9E-03 2.32
FC
Oral 1.62E-08 3.16E-08 9.91E-09 8.35E-07
Dermal 9.76E-07 2.53E-07 8.68E-08 1.37E-06
Inhalation 8.05E-03 5.39E-04 8.11E-05 7.35E-08
Total 8.05E-03 5.39E-04 8.12E-05 2.27E-06 1.00E+01 4.35E-01 4.83E-02 1.14E-02 5.57E-03 8.7E-03 10.50
CN
C
Oral 8.11E-09 1.57E-08 4.91E-09 7.05E-07
Dermal 1.02E-07 2.65E-08 9.07E-09 2.43E-07
Inhalation 3.20E-04 2.10E-05 3.16E-06 4.85E-09
Total 3.21E-04 2.10E-05 3.17E-06 9.52E-07 3.98E-01 1.70E-02 1.89E-03 4.78E-03 1.27E-03 3.5E-04 0.42
CC
Oral 6.34E-09 1.24E-08 3.87E-09 3.27E-07
Dermal 1.61E-07 4.17E-08 1.43E-08 2.25E-07
Inhalation 9.58E-04 6.26E-05 9.41E-06 8.55E-09
Total 9.58E-04 6.27E-05 9.43E-06 5.61E-07 1.19E+00 5.05E-02 5.65E-03 2.80E-03 1.31E-03 1.0E-03 1.25
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA (dichloroacetic acid), TCAA
(trichloroacetic acid). MNC (male noncompetitive swimmers), FNC (female noncompetitive swimmers), CNC (child, 11-14 years, non-
competitive swimmers). MC (male competitive swimmers), FC (female competitive swimmers), CC (child, 11-14 years, competitive
swimmer)
114
Table 6.7: Cancer risk and hazard index from DBPs measured in S17T swimming pool on swimmers
Group Exposure
route
Cancer risk Hazard Index Additive
Cancer
Risk
Hazard
Index TCM BDCM DBCM DCAA TCM BDCM DBCM DCAA TCAA
MN
C
Oral 4.68E-08 3.08E-08 7.58E-09 4.58E-06
Dermal 1.62E-06 1.41E-07 3.82E-08 4.30E-06
Inhalation 3.70E-03 8.18E-05 9.74E-06 6.30E-08
Total 3.70E-03 8.20E-05 9.79E-06 8.94E-06 4.61E+00 6.65E-02 5.80E-03 4.48E-02 1.36E-02 3.8E-03 4.74
MC
Oral 1.66E-07 2.24E-08 5.51E-09 3.33E-06
Dermal 1.15E-05 2.06E-07 5.56E-08 3.33E-06
Inhalation 8.37E-02 3.82E-04 4.53E-05 2.93E-07
Total 8.37E-02 3.82E-04 4.53E-05 6.95E-06 2.10E+01 3.08E-01 2.70E-02 4.93E-02 1.56E-02 1.7E-02 21.40
FN
C
Oral 5.59E-08 3.67E-08 9.07E-09 5.45E-06
Dermal 1.68E-06 1.47E-07 3.98E-08 4.47E-06
Inhalation 4.42E-03 9.80E-05 1.16E-05 7.50E-08
Total 4.42E-03 9.81E-05 1.16E-05 1.00E-05 5.50E+00 7.90E-02 6.95E-03 5.00E-02 1.51E-02 4.5E-03 5.65
FC
Oral 4.06E-08 2.67E-08 6.58E-09 3.98E-06
Dermal 2.44E-06 2.14E-07 5.78E-08 6.50E-06
Inhalation 2.09E-02 4.56E-04 5.41E-05 3.49E-07
Total 2.09E-02 4.57E-04 5.42E-05 1.08E-05 2.60E+01 3.68E-01 3.22E-02 5.43E-02 1.70E-02 2.1E-02 26.47
CN
C
Oral 2.03E-08 1.33E-08 3.28E-09 3.37E-06
Dermal 2.56E-07 2.23E-08 6.05E-09 1.16E-06
Inhalation 8.01E-04 1.77E-05 2.10E-06 2.31E-08
Total 8.01E-04 1.78E-05 2.11E-06 4.54E-06 9.96E-01 1.44E-02 1.26E-03 2.27E-02 3.90E-03 8.3E-04 1.04
CC
Oral 1.59E-08 1.05E-08 2.58E-09 1.56E-06
Dermal 4.03E-07 3.52E-08 9.52E-09 1.07E-06
Inhalation 2.40E-03 5.31E-05 6.29E-06 4.07E-08
Total 2.40E-03 5.31E-05 6.30E-06 2.67E-06 2.98E+00 4.29E-02 3.75E-03 1.34E-02 4.00E-03 2.5E-03 3.04
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and TBM (tribromomethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid). MNC (male noncompetitive swimmers), FNC (female noncompetitive swimmers),
CNC (child, 11-14 years, non-competitive swimmers). MC (male competitive swimmers), FC (female competitive swimmers), CC (child,
11-14 years) competitive swimmer)
115
The lifetime cancer risk developed by each swimming group in the three studied
indoor swimming pools is compared in Figure 6.1. Adult competitive swimmers either
male or female have more lifetime cancer risk from all hazardous DBPs and in all pools.
Male and female swimmers show comparable lifetime cancer risk from swimming in
chlorinated swimming pool water. The lifetime cancer risk was more in the two
swimming pools using electro generated chlorine. The pool with warm water exhibited
the highest lifetime cancer risk compared to the two pools operated at lower water
temperature. TCM imposed the highest cancer risk on all groups of swimmers in all
swimming pools evaluated, which is due to its higher concentration and more volatility.
The additive lifetime cancer risk from the three THMs (TCM, BDCM, and DBCM) and
DCAA in the three swimming pools on the six swimmers groups is shown in Figure 6.2.
The adult competitive male and female are shown to have the highest lifetime cancer risk
in the three pools. The additive cancer risk for DBPs of each swimming pool followed the
order: S17T ˃ S17L ˃ S16 pool. Again more additive cancer risk is shown by adult
competitive swimmers either male or female swimming in the three swimming pools
investigated in this study. The childhood duration time of swimming was four years
should be kept in mind when looking at the health effect shown in the results of the risk
assessment. Also children were assumed to spend only one hour in the pool in each
swimming event which is mostly not the case. One hour duration of swimming event and
the lowest water ingested volume were used in all the risk and hazard estimations to
avoid any overestimation of developed risk from swimming in chlorinated indoor
swimming pool water.
116
Figure 6.1: Lifetime cancer risk from TCM (a), BDCM (b), DBCM (c), and DCAA (d) estimated for different swimmers
groups in the three swimming pools. MNC (male noncompetitive swimmers), FNC (female noncompetitive swimmers), CNC
(child, 11-14 years, non-competitive swimmers). MC (male competitive swimmers), FC (female competitive swimmers), CC
(child, 11-14 years, competitive swimmer)
0.0E+00
5.0E-03
1.0E-02
1.5E-02
2.0E-02
2.5E-02
NCM CM NCF CF CNC CC
a
S16
S17L
S17T
0.0E+00
1.0E-04
2.0E-04
3.0E-04
4.0E-04
5.0E-04
6.0E-04
NCM CM NCF CF CNC CC
c
S16
S17L
S17T
0.0E+00
2.0E-05
4.0E-05
6.0E-05
8.0E-05
1.0E-04
NCM CM NCF CF CNC CC
b
S16
S17L
S17T
0.E+00
5.E-06
1.E-05
2.E-05
2.E-05
3.E-05
3.E-05
4.E-05
4.E-05
NCM CM NCF CF CNC CC
d
S16
S17L
S17T
117
Figure 6.2: Additive lifetime cancer risk from TCM, BDCM, DBCM, and DCAA in the
three swimming pools estimated for different swimmers groups. MNC (male non-
competitive swimmers), FNC (female noncompetitive swimmers), CNC (child, 11-14
years, non-competitive swimmers). MC (male competitive swimmers), FC (female
competitive swimmers), CC (child, 11-14 years, competitive swimmer)
The values for the hazard index of the four DBPs in the investigated swimming
pools were quite high (Figure 6.3). The maximum hazard index should not exceed one. In
the three swimming pools evaluated for additive non-carcinogenic hazardous indices
(Figure 6.4) caused by three THMs (TCM, BDCM, and DBCM) and two HAAs (DCAA,
and TCAA), the non carcinogenic additive hazard indices were always higher than one
and reached as high as 26 in the warm water pool. The major contribution of non-
carcinogenic hazard followed the order TCM ˃ BDCM˃ DCAA˃ DBCM ˃ TCAA in the
three pools for the six swimmers groups (Figure 6.4).
0.0E+00
5.0E-03
1.0E-02
1.5E-02
2.0E-02
2.5E-02
NCM CM NCF CF CNC CC
S16
S17L
S17T
118
Figure 6.3: Hazard index from TCM (a), BDCM (b), DBCM (c), DCAA (d), and TCAA (e) estimated for the different
swimmers groups in the three swimming pools. MNC (male noncompetitive swimmers), FNC (female noncompetitive
swimmers), CNC (child, 11-14, non-competitive swimmers). MC (male competitive swimmers), FC (female competitive
swimmers), CC (child, 11-14 years, competitive swimmer)
0.0E+00
1.0E+01
2.0E+01
3.0E+01
NCM CM NCF CF CNC CC
aS16 S17L S17T
0.0E+00
2.0E-01
4.0E-01
6.0E-01
NCM CM NCF CF CNC CC
bS16 S17L S17T
0.0E+00
2.0E-02
4.0E-02
6.0E-02
NCM CM NCF CF CNC CC
cS16 S17L S17T
0.0E+00
2.0E-02
4.0E-02
6.0E-02
NCM CM NCF CF CNC CC
d S16 S17L S17T
0.0E+00
1.0E-02
2.0E-02
NCM CM NCF CF CNC CC
e S16 S17L S17T
119
Figure 6.4: Additive hazard indices from TCM, BDCM, DBCM, DCAA, and
TCAA in the three swimming pools for the different swimmers groups. MNC
(male noncompetitive swimmers), FNC (female noncompetitive swimmers), CNC
(child, 11-14 years, non-competitive swimmers). MC (male competitive
swimmers), (female competitive swimmers), CC (Child, 11-14 years, competitive
swimmer). The dashed line represents a hazard index of 1.0
Lifeguards Exposure and Health Risk Assessment
Swimming pool operation regulations require the presence of a lifeguard during
the working hours of the pool. Lifeguards are either an adult male (MLG) or female
(FLG). Samples of urine and alveolar air from workers at indoor swimming pools showed
an increase in chloroform directly after begin their work day (Fantuzzi et al., 2001; Caro
and Gallego, 2007; 2008). Blood THMs measured after different activities related to
chlorinated water show that inhalation during showering, bathing, and manual dish
washing is a major intake pathway, and the blood THMs increased and varied according
to the water THM content variation (Ashley et al., 2005). The main exposure route of
0
5
10
15
20
25
30
NCM CM NCF CF CNC CC
S16
S17L
S17T
120
lifeguards is the inhalation route. The gaseous dermal absorption as an exposure route for
volatile DBPs is not mentioned in the literature or in any other available resources about
exposure routes factors. The time of lifeguards existence in water during their duty is
negligible since they should be in a position to watch the swimmers in the swimming
pool all the time. To estimate the lifetime cancer risk and non-cancer hazard of lifeguards
we assumed a duty time of three hours per working event for three times a week for 44
weeks a year. This results with approximately 130 working events per year. The different
parameters, time duration and exposure variables used in estimating the health risk
assessment for swimming pools male and female lifeguards are summarized in Table 6.8.
The exposure duration and frequencies were considered at the minimum to avoid any
overestimation of lifetime cancer risk and hazard index. Thus the estimated cancer risk
and hazard reported here may be lower than the actual risk. Also we should keep in mind
that lifeguards likely practice swimming, which may add to the risk developed from their
lifeguard job.
The lifetime cancer risk and non-cancer hazard indices from DBPs in the
atmosphere of the three swimming pools investigated in this study are summarized in
Tables 6.9, 6.10, and 6.11. The results of lifetime cancer risk and hazard index on non-
carcinogenic health impacts developed by lifeguards working for 10 years in the three
indoor pools used in this study are more than those developed by adult male and female
noncompetitive swimmers swimming for 30 years. The lifeguard lifetime cancer risk is
above the negligible risk level of 10-6
by a factor of 1000 in the pools. The main cancer
121
risk is due to inhalation of chloroform. Hazard indices of DBPs on life guards were
always higher than 1 and reached a maximum hazard quotient equal to 5.65.
122
Table 6.8: Lifeguard body information (personal information), working hours, and frequencies assumed for
exposure estimation (US EPA, 2009b).
Lifeguard
Body
weight
Body
surface area
Working
frequency
Working
duration
Inhalation
rate
Event
duration
kg m2 event/year years m
3/hr hr/event
Male 78.1 1.94 130 10 1 3
Female 65.4 1.69 130 10 1 3
Table 6.9: Cancer risk and hazard index from DBPs measured in S16 swimming pool on lifeguards
Group Exposure
route
Cancer risk Hazard Index Additive
Cancer
Risk
Hazard
Index TCM BDCM DBCM DCAA TCM BDCM DBCM DCAA TCAA
Male
Lifeg
uard
Oral 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Dermal 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Inhalation 1.25E-03 8.06E-06 0.00E+00 1.79E-08
Total 1.25E-03 8.06E-06 0.00E+00 1.79E-08 1.55E+00 6.50E-03 0.00E+00 8.93E-05 1.91E-05 1.3E-03 1.56
Fem
ale
Lifeg
uard
Oral 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Dermal 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Inhalation 1.50E-03 9.67E-06 0.00E+00 4.26E-07
Total 1.50E-03 9.67E-06 0.00E+00 4.26E-07 1.86E+00 7.80E-03 0.00E+00 1.07E-04 2.28E-05 1.5E-03 1.87
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA (dichloroacetic acid), TCAA
(trichloroacetic acid)
123
Table 6.10: Cancer risk and hazard index from DBPs measured in S17L swimming pool on lifeguards
Group Exposure
route
Cancer risk Hazard Index
Additive
Cancer
Risk
Hazard
Index
TCM BDCM DBCM DCAA TCM BDCM DBCM DCAA TCAA
Male
Lifeg
uard
Oral 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Dermal 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Inhalation 1.60E-03 1.05E-04 1.58E-05 1.43E-08
Total 1.60E-03 1.05E-04 1.58E-05 1.43E-08 1.99E+00 8.45E-02 9.40E-03 7.15E-05 4.93E-05 1.7E-03 2.08
Fem
ale
Lifeg
uard
Oral 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Dermal 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Inhalation 1.92E-03 1.25E-04 1.89E-05 1.71E-08
Total 1.92E-03 1.25E-04 1.89E-05 1.71E-08 2.38E+00 1.01E-01 1.13E-02 8.53E-05 5.90E-05 2.1E-03 2.49
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA (dichloroacetic acid), TCAA (trichloroacetic
acid)
Table 6.11: Cancer risk and hazard index from DBPs measured in S17W swimming pool on lifeguards
Group Exposure
route
Cancer risk Hazard Index
Additive
Cancer
Risk
Hazard
Index
TCM BDCM DBCM DCAA TCM BDCM DBCM DCAA TCAA
Male
Lifeg
uard
Oral 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Dermal 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Inhalation 4.01E-03 8.87E-05 1.05E-05 6.80E-08
Total 4.01E-03 8.87E-05 1.05E-05 6.80E-08 4.98E+00 7.15E-02 6.25E-03 3.40E-04 1.51E-04 4.1E-03 5.06
Fem
ale
Lifeg
uard
Oral 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Dermal 0.00E+00 0.00E+00 0.00E+00 0.00E+00
Inhalation 4.79E-03 1.06E-04 1.26E-05 8.15E-08
Total 4.79E-03 1.06E-04 1.26E-05 8.15E-08 5.95E+00 8.55E-02 7.50E-03 4.08E-04 1.80E-04 4.9E-03 6.04
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA (dichloroacetic acid), TCAA
(trichloroacetic acid)
124
There is a variation in the cancer risk and non-cancer hazard among the three swimming
pools, three of them have a high cancer risk and hazard. Figure 6.5 shows the summary of
cancer risk and non-cancer risk developed by different swimming groups and also male
lifeguards (MLG) and female lifeguards (FLG) swimming or working in the three
swimming pools. The results show that lifeguards are exposed to similar risk and hazard
even for working ten years during their lifetime for a short working shift (three hours).
Two of the swimming pools used electro-generated chlorine for disinfection, which poses
more cancer risk on swimmers and workers. The warm pool has higher adverse health
effect on swimmers and workers, too.
125
Figure 6.5: Lifetime cancer risk (a) and non-cancer hazard (b) on swimmers and
lifeguards associated with the three swimming pools. MNC (male noncompetitive
swimmers), FNC (female noncompetitive swimmers), CNC (child, 11-14 years, non-
competitive swimmers). MC (male competitive swimmers), (female competitive
swimmers), CC (child, 11-14 years, competitive swimmer), MLG (male lifeguard), FLG
(female lifeguard). The dashed line represents a hazard index of 1.0
0.0E+00
5.0E-03
1.0E-02
1.5E-02
2.0E-02
2.5E-02
MNC MC FNC FC CNC CC MLG FLG
aS16 S17L S17T
0
5
10
15
20
25
30
MNC MC FNC FC CNC CC MLG FLG
b S16 S17L S17T
126
Conclusions
Through different pathways, the lifetime cancer risk and hazard index for THMs
and HAAs in the water of three swimming pools using chlorine for disinfection were
evaluated. Results show that
Swimmers had higher cancer risk than the negligible risk level of 10-6
.
The results show that inhalation of TCM is the major exposure route and hence
the cause of the highest lifetime cancer risk. Dermal and oral exposure routes
cause more lifetime cancer risk from DCAA.
The cancer risk from swimming in chlorinated indoor swimming pool water is
more than that reported from drinking chlorinated water. Most the studies that
estimated lifetime cancer risk from drinking water via ingestion and other
exposure routes such as dermal absorption and inhalation while showering
reported less cancer risk from drinking water compared to swimming.
Non-carcinogenic hazard indices from swimming pool water are high especially
for adults who are either competitive or non competitive swimmers. Competitive
swimmers show higher hazard index due to the large inhalation volume
(aspirated) air. On the other hand, noncompetitive swimmers swallow more water,
which caused an increase in oral exposure of DBPs while swimming.
It should be noted that the swimming by children for extended periods of time
will cause more risk of adverse health effects. Calculated values were for one
hour and for the lower swallowed water volume during swimming. In actuality
127
children spend longer time and thus are exposed to more DBPs either via
inhalation or through water ingestion and dermal absorption also.
Lifeguards are at higher risk than swimmers. Lifeguards and other workers that
stay for extended periods in an indoor swimming pool are mainly exposed to
DBPs via the inhalation route. Their time at the pool and frequency of exposure
are critical factors that should be considered to minimize the risk they are
developing by inhaling contaminated air in the indoor swimming pool facility.
128
CHAPTER SEVEN
THE CONTRIBUTION OF FILLING WATER NATURAL ORGANIC MATTER AND
BODY FLUIDS TO THE FORMATION OF DIFFERENT CLASSES OF
DISINFECTION BY-PRODUCTS IN SWIMMING POOLS
Introduction and Objectives
Swimming pool waters contain a complex mixture of organic compounds that can
react with aqueous chlorine to form DBPs. In swimming pool waters, there are two types
of organic matter that act as precursors of DBPs: (i) the natural organic matter (NOM)
that comes with the filling water, and (ii) the organic matter introduced to water by
swimmers (organic matter of human origin) which is referred to as bathers load. Total
organic carbon (TOC) of swimming pool water increases with time due to the continuous
release of body fluids (BFs), mainly urine and sweat, by swimmers even under stringent
hygienic conditions. NOM and BFs are different in their chemical composition and
properties; thus it is hypothesized that their reactions with chlorine will produce different
amount and types of DBPs. The objective of the work presented in this chapter was to
investigate and compare the reactivity of these different organic precursors in the
formation of three DBP classes (THMs, HAAs, and HNMs). Reactivity of the precursors
was investigated by conducting a series of DBP formation potential (FP) tests using
NOM samples collected from five drinking water treatment plants in South Carolina and
three different body fluid analogs (BFAs) proposed in the literature to simulate human
BFs. Formation potential (FP) tests have been designed to provide the maximum amount
of DBPs that can form in a water sample disinfected with a disinfectant; therefore, it is a
129
good measure of the overall formation of DBPs that can partition among different phases
in a swimming pool (water, air, human bodies).
Approach
Five drinking water samples (i.e., filling water of the swimming pools that
contains ―treated‖ NOM) were obtained from water treatment plants in South Carolina at
three different times during 2008 and 2009. Each sample was diluted to bring the organic
matter concentration to a constant level of 1 mg/L TOC, unless the original sample TOC
was lower (Table 4.1). During FP tests, free chlorine was injected to each sample at the
constant initial dose of 50 mg/L. Therefore, Cl2/TOC levels were maintained constant for
the majority of the experiments. Chlorinated water was incubated in brown glass bottles
(free of head space) for 5 or 10 days at 26 or 40°C using a water bath to examine the
effects of reaction time and temperature. The same experimental conditions were also
used for the FP tests of three BFAs [(BFA(G), BFA(J), and BFA(B)] which are described
in Table 4.2. The concentrations of THM, HAA, and HNM species were quantified at the
end of the experiments that are described in Figure 3.2.
Materials and Methods
Filling Water NOM
Filling water NOMs with different characteristics were obtained from five
drinking water plants after conventional treatment processes (before any oxidant and
disinfectant addition) in South Carolina: Spartanburg (SP), Startex-Jackson-Wellford-
130
Duncan (SJWD), Greenville (GV), Myrtle Beach (MB), and Charleston (CH). The water
samples were collected three times during 2008 and 2009 (Table 4.1). Samples were
filtered with pre-washed 0.2 μm Supor® membrane filters to eliminate the particles and
biological activity immediately after arrival at the laboratory, and stored in a dark
constant temperature room (4°C) until the experiments, which were usually performed
within a few (2-4) days of storage. For each sample, the TOC, TN, UV254 and bromide
concentrations were determined before the experiments (Table 4.1). As indicated before,
TOC concentration of samples was adjusted to 1 mg/L, unless it was initially less than 1
mg/L.
Body Fluid Analogs (BFAs)
BFAs were prepared following three different recipes that have been proposed in
literature (Table 4.2). These are BFA(G) (Goeres et al., 2004), BFA(J) (Judd and
Bullock, 2003), and BFA(B) (Borgmann-Strahsen, 2003). Components of each BFA are
shown in Table 4.2. The same FP test protocol (described above) was used for both the
filling water NOMs and three BFAs.
Chlorination
Freshly prepared stock solutions of sodium hypochlorite (5%) were used to
chlorinate the BFAs and filling water NOM samples. The initial chlorine dose was 50
mg/L to ensure excess chlorine.
131
Analytical Procedures
Four THMs (TCM, BDCM, DBCM, and TBM), and nine HNMs (CNM, DCNM,
TCNM, BNM, BCNM, BDCNM, DBNM, DBCNM, and TBNM) were quantified by
liquid/liquid extraction with MtBE followed by gas chromatography with electron
capture detection (GC/ECD) according to US EPA Method 551.1 with some
modifications. Nine HAAs (CAA, BAA, DCAA, BCAA, DBAA, BDCAA, DBCAA,
TCAA, and TBAA) were analyzed by liquid/liquid extraction with MtBE followed by
derivatization with diazomethane and analysis by GC/ECD. The details of the analytical
protocols were provided in Chapter Four.
Results and Discussion
Reactivity and Formation Potential of DBPs from BFAs
The results of FP tests are summarized in Table 7.1. Since there was no bromide
present in the background water, chlorinated DBP species were the main species formed
during the experiments: TCM (chloroform) for THM, DCAA and TCAA for HAA and
TCNM (chloropicrin) for HNM. The chlorine demand measured during the FP tests was
relatively high, which was attributed to the chlorine demand of the nitrogenous and
carbonaceous compounds that are present in the three BFAs. The high chlorine demands
are consistent with previous reports testing some of the same BFA components as model
compounds during chlorination studies (Hureiki et al., 1994; Li and Blatchley III, 2007;
Hong et al., 2008).
132
The formation of total THMs (chloroform) from the BFAs was always lower than
total HAAs (DCAA and TCAA) at the same conditions (Table 7.1). THMs
concentrations ranged from 21 µg/L (at 26°C for five days contact time) to 77 µg/L (at 40
133
Table 7.1: Disinfection By-Products formation from BFAs at pH 7, TOC 1mg/L, and initial chlorine dose 50 mg/L
Body Fluid Analog
(BFA)
T FAC Incubation TCM DCAA TCAA THAA TCNM
°C mg/L days µg/L µg/L µg/L µg/L µg/L
BFA(G)
26 31 5 21 15 19 35 1.5
26 30 10 28 22 24 46 1.3
40 28 5 29 20 19 39 1.1
40 25 10 35 18 18 36 0.8
BFA(J)
26 33 5 30 51 19 69 1.6
26 32 10 38 54 21 75 1.1
40 29 5 50 66 15 81 1.1
40 28 10 77 68 27 95 0.9
BFA(B)
26 28 5 16 63 11 74 2.0
26 27 10 18 70 12 82 1.0
40 26 5 18 63 8 72 1.1
40 24 10 33 66 14 80 1.0
T (temperature), FAC (free available chlorine), TCM (chloroform), DCAA (dichloroacetic acid), TCAA
(trichloroacetic acid), THAA (total HAA), TCNM (trichloronitromethane)
134
Figure 7.1: Chloroform formed after 5 and 10 days chlorination of the three
BFAs (1mg/L TOC) at pH 7 and 26°C (a) and 40°C (b). (error bars are standard
deviation)
0
10
20
30
40
50
60
70
80
90
BFA(G) BFA(J) BFA(B)
µg/L
a
5 days 10 days
0
10
20
30
40
50
60
70
80
90
BFA(G) BFA(J) BFA(B)
µg/L
b
135
°C for ten days contact time) (Figure 7.1). Chloroform concentration increased with time
and temperature. However, the majority of ten-day chloroform yield (55 to 88%) had
already formed after five days of reaction time. Among the three BFAs, the maximum
amount of THM was produced by BFA(J).
In order to examine the reactivity of each BFA component, FP tests were also
conducted for each component alone (Table 7.2).
Table 7.2: Disinfection By-Products formation from 1 mg/L BFA components at 22°C,
pH 7, initial chlorine dose 50 mg/L, and 5-days contact time
BFA Component
FAC
mg/L
TCM
µg/L
DCAA
µg/L
TCAA
µg/L
THAA
µg/L
TCNM
µg/L
Urea 37 13 4 6 10 0.7
Albumin 43 23 16 23 39 0.8
Creatinine 37 12 2 4 6 0.7
Citric acid 45 307 173 8 181 0.8
Hippuric acid 46 14 2 4 6 0.9
Glucuronic acid 41 13 2 4 6 0.8
Lactic acid 41 14 2 5 7 0.8
Uric acid 39 15 2 4 6 <MRL
Histidine* ** 1 27 15 42 NM
Aspartic acid* ** <2 26 4 30 NM
Glycine* ** ND ND ND NM
Lysine* ** <1 3 <1 <4 NM
*Hong et al., 2008
** Cl2/DOC= 10, 4-days contact time at 20°C
FAC (free available chlorine), TCM (chloroform), DCAA (dichloroacetic acid), TCAA
(trichloroacetic acid), THAA (total HAA), TCNM (trichloronitromethane)
The results showed that citric acid, a component present only in BFA(J), exhibits
significantly higher reactivity toward THM and HAA formation than all other individual
components (Table 7.2). The occurrence of citric acid in tap waters (28-35 µg/L) and
136
natural waters (44-85 µg/L) has been documented in literature (Afghan et al., 1974;
Bjork, 1975; Larson and Rockwell, 1979). Also citric acid from metabolic activity of
both human body (sweat and urine) and microbial cells is introduced continuously into
pool water. Chlorination of citric acid from a previous study also produced considerable
amount of chloroform at a very fast rate (within two hours) at pH 7, but the amount of
chloroform formed decreased at higher pH values (Larson and Rockwell, 1978).
Therefore, the higher THM and HAA formation from BFA(J) was attributed primarily to
the presence of citric acid in its composition. All other BF components showed similar
formation potentials of THMs and HAAs, except the THM and HAA formation potential
of albumin was higher than the others, however, at much lower levels than citric acid.
Chloroform formation potential from 5 mg/L albumin at 20°C and pH 7 was
reported to be 97 µg/L (i.e., 19 g/mg) (Scully et al., 1988). This is comparable to the
yield obtained in this study (23 g/mg). The slightly higher yield observed was attributed
to the higher temperature and initial chlorine dose used in this study as compared to the
conditions used by Scully and coworkers (1988). The researchers also concluded that
different proteins exhibit similar yields of chloroform when chlorinated since they have
similar types of monomers (i.e., amino acids).
The results of BFAs reactivity tests show that all BFAs have high HAA,
especially DCAA, formation potentials (Table 7.1). The HAAs formed from each of the
three BFAs is shown in Figure 7.2. BFA(B) and BFA(J) exhibited higher HAA formation
potential due to their free amino acids, histidine and aspartic acids. These particular two
amino acids showed high HAA formation potentials in previous studies (Hong et al.,
137
2008). In general, formation of HAAs from the three BFAs used in this study were
always higher than the formation of THMs. BFA components are hydrophilic low
molecular weight organic compounds which are considered major precursors of HAAs,
especially dihaloacetic acids (Hua and Reckhow, 2007).
As was observed for THMs, only chlorinated HAAs (DCAA and TCAA) species
were formed from BFAs (Table 7.1). The formation of DCAA was higher than the
formation of TCAA, especially for BFA(J) and BFA(B), which was attributed to free
amino acids (histidine and aspartic acid). DCAA to TCAA mass ratio for BFA(G) was
nearly 1:1, while it ranged from 2.5 to almost 8 for BFA(J) and BFA(B). The higher
DCAA formation from amino acids has also been reported in a recent study (Hong et al.,
2008).
138
Figure 7.2: HAAs formed after 5 and 10 days chlorination of the three BFAs
(1mg/L TOC) at pH 7 at 26°C (a) and 40°C (b). (error bars are standard deviation)
THMs and HAAs values measured in the actual swimming pool samples (Chapter
Five) are in agreement with these findings. Higher HAA than THM concentrations were
always observed in swimming pool water samples, although the DCAA levels were
0
20
40
60
80
100
120
BFA(G) BFA(J) BFA(B)
µg/L
a
5days 10 days
0
20
40
60
80
100
120
BFA(G) BFA(J) BFA(B)
µg/L
b
139
comparable to the levels of TCAA, as observed for BFA(G). This observation implies
that HAAs precursors in pools are not exclusively free amino acids but also include
peptides and proteins (e.g., such as albumin) and also from other organics of human body
origin.
HNMs formed from all three BFAs were comparable and ranged from 0.8 to 2
µg/L. The only species of HNM that was detected in all these formation potential
experiments was TCNM, which is known as chloropicrin.
140
Figure 7.3: Chloropicrin formed after 5 and 10 days chlorination of the three
BFAs (1mg/L TOC) at pH 7 and 26°C (a) and 40°C (b). (error bars are standard
deviation)
0.0
0.5
1.0
1.5
2.0
2.5
BFA(G) BFA(J) BFA(B)
µg/L
a
5days 10 days
0.0
0.5
1.0
1.5
2.0
2.5
BFA(G) BFA(J) BFA(B)
µg/L
b
141
Reactivity and Formation Potential of DBPs from Filling Water NOMs
Filling water NOMs were sampled three times during 2008 and 2009. These
samples were characterized for their TOC, TN, UV254, and bromide content, and the
SUVA254 values were calculated (Table 4.1). Because Greenville water TOC is already
less than 1 mg/L, it was used as collected from the source without any dilution. The
results of FP tests with filling water NOMs are presented in Tables 7.3 and 7.4. The
chlorine demands were much less than those of the BFAs under the same experimental
conditions. In general, the NOMs exhibited significantly higher reactivity toward
producing THMs than HAAs. THM concentrations were twice and sometimes more than
HAAs concentrations. This trend is opposite to the observations with BFAs, where all
produced higher amounts of HAAs than THMs. The difference also explains the
occurrence of high HAA concentrations and their potential precursors in swimming pool
water samples. Since (i) the BF components are continuously introduced and added from
bathers to swimming pools waters, (ii) the pool waters are not diluted at high percentages
and not periodically replaced, resulting in very long water ages (months to years), and
(iii) HAAs are highly soluble in water, the accumulation of HAAs in pool waters is
primarily due to releases of the BF components and their reactions with high chlorine
concentrations. The contributions of filling water NOM to HAA concentrations is
minimal. The higher THM formation potential of NOM than proteins and free amino
acids was also observed in early DBP studies when proteins, free amino acids and humic
acid were chlorinated and compared under the same conditions (Morris et al., 1980;
Scully et al., 1988). Increasing the reaction contact time increased both THM and HAA
142
formation, but HAAs increased more than THM with time. The issue of formation
kinetics of THM and HAA in swimming pools will be further addressed in Chapter Nine.
On the other hand, the effect of temperature was greater on the yield of THMs than on the
yield of HAAs.
For HNMs, only TCNM was detected in the FP experiments, most of the time it
ranged between 0.7 and 1.7 µg/L, at the two temperatures and contact periods tested. The
narrow ranges of TCNM measured indicate low reactivity of the filling water NOMs to
produce HNMs, as compared to THMs and HAAs.
143
Table 7.3: Trihalomethanes (THMs), haloacetic acids (HAAs), and halonitromethanes (HNMs) formation potentials of treated
drinking water samples at 26°C, pH 7, and initial chlorine dose 50 mg/L
Sample Date FAC Incubation TCM BDCM DBCM TTHM DCAA BCAA TCAA BDCAA DBCAA THAA TCNM
mg/L days µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L
SJWD
No
vem
ber-0
8
47 5 64 5 1 70 13 1 20 3 <MRL 37 1.5
SP 47 5 70 5 1 75 13 1 22 2 <MRL 39 1.7
GV 47 5 44 3 1 48 7 <MRL 12 1 <MRL 20 1.1
CH 45 5 64 12 2 77 13 2 23 8 2 47 1.3
MB 45 5 80 4 1 85 13 <MRL 27 3 <MRL 43 1.1
SJWD 44 10 83 7 1 91 9 <MRL 18 3 <MRL 31 1.1
SP 47 10 94 5 1 99 10 <MRL 21 2 <MRL 33 1.2
GV 47 10 58 4 1 63 10 <MRL 16 2 <MRL 28 1.1
CH 42 10 82 14 3 98 14 2 26 9 <MRL 50 1.3
MB 43 10 100 5 1 106 13 <MRL 30 3 <MRL 46 1.0
SJWD
March
-09
44 5 69 5 1 75 ND 1 14 3 <MRL 18 1.1
SP 46 5 79 4 1 84 ND 1 22 2 <MRL 25 1.3
GV 46 5 70 4 1 75 ND 1 11 2 <MRL 14 1.1
CH 45 5 71 10 2 82 ND 1 14 5 <MRL 20 1.0
MB 45 5 78 3 1 81 ND 1 16 1 <MRL 18 1.1
SJWD 43 10 95 6 1 103 39 2 48 7 <MRL 97 0.8
SP 44 10 99 5 1 104 52 3 59 5 <MRL 119 1.0
GV 45 10 87 5 1 92 29 1 33 4 <MRL 68 <MRL
CH 44 10 90 11 2 104 36 4 45 12 <MRL 97 <MRL
MB 44 10 94 12 2 108 27 3 43 12 <MRL 86 0.7
SJWD
Sep
temb
er-09
47 5 85 5 1 91 ND 2 18 5 <MRL 25 <MRL
SP 48 5 90 4 1 95 ND 1 20 3 <MRL 24 0.7
GV 47 5 101 3 1 106 ND 3 31 5 <MRL 39 1.0
CH 43 5 83 10 2 96 ND 3 29 17 <MRL 50 0.7
MB 46.5 5 97 4 1 103 ND <MRL 24 5 <MRL 29 <MRL
SJWD 44 10 103 6 1 110 25 1 31 8 <MRL 65 0.7
SP 44.5 10 110 4 1 115 32 2 49 6 <MRL 89 0.8
GV 47 10 121 4 1 126 48 2 49 6 <MRL 105 1.0
CH 42 10 102 12 2 117 21 2 33 18 <MRL 73 0.7
MB 45 10 117 5 1 123 20 1 39 6 <MRL 66 0.7
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and TBM (tribromomethane). THNM (total halonitromethane),
DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA (trichloroacetic acid), BDCAA (bromodichloroacetic acid), DBCAA
(dibromoacetic acid), THAA (total HAA), TCNM (trichloronitromethane)
144
Table 7.4: Trihalomethanes (THMs), haloacetic acids (HAAs), and halonitromethanes (HNMs) formation potentials of treated drinking
water samples at 40°C, pH 7, and initial chlorine dose 50 mg/L
Sample Date FAC Incubation TCM BDCM DBCM TTHM DCAA BCAA TCAA BDCAA DBCAA THAA TCNM
mg/L days µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L
SJWD
No
vem
ber-0
8
45 5 115 9 1 125 19 1 26 3 <MRL 49 1.1
SP 42 5 125 6 1 131 19 1 29 2 <MRL 51 1.6
GV 43 5 73 4 1 78 8 <MRL 15 1 <MRL 24 0.8
CH 45 5 118 19 3 140 14 2 24 7 <MRL 47 1.3
MB 44 5 159 6 1 166 14 <MRL 31 2 <MRL 47 1.4
SJWD 41 10 163 11 1 175 10 <MRL 21 2 <MRL 33 1.1
SP 42 10 172 7 1 180 11 <MRL 22 1 <MRL 34 1.3
GV 42 10 103 5 1 110 11 <MRL 18 1 <MRL 31 1.3
CH 42 10 152 24 4 180 15 1 26 5 <MRL 47 1.3
MB 42 10 191 7 1 199 23 <MRL 38 2 <MRL 64 1.3
SJWD
March
-09
43 5 138 8 1 147 ND 1 25 3 <MRL 29 1.3
SP 44 5 146 6 1 152 ND 1 31 2 <MRL 34 1.7
GV 44 5 133 6 1 140 ND 1 20 2 <MRL 23 1.6
CH 44 5 138 14 2 154 ND 2 22 5 <MRL 29 1.4
MB 44 5 149 4 1 154 ND 1 25 1 <MRL 28 1.3
SJWD 42 10 196 9 1 206 52 3 65 6 <MRL 126 0.9
SP 43 10 198 6 1 205 66 3 74 4 <MRL 147 1.0
GV 43 10 179 6 1 186 37 2 50 3 <MRL 92 0.7
CH 42.5 10 193 17 2 212 43 4 58 9 <MRL 114 0.8
MB 42 10 205 4 1 210 42 1 65 2 <MRL 111 1.1
SJWD
Sep
temb
er-09
41 5 138 8 1 147 ND 1 30 6 <MRL 36 0.7
SP 44 5 148 5 1 154 ND 1 28 3 <MRL 32 0.9
GV 45.2 5 166 4 1 172 ND 1 37 4 <MRL 42 1.0
CH 42.5 5 145 15 3 162 ND 2 38 11 <MRL 51 0.7
MB 45.5 5 160 6 1 168 ND <MRL 36 5 <MRL 41 0.7
SJWD 40 10 177 9 1 187 29 1 41 7 <MRL 78 0.9
SP 43 10 195 6 1 201 43 1 54 5 <MRL 102 0.8
GV 44 10 197 5 1 203 66 2 72 6 <MRL 147 1.0
CH 41 10 191 18 3 212 58 5 70 14 <MRL 147 0.8
MB 43.5 10 204 7 1 212 30 2 55 5 <MRL 92 0.8
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and TBM (tribromomethane). THNM (total halonitromethane),
DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA (trichloroacetic acid), BDCAA (bromodichloroacetic acid), DBCAA
(dibromoacetic acid), THAA (total HAA), TCNM (trichloronitromethane)
145
THMs, HAAs, and HNMs produced from the filling water NOMs collected at
three different times but tested under the same conditions are shown in Figures 7.4, 7.5,
and 7.6. Noticeable differences were observed between the THM and HAA formation
patterns. For THM, although five treatment plants use water from different sources in
South Carolina with significantly different characteristics, THM formation potential was
relatively independent of source and location, and did not show time dependence for the
three samples collected at different times during 2008-2009 period (Figure 7.4). For
HAAs, there was more variability as a function of time and location, especially
considering the results for the ten-day FP test (Figure 7.5). This suggested that the
removal of HAA precursors during conventional treatment processes was more variable
than THM precursors in the treatment plants monitored in this study. The temporal
variability of HAAs formation was reported also by others when chlorination of different
water types was carried out at the same conditions but at different sampling dates or
seasons (Rodriguez et al., 2007). Especially after 10 days reaction time, DHAA appeared
and increased significantly. This may be due to the oxidation and further hydrolysis of
the organic matter after extended contact and reaction time, which produces more
hydrophilic and low molecular weight precursors fractions that have been shown to have
high HAAs (especially DHAA) yields in previous studies (Hua and Reckhow, 2007;
Bond et al., 2009).
146
Figure 7.4: THMs formed from five water types (NOMs) sampled three times during 2008-2009 at 1 mg/L TOC
(except GV water), pH 7, initial chlorine dose 50 mg/L, 5 days incubation at 26°C (a) and 40°C (b), and 10 days
incubation at 26°C (c) and 40°C (d). SJWD (Startex-Jackson-Wellford-Duncan), SP (Spartanburg), GV (Greenville),
MB (Myrtle Beach), CH (Charleston) (error bars are standard deviation)
0
50
100
150
200
250
SJWD SP GV CH MB
µg/L
a
Nov 08 Mar 09 Sep 09
0
50
100
150
200
250
SJWD SP GV CH MB
µg/L
c
0
50
100
150
200
250
SJWD SP GV CH MB
µg/L
b
0
50
100
150
200
250
SJWD SP GV CH MB
µg/L
d
147
Figure 7.5: HAAs formed from five water types (NOMs) sampled three times during 2008-2009 at 1 mg/L TOC
(except GV water), pH 7, initial chlorine dose 50 mg/L, 5 days incubation at 26°C (a) and 40°C (b), and 10 days
incubation at 26°C (c) and 40°C (d). SJWD (Startex-Jackson-Wellford-Duncan), SP (Spartanburg), GV (Greenville),
MB (Myrtle Beach), CH (Charleston) (error bars are standard deviation)
-40
10
60
110
160
SJWD SP GV CH MB
µg/L
a
Nov 08 Mar 09 Sep 09
0
20
40
60
80
100
120
140
160
SJWD SP GV CH MB
µg/L
c
0
20
40
60
80
100
120
140
160
SJWD SP GV CH MB
µg/L
b
0
20
40
60
80
100
120
140
160
SJWD SP GV CH MB
µg/L
d
148
Figure 7.6: HNMs (chloropicrin) formed from five water types (NOMs) sampled three times during 2008-2009 at 1 mg/L TOC
(except GV water), pH 7, initial chlorine dose 50 mg/L, 5 days incubation at 26°C (a) and 40°C (b), and 10 days incubation at
26°C (c) and 40°C (d). SJWD (Startex-Jackson-Wellford-Duncan), SP (Spartanburg), GV (Greenville), MB (Myrtle Beach), CH
(Charleston) (error bars are standard deviation)
0.0
0.4
0.8
1.2
1.6
2.0
2.4
SJWD SP GV CH MB
µg/L
aNov 08 Mar 09 Sep 09
0.0
0.4
0.8
1.2
1.6
2.0
2.4
SJWD SP GV CH MB
µg/L
c
0.0
0.4
0.8
1.2
1.6
2.0
2.4
SJWD SP GV CH MB
µg/L
b
0.0
0.4
0.8
1.2
1.6
2.0
2.4
SJWD SP GV CH MBµ
g/L
d
149
In all NOMs tested in these experiments DCAA was less than TCAA and in
several cases DCAA was not detected which was noted in previous studies that showed
that DCAA production decreased by increasing chlorine to NOM ratio (Miller and Uden,
1983; Zhuo, et al., 2001; Hua and Reckhow, 2008). Hua and Reckhow (2008) explained
the DCAA decrease at high Cl2/NOM ratios by differences in the reactivity of the
precursors of each species under different chlorine doses and that DCAA and TCAA
formation have different formation pathways also.
The chlorinated species were the dominant species of the three classes of DBPs
(THMs, HAAs, and HNMs) since bromide was either absent (in BFAs solutions) or at
low levels after diluting the waters to 1 mg/L TOC. Few brominated THM and HAA
species were observed in filling water tests. The speciation of the THMs and HAAs
produced from the November samples at 26°C for five days incubation time are
illustrated in Figures 7.7 and 7.8, respectively. The speciation of the of March-09 and
September-09 samples showed similar patterns (Tables 7.3 and 7.4).
150
Figure 7.7: THM species formed from BFAs and treated drinking waters in
November-08 samples (i.e, filling waters) during the FP tests at 1 mg/L TOC
(except GV water, 0.7 mg/L), 26°C, pH 7, initial chlorine dose 50 mg/L, and 5
days contact time.
Figure 7.8: HAA species formed from BFAs and treated drinking waters in
November-08 samples (i.e., filling waters) during the FP tests at 1 mg/L TOC
(except GV water, 0.7 mg/L) 26°C; pH 7, initial chlorine dose 50 mg/L, and 5
days contact time.
0
20
40
60
80
100
BFA(G) BFA(J) BFA(B) SJWD SP GV CH MB
µg/L
Chloroform DCBM DBCM
0
20
40
60
80
100
BFA(G) BFA(J) BFA(B) SJWD SP GV CH MB
µg/L
DCAA BCAA TCAA BDCAA DBCAA
151
The increase in the contact time and temperature resulted in an increase in both
THMs and HAAs for both BFAs and NOMs tested. Figure 7.9 shows the effect of contact
time on THM formation, which was greater for the treated drinking water NOM than
BFAs.
More time effect was noticed on the formation of HAAs. Figure 7.10 shows
HAAs formed from the five water sampled on March 2009 after five and ten days contact
period at 26°C. The same pattern applied for the other two samples of November 2008
and September 2009 (Figure 7.5). This temporal change in HAA formation is mostly
because of the change on the organic precursor due to prolong contact with the oxidant
which may result with more available HAAs precursor especially DHAAs ones.
The temperature dependence was greater for THM than HAAs formation, as
illustrated for the March samples in Figures 7.11 and 7.12. It is evident that the increase
in water temperature increased THM and HAA formation by enhancing reactions
between chlorine and DBP precursors that did not occur at the lower temperature (Weasel
and Chen, 1994; Al-Omari et al., 2004). The HNM (chloropicrin) formation did not show
any considerable change by time and temperature (Tables 7.3 and 7.4).
152
Figure 7.9: THMs (a) and HAAs (b) yield from BFAs and five NOMs
(November 08 samples) after 5 and 10 days under the same conditions. (error bars
are standard deviation)
0
20
40
60
80
100
120
BFA(G) BFA(J) BFA(B) SJWD SP GV CH MB
µg/L
a5-days 10-days
0
20
40
60
80
100
120
BFA(G) BFA(J) BFA(B) SJWD SP GV CH MB
µg/L
b
153
Figure 7.10: HAAs yield from five NOMs (March 09 samples) after 5 and 10
days under the same chlorination conditions. (error bars are standard deviation)
Figure 7.11: THMs yield from five NOMs (March 09 samples) chlorination after
10 days at 26°C and 40°C. (error bars are standard deviation)
0
20
40
60
80
100
120
140
SJWD SP GV CH MB
µg/L
5-days 10-days
0
20
40
60
80
100
120
140
160
SJWD SP GV CH MB
µg/L
THM at 26 °C THM at 40 °C
154
Figure 7.12: HAAs yield from five NOMs (March 09 samples)
chlorination after 10 days at 26°C and 40°C. (error bars are standard
deviation)
Conclusions
The main findings from this phase of the study are as follows:
FP tests demonstrated that BFAs were more reactive toward chlorine than filling
water (i.e., treated drinking water) NOMs.
BFAs formed more HAAs than THMs, while filling water NOMs produced more
THMs than HAAs. On the other hand, both NOMs and BFAs produced a similar
amount of HNMs (chloropicrin), which was significantly lower as compared to
THM and HAA formation.
Among the three BFAs tested, BFA(J) proposed by Judd and Bullock (2003)
exhibited the highest degree of THM and HAA formation. Analysis of individual
0
20
40
60
80
100
120
140
160
SJWD SP GV CH MB
µg/L
HAA at 26 °C HAAs at 40 °C
155
BFA components demonstrated that citric acid had significantly higher reactivity
toward THM and HAA formation than other components, which showed
relatively similar THM and HAA yields. The high reactivity exhibited by BFA(J)
as compared to the other BFAs was attributed to the presence of citric acid and
free amino acids in its composition.
Filling waters collected from five different treatment plants in three different
sampling events during a one year period exhibited comparable THM formation
relatively independent of time and location, whereas HAA yields exhibited more
spatial and time dependent variability.
Swimming pool water temperature affected THMs, HAAs, and HNMs formation
differently. At 40°C more THMs and HAAs were formed than at 26°C. Though,
more temperature dependence was observed for increasing THMs formation
while less effect was noticed on HAAs formation.
The contact time increased both THMs and HAAs. The effect of time was
different for THMs and HAAs. More HAAs were formed with an increase in
incubation time whereas less THMs were formed for the same incubation time
increase. Chloropicrin tends to decrease by increasing contact time, although a
very slight decrease was observed. These conclusions are applied for both NOMs
and BFAs.
The temporal effect on the formation of DBPs from NOMs was not the same on
the THMs, HAAs, and HNMs. THMs formed from the three sampling dates of the
five water recourses did not show large variation among the three seasons. Yet an
156
increasing trend was noticed from November 08 to September 09 which was most
probably due to the increase in the precipitation and runoff that took place during
this time period in the region. The HAAs formed from the three sampling events
were more variable for each water source. The different temporal effect on THMs
and HAAs suggests that the HAAs and THMs that may form from the NOMs
coming to swimming pools are not the same around the year and may vary
depending on the season and weather changes. Chloropicrin showed a decreasing
trend from the drought period (November 08) to the wet period (September 09).
157
CHAPTER EIGHT
SWIMMING POOL OPERATION PARAMETERS EFFECT ON DISINFECTION BY-
PRODUCTS FORMATION
Introduction and Objectives
During typical operation, swimming pool water is continuously circulated, filtered
and disinfected, as described and discussed in detail in Chapter 2. The aim of swimming
pool water treatment is to maintain clean, clear and biologically safe water to prevent
transmission of diseases among swimmers. Chlorine is the most widely used disinfectant
due to its stability, availability, ease of use, and ability to provide and maintain the
required free available chlorine residual (FAC) (Judd and Black, 2000; Borgmann-
Strahsen, 2003). However, as discussed in previous chapters, chlorine also reacts with
organic matter in water resulting in the formation of a wide variety of halogenated and
non-halogenated by-products that are known as disinfection by-products (DBPs) (Rook,
1974; 1976; Richardson et al., 2007). Although intensive work has been devoted to
investigate the factors affecting the formation of regulated THMs and HAAs in drinking
water, the effects of swimming pool operational parameters on the formation and
speciation of DBPs in swimming pools has not been systematically investigated.
The objective of the research in this chapter was to investigate the effects of
different swimming pool operational parameters such as free available chlorine
concentration, pH, TOC concentration (bathers load), and temperature on the formation
and speciation of three classes of DBPs (THMs, HAAs, and HNMs). The effect of
bromide was also examined because different levels of bromide may be present in the
158
filling water and bromide may also enter water through the impurities in some of the
chemicals (e.g., NaCl used for electrochemical production of Cl2) used for pool
operations. The presence of bromide can significantly change the speciation of DBP in
the pool water, and it has been shown that brominated DBPs have more adverse health
effects than chlorinated DBPs (Icihashi, et al., 1999; Westerhoff et al., 2004; Duirk and
Valentine, 2007). Understanding the effect of swimming pool operational parameters on
the formation and speciation of DBPs is important for developing approaches that will
reduce the exposure of swimmers and swimming pool attendants to DBPs.
Approach
Two synthetic pool waters were prepared using two different filling waters and a
body fluids analog developed by Geores and co-workers (2004), BFA(G), as described in
Chapter Four (Table 4.2). The filling waters were obtained as the finished waters from
Myrtle Beach (MB) and Startex-Jackson-Wellford-Duncan (SJWD) water treatment
plants in South Carolina prior to final disinfectant addition. The BFA(G) was used to
simulate the body fluids that are introduced in swimming pool water by swimmers. The
TOC concentration of the synthetic pool water was 6 mg/L, of which 5 mg/L was from
BFA(G) and 1 mg/L from the filling water. These concentrations are representative of the
TOC levels in indoor pools and contributions from swimmer body fluid releases and
filling waters as it was determined during monitoring of the swimming pools (Chapter
Five). The experiments of this task are described in Chapter Three (Figure 3.3)
159
Materials and Methods
Synthetic Swimming Pool Waters
Two synthetic swimming pool water solutions, BFA(G)-MB and BFA(G)-SJWD,
were prepared by mixing one filling water, MB or SJWD, with BFA(G). As indicated
previously, filling waters were collected from the effluent of MB and SJWD drinking
water treatment plants in South Carolina prior to post-disinfection. MB and SJWD waters
are from two different sources with significantly different characteristics. Myrtle Beach
source water has high TOC concentrations (15-20 mg/L) and is rich in aromatic organic
components (SUVA254= 4-6 mg/L-m), whereas SJWD source water has low TOC
concentrations (2-4 mg/L) and is low in aromatic organic components (SUVA254= 2-3
mg/L-m). After water treatment processes, the effluent waters (or filling waters) had
different characteristics. MB filling water had higher TOC and bromide, and slightly
higher SUVA254 values as compared to SJWD water (Table 4.1). These two filling waters
served as two different background matrices for the synthetic swimming pool waters.
Since they had different TOC values, they were both diluted to provide the same amount,
1 mg/L TOC, of background organic carbon in the synthetic solution. The remaining
TOC was provided by the BFA(G).
The BFA proposed by Goeres et al. (2004) was selected for preparing the
synthetic swimming pool waters because the other two BFAs formed high amounts of
THMs and HAAs due to the presence of citric acid and/or specific amino acids (histidine
and asparaginic acid) selected for their formulations, as discussed in the previous chapter.
160
The composition of BFA(G) was provided in Chapter Four (Table 4.2). The TOC and TN
of the synthetic stock solutions were confirmed with measurements prior to experiments.
Chlorination Experiments
Sodium hypochlorite (NaOCl) with 5% available chlorine was used as chlorine
source. The stock chlorine solution was always standardized by the N, N-diethyl-p-
phenylenediamine (DPD) titrimetric method, 4500-Cl F (Standard Methods, 1995). The
chlorination experiments were conducted in 125-mL amber glass bottles closed tightly
with Teflon-faced septa screw cap. After mixing well using magnetic stir bars, the bottles
were stored headspace free in a water bath for five days at constant temperature (26 or
40°C). The contact time of five days was used to simulate the long contact time between
disinfectant and organic precursors in a swimming pool. Initial chlorine doses were
selected to achieve 1 mg/L, 3 mg/L and 5 mg/L FAC residual after five days of contact
time. The water samples were buffered by addition of 4 mM sodium bicarbonate (336
mg/L) and then pH was adjusted as necessary with HCl (1M) or NaOH (1N) solutions.
Analytical Methods
Detailed information about the analytical methods can be found in Chapter Four.
161
Results and Discussion
Effect of Free Available Chlorine on DBP Formation
The required disinfectant residual levels in swimming pools vary widely around
the world ranging from as low as 0.3 mg/L to 5 mg/L as FAC (WHO, 2006; SC DHEC,
2007; Zwiener et al., 2007). To investigate the effect of FAC on the formation of DBPs in
swimming pools, three FAC levels were tested: 1, 3, and 5 mg/L. THM concentration
increased slightly, 5% for BFA(G)-MB and 14% for BFA(G)-SJWD, with increasing free
available chlorine concentrations from 1 to 5 mg/L (Table 8.1 and Figure 8.1). On the
other hand, the effect of chlorine concentration on HAA and HNM formation was greater
as compared to THM. Increasing chlorine dose from 1 mg/L to 5 mg/L, increased HAA
formation by 25% and 27% for BFA(G)-MB and BFA(G)-SJWD, respectively, (Table
8.1). HNM concentration was doubled during the same experiments in the two synthetic
swimming pool water solutions. The lower impact of chlorine concentrations on THM
than HAA and HNM was attributed to the impact of chlorine dose on the formation of
different DBPs. Previous research showed a linear relationship between chlorine demand
and THMs formation (Boccelli et al., 2003), and a weak correlation between the chlorine
levels and chloroform formation after satisfying the demand (Garcia-Villanova et al.,
1997). Consistent with these observations, the results indicate that once chlorine demand
was satisfied after five days of reaction time, there was no impact of chlorine dose on the
THM formation. Chloroform was the dominant species formed during the experiments
with very few or trace brominated species. The lack of brominated species of DBPs was
162
Table 8.1: Trihalomethanes (THMs) and haloacetic acids (HAAs) formed from synthetic swimming pool water
Pa
ram
eter
Synthetic
pool water*
TO
C m
g/L
Tem
p. °C
FA
C m
g/L
pH
Br
- µg
/L
THMs (µg/L) HAAs (µg/L)
TC
M
DC
BM
DB
CM
TB
M
TT
HM
BA
A
DC
AA
BC
AA
TC
AA
DB
AA
DC
BA
A
DB
CA
A
TB
AA
TH
AA
FA
C
BFA(G)-MB 6 26 1 7 ambient 84 4 1 ND 89 ND 82 3 86 ND 7 ND ND 178
6 26 3 7 ambient 87 5 1 ND 93 ND 98 2 93 ND 7 ND ND 200
6 26 5 7 ambient 89 4 1 ND 94 ND 105 2 111 ND 4 ND ND 222
BFA(G)-SJWD 6 26 1 7 ambient 73 7 1 ND 81 ND 74 5 70 ND 11 ND ND 160
6 26 3 7 ambient 77 9 2 ND 87 ND 89 3 84 ND 7 ND ND 183
6 26 5 7 ambient 84 9 1 ND 93 ND 95 4 101 ND 4 ND ND 204
pH
BFA(G)-MB 6 26 1 6 ambient 71 4 1 ND 76 ND 52 2 69 ND 5 ND ND 129
6 26 1 8 ambient 120 5 1 ND 126 ND 115 3 98 ND 10 ND ND 226
BFA(G)-SJWD 6 26 1 6 ambient 64 6 1 ND 71 ND 45 4 59 ND 8 ND ND 116
6 26 1 8 ambient 106 9 1 ND 116 ND 105 6 77 ND 13 ND ND 201
TO
C
BFA(G)-MB 11 26 1 7 ambient 131 10 1 ND 142 ND 111 3 141 ND 6 ND ND 262
16 26 1 7 ambient 154 8 1 ND 163 ND 126 2 150 ND 6 ND ND 284
BFA(G)-SJWD 11 26 1 7 ambient 117 12 1 ND 130 ND 92 4 112 ND 10 ND ND 219
16 26 1 7 ambient 142 12 1 ND 155 ND 112 4 150 ND 9 ND ND 275
T
BFA(G)-MB 6 40 1 7 ambient 176 6 <MRL ND 182 ND 158 3 120 ND 5 ND ND 287
BFA(G)-SJWD 6 40 1 7 ambient 157 11 <MRL ND 168 ND 146 7 103 ND 8 ND ND 264
Br
-
BFA(G)-MB 6 26 1 7 100 88 47 11 1 147 4 83 21 66 3 35 6 0 218
6 26 1 7 300 52 68 51 13 184 6 62 31 39 10 45 23 2 218
6 26 1 7 600 36 78 87 38 238 8 42 39 26 20 45 36 6 222
BFA(G)-SJWD 6 26 1 7 100 74 53 13 1 140 4 74 21 57 3 35 8 0 202
6 26 1 7 300 47 71 46 12 175 6 52 31 36 11 43 24 2 205
6 26 1 7 600 31 75 73 33 212 8 44 39 27 21 43 35 6 223
* Synthetic pool water was prepared from BFA(G) and two different background waters: BFA(G)-MB= body fluid analog and Myrtle Beach water;
BFA(G)-SJWD=body fluid analog and SJWD water. The values are the average of duplicate or triplicate measurements. TCM (chloroform), BDCM
(bromdichloromethane), DBCM (dibromochloromethane), and TBM (tribromomethane). THNM (total halonitromethane), DCAA (dichloroacetic acid),
BCAA (bromochloroacetic acid), TCAA (trichloroacetic acid), BDCAA (bromodichloroacetic acid), DBCAA (dibromoacetic acid), THAA (total
HAA).
163
Figure 8.1: Effect of free available chlorine (FAC) on THM (a), HAA (b), and
HNM (c) formation during chlorination of two synthetic pool waters. (error bars
are standard deviation)
0
50
100
150
200
1 3 5
µg/L
a BFA-MB BFA-SJWD
0
50
100
150
200
250
1 3 5
µg/L
b
0.0
0.4
0.8
1.2
1.6
2.0
1 3 5
µg/L
FAC (mg/L)
c
164
attributed to the low bromide levels in the filling water samples (especially after dilution
to obtain 1 mg/L TOC) and high chlorine dose applied to satisfy the demand and achieve
the required free available chloride after five days.
In contrast to THMs, some dependence of HAA formation on chlorine dose was
observed, with the HAA formation increasing approximately 25% with increasing FAC
concentration from 1 to 5 mg/L. The dependence was attributed to the reaction(s) of
chlorine with albumin in BFA(G). With increasing dose, a higher degree of albumin
decomposition (hydrolysis) occurred generating more HAA precursors (free amino acids)
than THM. The observed dependence is consistent with the results presented in Table 7.1
in the previous chapter showing that under the same chlorination condition BFA(G)
formation of HAA was higher than THMs. As was observed for THMs, HAA formation
mainly consisted of chlorinated species (DCAA and TCAA). Similar to HAAs, formation
of HNMs increased with increasing FAC levels (Tables 8.1 and 8.2). Chloropicrin was
the only HNM species detected.
Comparison of the results between MB and SJWD samples showed that formation
of THM and HAA was approximately 10% higher in MB than in SJWD water. Although
both synthetic pool waters had similar composition (1 mg TOC from filling water and 5
mg TOC from BFA(G)), slightly higher THM and HAA formation in MB than in SJWD
water was attributed to the more aromatic nature of the former than the latter source
waters. Although the filling waters had similar TOC values, MB water had somewhat
higher SUVA254 (~2.0 L/mg-m) as compared to SJWD water (~1.7 L/mg-m) (Table 4.2),
165
Table 8.2: Halonitromethanes (HNMs) formed from synthetic swimming pool water
Para
meter
Synthetic pool water*
TO
C m
g/L
Tem
p. °C
FA
C m
g/L
pH
Br
- µg/L
HNMs (µg/L)
TC
NM
BN
M
BC
NM
DC
BN
M
DB
CN
M
TB
NM
TH
NM
FA
C
BFA(G)-MB 6 26 1 7 ambient 0.7 ND ND ND ND ND 0.7 6 26 3 7 ambient 1.2 ND ND ND ND ND 1.2 6 26 5 7 ambient 1.4 ND ND ND ND ND 1.4
BFA(G)-SJWD 6 26 1 7 ambient 0.7 ND ND ND ND ND 0.7 6 26 3 7 ambient 1.0 ND ND ND ND ND 1.0 6 26 5 7 ambient 1.4 ND ND ND ND ND 1.4
pH
BFA(G)-MB 6 26 1 6 ambient 0.6 ND ND ND ND ND 0.6 6 26 1 8 ambient 0.9 ND ND ND ND ND 0.9
BFA(G)-SJWD 6 26 1 6 ambient 0.6 ND ND ND ND ND 0.6 6 26 1 8 ambient 0.9 ND ND ND ND ND 0.9
TO
C
BFA(G)-MB 11 26 1 7 ambient 1.3 ND ND ND ND ND 1.3 16 26 1 7 ambient 1.6 ND ND ND ND ND 1.6
BFA(G)-SJWD 11 26 1 7 ambient 1.3 ND ND ND ND ND 1.3 16 26 1 7 ambient 1.6 ND ND ND ND ND 1.6
Tem
p.
BFA(G)-MB 6 40 1 7 ambient 1.9 ND ND ND ND ND 1.9
BFA(G)-SJWD 6 40 1 7 ambient 1.8 ND ND ND ND ND 1.8
Br
-
BFA(G)-MB 6 26 1 7 100 0.7 2.5 0.9 2.4 <MRL <MRL 6.5 6 26 1 7 300 <MRL 6.3 0.1 2.4 1.8 4.5 15.4 6 26 1 7 600 <MRL 8.6 0.0 2.2 2.0 11.5 24.5
BFA(G)-SJWD 6 26 1 7 100 <MRL 3.2 1.6 2.5 ND ND 7.9 6 26 1 7 300 <MRL 6.6 0.3 2.4 1.9 3.6 15.1 6 26 1 7 600 <MRL 6.6 0.1 2.2 1.9 12.1 23.1
* Synthetic pool water was prepared from BFA(G) and two different background waters: BFA-
MB= body fluid analog and Myrtle Beach water; BFA-SJWD=body fluid analog and SJWD
water. The values are the average of duplicate or triplicate measurements.
TCNM (trichloronitromethane), BNM (bromonitromethane), BCNM (bromochloronitromethane),
DCBNM (dichlorobromonitromethane), DBNM (dibromonitromethane), THNM (total
halonitromethane)
166
indicating that the former filling water had slightly higher aromatic character than the
latter.
Effect of pH on DBP Formation
The pH of swimming pool water is continuously adjusted and maintained within
the values required by regulations, mainly to assure an acceptable level of disinfection
efficiency. In addition, pH control makes the water comfortable for swimmers and
prevents damage of the swimming pool structures and pipes. Some swimming pool
regulations require a pH maintained between 6.5 and 7.2 (Erdinger et al., 2005; Uhl and
Hartmann, 2005; Zwiener et al., 2007), while others demand a higher range between 7.2
and 7.8 (NSPF, 2006; Zwiener et al., 2007). The formation of DBPs was examined at
three pH conditions (6, 7 and 8). The results show that the three studied DBPs (THMs,
HAAs, and HNMs) increased with increasing pH (Figure 8.2). It has been previously
reported in the drinking water literature that THM formation increases with an increase in
pH, while the trend is the opposite for HAA formation (Hua and Reckhow, 2008).
However, in this study, an increasing trend was observed for both THM and HAA with
an increase in pH. The opposite behavior observed for pH dependence of HAAs in
synthetic swimming water solution was attributed to the hydrolysis of albumin, one of the
important ingredients in the BFA(G), and its reactivity with chlorine. Albumin hydrolysis
and reaction with chlorine is favored at higher pH (a base catalyzed reaction) (Mabey and
Mill, 1978); therefore, decomposition of albumin increases with an increase in pH,
releasing more precursors forming HAAs. The HNM formation was 30% higher at pH 8
167
as compared to pH 6 (Table 8.2). Increasing HNM formation with increasing pH was also
reported by other researchers (Hu, 2009). The overall amount of HNMs (chloropicrin)
was very low compared to THMs and HAAs.
The observed pH trends for HAAs also indicate that filling water NOM was not a
major factor contributing to HAA formation in synthetic pool waters because in drinking
waters HAA concentration decreases with an increase in pH, as previously mentioned. At
all three pH conditions, the formation of THM and HAAs was about 10% higher in MB
water than in SWJD water, indicating that filling water characteristics had only a slight
impact on DBP formation. Finally, the results clearly indicate that reducing pH from 8 to
6 decreased THM and HAA formations approximately 40 to 60% (Table 8.1).
Furthermore, disinfection efficiency of chlorine increases with decreasing pH, especially
below the pKa of HOCl where HOCl is a more effective disinfectant agent than OCl-
[AWWA, 1990; White, 1999]. Therefore, operating swimming pools at neutral pHs or
slightly below neutral conditions has an advantages for control of DBPs.
168
Figure 8.2: Effect of pH on THM (a), HAA (b), and HNM (c) formation during
chlorination of two synthetic pool water types at three different pH levels. (error
bars are standard deviation)
0
20
40
60
80
100
120
140
6 7 8
µg/L
a BFA-MB BFA-SJWD
0
50
100
150
200
250
6 7 8
µg/L
b
0
0.2
0.4
0.6
0.8
1
1.2
6 7 8
µg/L
pH
c
169
Effect of TOC on DBP Formation
In indoor swimming pools, body fluids and excretions are continuously released
by swimmers in the pool water and they constitute the main source of organic carbon and
precursors of DBPs. As a result, the TOC concentrations continuously increase in the
pool waters, as reported in the literature (Zwiener et al., 2007). In this study, the BFA
was used to increase the TOC in the synthetic pool water to imitate levels of TOC that
had been reported in swimming pools. The results for the effect of increasing TOC
concentration are provided in Figure 8.3. As expected, formation of DBPs (THM, HAA
and HNM) increased with the increase in the TOC concentrations. The dependence on
TOC concentration confirms that the DBP formation in swimming pools is highly
correlated with the bather load. However, the increase in DBP concentrations was not
proportional to the increase in TOC concentrations (Table 8.3). One reason for this
behavior was the fact that during the experiments the contributions of BFA and filling
water to the overall TOC of the synthetic swimming pool solutions increased with TOC
concentrations: for TOC 6 mg/L [1 mg filling water (17%) and 5 mg BFA (83%)], 11
mg/L [1 mg filling water (9%) and 10 mg BFA (91%)], and 16 mg/L [1 mg filling water
(6%) and 15 mg BFA (94%)]. As a result, the chlorine dose to TOC ratio to maintain 1
mg/L residual after five days of contact time also increased (Table 8.3) since BFA(G) had
higher chlorine reactivity than the filling water NOM, as demonstrated in Chapter Seven.
170
Table 8.3: Trihalomethane (THM) and haloacetic acid (HAA) yields from different
chlorine to total organic carbon ratio
Synthetic swimming
pool water
TOC
mg/L
Injected Cl2
mg/L Cl2/TOC
THM
Yield
µg/mg C
HAA
Yield
µg/mg C
BFA(G)-MB
6 75 12.5 15 30
11 150 13.6 13 24
16 225 14 10 18
BFA(G)-SJWD
6 75 12.5 13.5 27
11 150 13.6 12 20
16 225 14 9.7 17
TOC (total organic carbon), THM (trihalomethane), HAA (haloacetic acid)
However, it was also found that THM and HAA yields decreased with increasing TOC
concentrations despite the increase in the Cl2/TOC dose. The decrease in the yields was
attributed to the reactivity of BFA components with chlorine and formation of by-
products other than THM and HAA with increasing BFA fraction in the synthetic pool
water. This yield decrease also suggests that although continuous release of BFs by
swimmers increases THM and HAA concentrations in the pools, they also produce more
of other DBPs. In this study, the concentration of total organic halides (TOX) was not
measured because the necessary analyzer was not available. It will be beneficial to
monitor TOX concentrations in future studies. The yield of THMs and HAAs per mg C is
presented in Table 8.3. There is a clear decrease in the yield while the TOC is increasing
in both types of synthetic pool waters.
171
Figure 8.3: Effect of TOC on the formation of THMs (a), HAAs (b), and HNM
(c) from two synthetic pool water types under the same conditions of swimming
pool operation parameters at TOC 6, 11, and 16 mg/L. (error bars are standard
deviation)
0
100
200
6 11 16
µg/L
a
BFA-MB BFA-SJWD
0
100
200
300
400
6 11 16
µg/L
b
0.0
1.0
2.0
6 11 16
µg/L
TOC (mg/L)
c
172
Effect of Bromide on DBP Formation
Filling and make-up water of swimming pools are obtained from the distribution
system in the swimming pool area. As a result bromide concentrations in swimming
pools are highly dependent on the location and drinking water source of the pool.
According to previous studies and the Information Collection Rule monitoring conducted
by US EPA during 1997-1998 the bromide concentration at 500 water treatment plants in
the US ranged between 36 g/L and 2230 µg/L with a mean of 69 g/L (Amy et al.,
1994; Obolensky and Singer, 2005). Another important source of bromide is the
impurities in chemicals used for swimming pool operations. For example,
electrochemical generation of chlorine from sodium chlorine is used in swimming pools
and bromide is usually present in the sodium chloride. When bromide at three levels
(100, 300, and 600 µg/L) was spiked in the two synthetic pool waters (BFA(G)-MB and
BFA(G)-SJWD) at 6 mg/L TOC, the formation of both THMs and HAAs and the
concentrations of brominated species increased while the concentrations of chlorinated
species decreased (Table 8.1, Figure 8.4 and Figure 8.5). The impact of bromide was
higher on THM than HAA formation. On a mass basis, THM concentrations increased by
65-72%, 106-116%, and 162-167% in synthetic pool waters at 100, 300, and 600 µg/L
bromide concentrations, respectively. In order to evaluate bromine incorporation an
incorporation factor n (a dimensionless factor) was introduced by Gould et al. (1983).
The factor n is the molar amount of bromine in the halogenated compound (THM or
HAA) divided by the molar total of that halogen.
173
Figure 8.4: Effect of bromide on the formation and speciation of THMs from
BFA-MB (a) and BFA-SJWD (b) synthetic pool water.
0
20
40
60
80
100
ambient 100 300 600
µg/L
a
TCM DCBM DBCM TBM
0
20
40
60
80
100
ambient 100 300 600
µg/L
Bromide concentration (µg/L)
b
174
Figure 8.5: effect of bromide on the formation of HAAs and speciation from
BFA-MB (a) and BFA-SJWD (b) synthetic pool water.
0
20
40
60
80
100
ambient 100 300 600
µg/L
a
BAA DCAA BCAA TCAA DBAA BDCAA DBCAA TBAA
0
20
40
60
80
100
ambient 100 300 600
µg/L
Bromide concentration (µg/L)
b
175
For THMs the following equation was used to calculate the bromide substitution.
𝑛 =𝐶𝐻𝐵𝑟𝐶𝑙2 + 2𝐶𝐻𝐶𝑙𝐵𝑟2 + 3𝐶𝐻𝐵𝑟3
𝑇𝑇𝐻𝑀 0 ≤ 𝑛 ≤ 3 (8.1)
When n is 0 it means that the only formed compound(s) are chlorinated ones whereas n˃0
mean that brominated species are starting to appear. For HAAs a similar equation was
used considering the nine HAA species. On the other hand, the increase in HAA
concentrations during the same experiments remained only between 22 and 39%.
Bromine incorporation factors calculated for THM and HAAs also confirmed this
observation (Figure 8.6). Results show that the presence of bromide will result in a higher
impact on brominated THM than HAA formation (Figure 8.6). When bromide was 600
µg/L the incorporation factor n was 1.3 for THMs but for HAAs its value was only 0.8 in
both synthetic swimming waters. This difference in bromide incorporation is also
consistent with higher bromine incorporation of THMs than HAAs in drinking water
samples (Kitis et al., 2002).
176
Figure 8.6: BIF (bromide incorporation factor) (n) into THM (a) and HAA (b) at
three different bromide levels spiked into two synthetic pool waters
0.0
0.4
0.8
1.2
1.6
100 300 600
BIF
(n)
a
BFA-MB BFA-SJWD
0
0.4
0.8
1.2
1.6
100 300 600
BIF
(n)
Br (µg/L)
b
177
The increase in bromide also increased HNM formation and shifted speciation
toward brominated species (Table 8.2 and Figure 8.7). In both synthetic pool waters the
HNMs ranged between 6.5 and 24.5 µg/L as bromide increased from 100 to 600 µg/L
(Table 8.3). These are very high levels considering the significantly higher geno- and
cytotoxicity of HNM as compared to regulated carbonaceous DBPs (C-DBPs). These
HNM values are consistent with the measured values in swimming pools samples shown
in Chapter Five.
For the three DBPs discussed above, bromide is highly reactive in the formation
of DBPs and incorporation to form brominated species. Such bromide reactivity has also
been noticed by other researchers especially when precursors are hydrophilic low
molecular weight organic compounds similar to BF components. However, chlorine has
exhibited an opposite reactivity (Huang and Yeh, 1997; Kitis et al., 2002; Liang and
Singer, 2003). Chlorine acts more as an oxidant, while bromine is a more efficient as a
substituting halogen (Westerhoff et al., 2004).
Overall, these results clearly demonstrate using water with low bromide levels to
fill swimming pools or use as make up water is critical to reduce DBP formation,
especially THMs and HNMs. Likewise, using seawater or saline water as make-up or
filling water should be avoided to reduce the DBP formation in swimming pools.
178
Figure 8.7: Effect of bromide on HNM formation and speciation during
chlorination of two synthetic pool waters, BFA-MB (a) and BFA-SJWD (b).
0
5
10
15
20
25
30
ambient 100 300 600
µg/L
a
TCNM BNM BCNM DCBNM DBCNM TBNM
0
5
10
15
20
25
30
ambient 100 300 600
µg/L
Bromide concentration (µg/L)
b
179
Effect of Temperature on DBP Formation
Swimming pool water temperature is maintained constant using a heat exchanger
placed in the treatment train after filtration (Figure 2.1). The whole experimental matrix
and results discussed until now in this chapter were performed at 26°C, which is a typical
value used during the operation of indoor swimming pools. To examine the effect of
temperature on DBP formation, chlorination of the two synthetic swimming pool water
was also conducted at the highest temperature, 40°C, allowed in pools. This temperature
is typically used in therapeutic swimming pools, hot tubs, and whirlpool spas. The
increase in temperature effect doubled the amount of THMs and HNMs formed in both
synthetic pool waters used as compared to 26°C (Table 8.1 and 8.2, and Figure 8.8). The
increase in HAAs formation was about 60%. It is evident that exposure to DBPs in hot
tubs or any other type of elevated temperature indoor swimming pools will be
substantially higher, but usually people spend shorter time in hot tubs compared to
swimming time. The increase in DBP formation with temperature can be explained by
reaction of un-reacted DBPs precursors with chlorine and increase in the reactivity of
chlorine with precursors (Weisel and Chen, 1994; Al-Omari et al., 2004).
180
Figure 8.8: Formation of THMs (a), HAAs (b) and HNMs (c) at 26 and 40°C
from two synthetic pool waters. (error bars are standard deviation)
0
50
100
150
200
BFA-MB BFA-SJWD
µg/L
a26˚C 40˚C
0
50
100
150
200
250
300
350
BFA-MB BFA-SJWD
µg/L
b
0.0
0.4
0.8
1.2
1.6
2.0
BFA-MB BFA-SJWD
µg/L
c
181
HAAs and THMs Formation Relation
It was noticed that the yield of HAAs formed by chlorination of body fluids was
always more than THMs (Table 8.1). High HAAs yields indicate that body fluid
components are richer with HAAs formation precursors than THM precursors. Reactivity
tests presented earlier in Chapter Seven and other studies of amino acids chlorination
showed that HAAs are formed at a higher yield than THMs from amino acids (Michael et
al., 1986; Hureiki, et al., 1994; Hong et al., 2008). The ratio of HAAs to THMs was
consistently around 1.9:1 when bromide was at ambient concentration and pH is not 6.
When bromide was at a higher concentration than ambient especially at 300 and 600
µg/L, the ratio of HAAs to THMs was around 1:1. The linership was strong when HAAs
vs. THMs formed under the same conditions (temperature 26°C and no bromide spiked)
were plotted against each other (Figure 8.9). The correlation (r2) is about 0.8 and the
slope is 1.86. This linear relation between the two main DBPs that may be found at high
concentrations in swimming pools is an important tool to estimate the whole amount of
THMs that are partitioning between water and air. If this is applicable, THMs that escape
to the air can be estimated also from the measurement of HAAs and THMs in the pool
water.
182
Figure 8.9: HAAs and THMs linear relation
Conclusions
This part of the study has focused on the effect of different operational parameters
on the formation of DBPs under swimming pool chlorination conditions. Results obtained
show that:
The DBPs formation is affected by the chlorine residual maintained in the pool
water as FAC.
Decreasing the chlorine demand and maintaining lower FAC in the pool water is
an important factor to improve the health environment in swimming pools.
Increasing the efficiency of filtration and pathogen chlorine resistant removal may
be an alternative for the high chlorine residual required to maintain safe water.
y = 0.5317x
r² = 0.8461
0
50
100
150
200
250
300
350
400
0 50 100 150 200 250 300
TH
M (
µg/L
)
HAA (µg/L)
183
The approach of increasing pathogen removal by filtration and minimizing
chlorine will provide both chemical and biological safe water.
The pH as a controlled parameter can be lowered to about 7 for both increasing
the chlorine disinfection efficiency by favoring HOCl (which is more efficient as
a disinfectant) over OClˉ at lower pH and also hindering the DBPs formation.
This possibility is applicable since the pH effect on the three tested DBPs formed
from BFA is similar (increasing pH increased THMs, HAAs, and HNMs).
TOC increase caused an increase in the three investigated DBP classes. Bathers
load, which is proportional to the number of pool users at a time and per day,
should be carefully observed and regulated to keep the pool water organic content
as low as possible. Also the turnover rate and dilution of the pool water on a daily
basis and number of pool users will contribute greatly to preventing the
accumulation of DBPs (especially nonvolatile and highly soluble) and also their
precursors in the pool water.
Since temperature increased DBPs significantly, avoiding higher temperature of
pool water is important to reduce the DBPs formation in pool water.
Bromide increased the overall DBPs and enhanced the formation of brominated
species in the three DBPs measured in this study (THMs, HAAs, and HNMs).
Brominated species of DBPs are more toxic (Bull et al., 1995) than chlorinated
ones.
184
THMs overall formation increased when bromide was spiked into the synthetic
pool water. The overall HAAs increase with the addition of bromide was much
less than THMs. Bromide affected the HNMs formation and speciation, too.
185
CHAPTER NINE
TRIHALOMETHANES AND HALOACETIC ACIDS FORMATION DURING
TURNOVER TIME OF SWIMMING POOL WATER
Introduction and Objectives
The turnover period in swimming pools typically ranges from four to eight hours.
Therefore, from a DBP control perspective, when fresh body fluids (BFs) are released by
a swimmer, this is the retention time for BFs to react with chlorine in the pool before
water goes through treatment outside of the pool that may remove some of the BF
components (Figure 2.1). Given the fast DBP formation kinetics with chlorine in drinking
waters (Gallard and Gunten, 2002; Nikolaou et al. 2004) and much higher free chlorine
residual concentrations in swimming pools than in drinking waters, it is postulated that
DBPs will form very rapidly in swimming pools. To date, there is no information in the
literature regarding the DBP formation kinetics in swimming pool conditions Therefore,
it is important to understand the formation kinetics of DBPs, especially at short reaction
times, at swimming pool conditions for developing DBP control strategies. The
objectives of the research presented in this chapter were to (i) determine how fast THMs,
HAAs, and HNMs are produced under swimming pool operation conditions, and (ii)
examine what percent of the one day and five day DBP formation levels are occurring
during the first ten hours, covering the range of water turnover periods in swimming
pools. The impact of bromide on DBP formation kinetics was also investigated due to its
practical relevance.
186
Approach
DBP formation kinetics were studied for three solutions: (i) a synthetic pool water
at 6 mg TOC/L (5 mg/L from BFA(G) and 1 mg/L from MB as the background filling
water), (ii) 5 mg TOC/L BFA(G) DDW, and (iii) 1 mg TOC/L BFA(G) in DDW. Two
solutions of BFAs were examined in DDW at two concentrations (i) to examine the DBP
formation kinetics from BFs alone, and (ii) the formation kinetics at two Cl2/TOC ratios.
Each solution was chlorinated, and several DBP samples were collected at early reaction
times during the experiments that continued for five days (e.g., 0.5, 1.0, 3.0, 5.0, 7.0,
10.0, 15.0, 24.0, 48.0, 72.0, 96.0, 120.0 hours). To examine the bromide effect on the
DBP formation kinetics, the experiments were repeated by spiking the same three waters
with 200 µg/L bromide. An initial dose of 100 mg/L chlorine was used in the experiments
to have a residual of 3-5 mg/L free chlorine after five days of contact time. The
experiments for this part of the study are shown in Figure 3.4.
Materials and Methods
The composition of BFA(G) and characteristics of MB filling water were
provided in Chapter Four along with the analytical methods used for DBP measurements,
and are not repeated here.
187
Results and Discussion
THMs Formation as Function of Time
The results of the THM experiments are provided in Tables 9.1, 9.2, and 9.3. The
results showed that 53% to 68% of five-day THM formation occurred during the first five
hours in the presence and absence of bromide for synthetic pool water and BFA(G)
solutions. This is a faster rate of THMs production at early contact times compared to the
rates reported in drinking waters. Gallard and Gunten (2002) and Nikolaou et al. (2004)
reported that 15-30% of THMs are only formed at five to six hours of chlorination of
different surface drinking water sources under drinking water chlorination scenarios. The
fast formation rate of THMs observed in this study indicates that a significant portion of
THMs will be formed in the pool before the pool water undergoes any treatment. Since
THM are volatile compounds, an appreciable fraction of the formed THM will also
partition in air once they are formed in water. Practically, these results strongly implies
that precursor (i.e., the release of human body excretes) control will be important in
reducing the formation of THMs in swimming pools. The precursor control requires
improving the practices and behavior of swimming pools users, and implementing more
strict hygienic conditions by swimming pools utilities. Better hygienic conditions include
showering immediately before swimming and not releasing urine intentionally during
swimming pool use.
188
Table 9.1: Trihalomethanes (THMs) formation change during 5 days reaction time from
synthetic pool water produced from BFA(G) (5mg/L TOC) and MB water source
(1mg/L), BFA(G)-MB, without and with bromide.
Synthetic pool
water
Br- Time TCM DCBM DBCM TBM TTHMs
µg/L hours µg/L µg/L µg/L µg/L µg/L
BFA(G)-MB 0 0.5 53 ND ND ND 53
BFA(G)-MB 0 1 55 ND ND ND 55
BFA(G)-MB 0 3 62 ND ND ND 62
BFA(G)-MB 0 5 70 ND ND ND 70
BFA(G)-MB 0 7 72 ND ND ND 72
BFA(G)-MB 0 10 74 ND ND ND 74
BFA(G)-MB 0 15 76 ND ND ND 76
BFA(G)-MB 0 24 83 ND ND ND 83
BFA(G)-MB 0 48 103 ND ND ND 103
BFA(G)-MB 0 72 111 ND ND ND 111
BFA(G)-MB 0 96 111 ND ND ND 111
BFA(G)-MB 0 120 133 ND ND ND 133
BFA(G)-MB 200 0.5 36 15 3 < MRL 54
BFA(G)-MB 200 1 38 17 3 < MRL 58
BFA(G)-MB 200 3 44 19 4 < MRL 68
BFA(G)-MB 200 5 48 27 4 < MRL 79
BFA(G)-MB 200 7 49 28 5 < MRL 82
BFA(G)-MB 200 10 56 32 5 < MRL 94
BFA(G)-MB 200 15 58 32 6 < MRL 96
BFA(G)-MB 200 24 64 37 7 < MRL 108
BFA(G)-MB 200 48 66 40 8 < MRL 115
BFA(G)-MB 200 72 76 47 10 < MRL 133
BFA(G)-MB 200 96 82 51 11 < MRL 144
BFA(G)-MB 200 120 91 51 11 < MRL 153
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane),
and TBM (tribromomethane), TTHM (total trihalomethanes)
189
Table 9.2: Trihalomethanes (THMs) formation change during 5 days incubation from
synthetic pool water produced from BFA(G) (5mg/L TOC) only, without and with
bromide.
Synthetic pool
water
Br- Time TCM DCBM DBCM TBM TTHMs
µg/L hours µg/L µg/L µg/L µg/L µg/L
BFA(G) 0 0.5 30 ND ND ND 30
BFA(G) 0 1 29 ND ND ND 29
BFA(G) 0 3 38 ND ND ND 38
BFA(G) 0 5 39 ND ND ND 39
BFA(G) 0 7 41 ND ND ND 41
BFA(G) 0 10 41 ND ND ND 41
BFA(G) 0 15 43 ND ND ND 43
BFA(G) 0 24 45 ND ND ND 45
BFA(G) 0 48 49 ND ND ND 49
BFA(G) 0 72 52 ND ND ND 52
BFA(G) 0 96 55 ND ND ND 55
BFA(G) 0 120 57 ND ND ND 57
BFA(G) 200 0.5 30 10 1 < MRL 41
BFA(G) 200 1 30 12 1 < MRL 44
BFA(G) 200 3 31 20 2 < MRL 53
BFA(G) 200 5 32 22 3 < MRL 57
BFA(G) 200 7 35 25 3 < MRL 63
BFA(G) 200 10 37 26 4 < MRL 67
BFA(G) 200 15 37 28 4 < MRL 69
BFA(G) 200 24 38 28 5 < MRL 72
BFA(G) 200 48 41 32 6 < MRL 80
BFA(G) 200 72 44 35 8 < MRL 89
BFA(G) 200 96 45 36 8 < MRL 90
BFA(G) 200 120 47 40 10 < MRL 97
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane),
and TBM (tribromomethane), TTHM (total trihalomethanes)
190
Table 9.3: Trihalomethanes (THMs) formation change during 5 days incubation from
synthetic pool water produced from BFA(G) (1mg/L TOC), without and with bromide.
Synthetic pool
water
Br- Time TCM DCBM DBCM TBM TTHMs
µg/L hours µg/L µg/L µg/L µg/L µg/L
BFA(G) 0 0.5 18 ND ND ND 18
BFA(G) 0 1 18 ND ND ND 18
BFA(G) 0 3 21 ND ND ND 21
BFA(G) 0 5 21 ND ND ND 21
BFA(G) 0 7 22 ND ND ND 22
BFA(G) 0 10 24 ND ND ND 24
BFA(G) 0 15 25 ND ND ND 25
BFA(G) 0 24 25 ND ND ND 25
BFA(G) 0 48 28 ND ND ND 28
BFA(G) 0 72 30 ND ND ND 30
BFA(G) 0 96 33 ND ND ND 33
BFA(G) 0 120 35 ND ND ND 35
BFA(G) 200 0.5 18 4 1 < MRL 23
BFA(G) 200 1 19 6 1 < MRL 27
BFA(G) 200 3 20 9 2 < MRL 31
BFA(G) 200 5 20 10 2 < MRL 32
BFA(G) 200 7 21 10 2 < MRL 33
BFA(G) 200 10 21 11 2 < MRL 34
BFA(G) 200 15 22 11 2 < MRL 35
BFA(G) 200 24 24 12 3 < MRL 38
BFA(G) 200 48 27 12 3 < MRL 43
BFA(G) 200 72 30 13 4 < MRL 47
BFA(G) 200 96 35 15 5 < MRL 55
BFA(G) 200 120 37 16 5 < MRL 58
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane),
and TBM (tribromomethane), TTHM (total trihalomethanes)
Figure 9.1(a) shows the percent of the five-day THM yield as a function of time
during the kinetic experiments for three solutions in the absence and presence of bromide,
respectively. Two BFA solutions (1 and 5 mg TOC/L) showed similar formation patterns
indicating that Cl2/DOC ratio (100 vs. 20 mg Cl2/mg TOC) did not have an impact on the
191
formation rates of THMs. Furthermore, it has been shown that once all chlorine demand
was satisfied, additional chlorine did not increase the formation of THMs (Boccelli et al.,
2003). Since there is always a high Cl2/fresh BF DOC mass ratio in pool water, the
formation rates observed in this study is a representative estimate of THM formation in
swimming pools. This is especially true for swimming pools in the United States where
the dilution of pool water with the filling water is not regularly practiced and the water
age in the pools reach years. Therefore, chlorine demand of filling water is exhausted at
the very early period of operation after filling the pool. Afterwards, the THM formation is
primarily from the reactivity of BF components with chlorine.
Figure 9.1(a) also shows that in the absence of bromide, the presence of NOM in
water (i.e., BFA-MB) reduced the THM formation rates by about 20% during the first 24
hours as compared to the absence of NOM (BFA-5 mg). This behavior is due to the
higher reactivity of NOM compared to BFA with chlorine to form THM but which occurs
at a slower rate, as compared to BFA.
192
Figure 9.1: THM formation fraction during five days without bromide (a)
and with bromide (200 µg/L) (b). THMt (THM formed at time t), THM120
(THM formed at 120 hours)
0.0
0.2
0.4
0.6
0.8
1.0
1.2
0 24 48 72 96 120 144
[TH
Mt]
/[T
HM
120]
a No Br
BFA-MB BFA-5mg BFA-1mg
0.0
0.2
0.4
0.6
0.8
1.0
1.2
0 24 48 72 96 120 144
[TH
Mt]
/[T
HM
120]
Hours
b Br=200 µg/L
193
Comparison of THM formation potential of MB filling water NOM and BFA(G)
at the same TOC level (1 mg/L) in Chapter Seven showed that THM yield of MB water
NOM (81 g/mg TOC) was four times higher than the THM yield of BFA(G) (18 g/ mg
TOC). Consistent with these observations, five-day THM concentration of synthetic pool
water solution (i.e., 5mg/L TOC from BFA(G) and 1 mg/L from MB) during the kinetics
experiment was 133 g/L, whereas it was only 57 g/L for the 5 mg/L TOC BFA(G)
solution. These observations suggests that if swimming pool water is diluted using the
filling water from the distribution system, overall THM concentration in the pool will
increase until the chlorine demand of NOM is consumed. However, the rate of THM
formation in the pool during this period will be lower as compared to no dilution case,
where BF components control the formation rate.
Figure 9.1(b) also shows that in the presence of bromide, the difference in the
formation rates of synthetic pool water and BFA solutions diminished. The decrease is
due to higher formation rates of brominated THM species from NOM at high bromide
concentrations, as also has been observed in drinking water samples (Westerhoff et al.,
2004). As the results demonstrate, in the absence of bromide, TCM (chloroform) was the
only THM species present, and bromo/chloro THM species formed when bromide was
present (Tables 9.1, 9.2, and 9.3).
194
HAA Formation as Function of Time
The results of the HAA kinetics experiments are provided in Tables 9.4, 9.5, and
9.6. Only 15% to 30% of five-day HAA formation occurred during the first five hours in
the presence and absence of bromide for synthetic pool water and BFA(G) solutions. The
formation of HAA was lower as compared to the formation rates of THMs. HAA
formation was below the minimum reporting level or at 1 g/L in the absence of
bromide. Although the five-day HAA yields were higher than those of THMs since
BFA(G) is more reactive to the formation of HAA than THM, the slower rate of HAA
formation indicates that there is more opportunity to remove their precursors through
treatment processes during water turnover. In contrast to THMs, since HAAs are highly
soluble in water, they will remain in water as they are formed. These results further
support previous conclusions from the THM results that precursor (i.e., the release of
human body excretes) control is probably the best and the most feasible way to control
the formation of DBPs in swimming pools.
195
Table 9.4: Haloacetic acids (HAAs) formation during 5days chlorination from synthetic
pool water BFA(G)-MB produced from BFA(G) (5mg/L TOC) and Myrtle Beach water
(1mg/L).
Synthetic
pool water
Br-
µg/L
Time
hours
BAA
µg/L
DCAA
µg/L
BCAA
µg/L
TCAA
µg/L
DBAA
µg/L
BDCAA
µg/L
DBCAA
µg/L
THAAs
µg/L
BFA(G)-MB 0 0.5 ND <MRL <MRL <MRL ND 1 ND 1
BFA(G)-MB 0 1 ND <MRL <MRL <MRL ND 1 ND 1
BFA(G)-MB 0 3 ND 13 <MRL <MRL ND 2 ND 15
BFA(G)-MB 0 5 ND 41 1 <MRL ND 4 ND 46
BFA(G)-MB 0 7 ND 41 2 60 ND 4 ND 107
BFA(G)-MB 0 10 ND 43 1 69 ND 4 ND 117
BFA(G)-MB 0 15 ND 61 1 82 ND 3 ND 148
BFA(G)-MB 0 24 ND 73 1 85 ND 4 ND 162
BFA(G)-MB 0 48 ND 95 1 92 ND 4 ND 192
BFA(G)-MB 0 72 ND 101 1 98 ND 4 ND 204
BFA(G)-MB 0 96 ND 103 1 99 ND 4 ND 207
BFA(G)-MB 0 120 ND 109 1 113 ND 4 ND 228
BFA(G)-MB 200 0.5 <MRL <MRL <MRL <MRL <MRL 3 4 7
BFA(G)-MB 200 1 <MRL <MRL 1 <MRL <MRL 4 4 8
BFA(G)-MB 200 3 <MRL 5 1 <MRL <MRL 11 7 24
BFA(G)-MB 200 5 <MRL 27 7 <MRL 1 21 6 62
BFA(G)-MB 200 7 <MRL 29 7 51 1 25 8 121
BFA(G)-MB 200 10 <MRL 42 11 54 2 28 10 147
BFA(G)-MB 200 15 <MRL 54 15 55 2 31 11 168
BFA(G)-MB 200 24 2 58 15 56 2 32 12 176
BFA(G)-MB 200 48 2 67 17 56 2 32 11 189
BFA(G)-MB 200 72 3 86 21 58 2 35 10 214
BFA(G)-MB 200 96 3 84 21 59 3 35 11 214
BFA(G)-MB 200 120 3 88 23 66 3 42 13 237
BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA
(trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA (dibromoacetic acid), THAA (total
HAA)
196
Table 9.5: HAAs formation during 5days chlorination from synthetic pool water
produced from BFA(G) (5mg/L TOC).
Synthetic
pool
water
Br-
µg/L
Time
hours
BAA
µg/L
DCAA
µg/L
BCAA
µg/L
TCAA
µg/L
DBAA
µg/L
BDCAA
µg/L
DBCAA
µg/L
THAAs
µg/L
BFA(G) 0 0.5 ND <MRL ND <MRL ND ND ND <MRL
BFA(G) 0 1 ND <MRL ND <MRL ND ND ND <MRL
BFA(G) 0 3 ND 6 ND <MRL ND ND ND 6
BFA(G) 0 5 ND 22 ND <MRL ND ND ND 22
BFA(G) 0 7 ND 23 ND <MRL ND ND ND 23
BFA(G) 0 10 ND 38 ND 8 ND ND ND 45
BFA(G) 0 15 ND 46 ND 56 ND ND ND 102
BFA(G) 0 24 ND 53 ND 62 ND ND ND 115
BFA(G) 0 48 ND 61 ND 63 ND ND ND 124
BFA(G) 0 72 ND 71 ND 68 ND ND ND 139
BFA(G) 0 96 ND 77 ND 69 ND ND ND 147
BFA(G) 0 120 ND 86 ND 71 ND ND ND 157
BFA(G) 200 0.5 <MRL <MRL <MRL <MRL <MRL 1 2 3
BFA(G) 200 1 <MRL <MRL <MRL <MRL <MRL 3 3 7
BFA(G) 200 3 <MRL 5 2 <MRL <MRL 8 6 21
BFA(G) 200 5 <MRL 22 5 <MRL 1 17 6 52
BFA(G) 200 7 <MRL 28 7 39 1 21 7 104
BFA(G) 200 10 <MRL 32 10 39 1 22 10 116
BFA(G) 200 15 1 35 11 40 2 24 10 121
BFA(G) 200 24 1 43 13 40 2 25 10 135
BFA(G) 200 48 2 51 15 41 2 28 11 150
BFA(G) 200 72 3 59 19 44 3 27 11 165
BFA(G) 200 96 3 64 19 44 3 26 10 169
BFA(G) 200 120 3 66 21 45 3 24 9 170
BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA
(trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA (dibromoacetic acid), THAA (total
HAA
197
Table 9.6: Haloacetic acids (HAAs) formation during 5days chlorination from synthetic
pool water produced from BFA(G) (1mg/L TOC).
Synthetic
pool
water
Br-
µg/L
Time
hours
BAA
µg/L
DCAA
µg/L
BCAA
µg/L
TCAA
µg/L
DBAA
µg/L
BDCAA
µg/L
DBCAA
µg/L
THAAs
µg/L
BFA(G) 0 0.5 ND ND ND <MRL ND ND ND <MRL
BFA(G) 0 1 ND ND ND <MRL ND ND ND <MRL
BFA(G) 0 3 ND ND ND 4 ND ND ND 4
BFA(G) 0 5 ND ND ND 5 ND ND ND 5
BFA(G) 0 7 ND ND ND 5 ND ND ND 5
BFA(G) 0 10 ND ND ND 5 ND ND ND 5
BFA(G) 0 15 ND ND ND 5 ND ND ND 5
BFA(G) 0 24 ND ND ND 7 ND ND ND 7
BFA(G) 0 48 ND ND ND 9 ND ND ND 9
BFA(G) 0 72 ND ND ND 10 ND ND ND 10
BFA(G) 0 96 ND ND ND 15 ND ND ND 15
BFA(G) 0 120 ND ND ND 16 ND ND ND 16
BFA(G) 200 0.5 <MRL ND <MRL <MRL ND ND ND <MRL
BFA(G) 200 1 <MRL ND <MRL <MRL ND ND 3 3
BFA(G) 200 3 <MRL ND <MRL 2 ND 1 3 6
BFA(G) 200 5 <MRL ND <MRL 2 ND 1 3 7
BFA(G) 200 7 <MRL ND <MRL 2 ND 1 3 7
BFA(G) 200 10 <MRL ND <MRL 2 ND 2 3 7
BFA(G) 200 15 <MRL ND <MRL 2 ND 2 3 7
BFA(G) 200 24 2 ND 1 2 ND 2 3 10
BFA(G) 200 48 2 ND 1 4 ND 4 4 15
BFA(G) 200 72 2 ND 1 4 ND 4 4 15
BFA(G) 200 96 2 ND 1 5 ND 4 4 17
BFA(G) 200 120 2 ND 1 5 ND 4 4 17
BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA
(trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA (dibromoacetic acid), THAA (total
HAA
Figure 9.2(a) shows the percent of the five-day HAA yield as a function of time
during the kinetic experiments for three solutions in the absence and presence of bromide,
respectively. The presence of NOM in water (i.e., BFA-MB) did not have an impact on
the formation rate of HAA as compared to the absence of NOM (BFA-5 mg). HAA
198
formation potentials of MB filling water NOM (18 g/mg) was lower than that of
BFA(G) (35 g/mg) at the same TOC level (1 mg/L) as reported in Chapter Seven. This
is why probably filling water NOM did not have an impact on the formation rate of HAA
given the fact that the contribution of NOM to the total TOC was only 20%.
Figure 9.2: HAA formation fraction during five days without bromide (a) and
with bromide (200 µg/L) (b). HAAt (HAA formed at time t), HAA120 (HAA
formed at 120 hours)
0.0
0.2
0.4
0.6
0.8
1.0
1.2
0 24 48 72 96 120 144
[HA
At]
/[H
AA
12
0]
a No Br
BFA-MB BFA-5mg BFA-1mg
0.0
0.2
0.4
0.6
0.8
1.0
1.2
0 24 48 72 96 120 144
[HA
At]
/[H
AA
12
0]
Hours
b Br=200 µg/L
199
Figure 9.2(b) also shows that in the presence of bromide, the difference in the
formation rates of synthetic pool water and BFA solutions diminished. This is due to
higher formation rates of brominated HAA species from NOM at high bromide
concentrations. The fast rate of bromide substitution to organic material to form
brominated DBPs during chlorination is well reported in the literature (Adin et al., 1991;
Cowman and Singer, 1996; Richardson et al., 1999). In the absence of bromide, TCAA
and DCAA were the major HAA species present, and bromo/chloro HAA species formed
when bromide was present (Tables 9.4, 9.5, and 9.6).
Some difference was observed between the trends of the two BFA solutions (1
and 5 mg TOC/L) indicating that the increase in Cl2/DOC ratio (from 20 to 100 mg
Cl2/mg TOC) reduced the formation rate of HAA. From Figure 9.3 and 9.4 it can be
observed that the increase in the Cl2/DOC ratio decreased both DHAA and THAA
formation although the decrease in DHAA formation as a function of time is more. The
difference in the decrease DHAA and THAA is due to the different pathways of their
formation. THAA can be formed directly or through halogenation of DHAA to THAA
(Hua and Reckhow, 2008). The Cl2/DOC ratio effect on decreasing DHAA formation
was noticed also on the experiments of formation potential of HAA as was shown in
Chapter Seven. In the presence of bromide (Figures 9.3 b and 9.4 b) the rate decrease was
observed but to a lesser degree due to the faster reaction of bromine than chlorine with
organic matter (Weserhoff et al., 2004).
200
Figure 9.3: DHAA and THAA formation fraction at 20 Cl2/mg TOC in the
absence of bromide (a) and at 200 µg/L bromide (b). Ct (concentration measured
at time t), C120 (concentration measured at 120 hours)
0.0
0.2
0.4
0.6
0.8
1.0
1.2
0 24 48 72 96 120 144
Ct/C
12
0
a BFA (5 mg/L)
DHAA
THAA
0.0
0.2
0.4
0.6
0.8
1.0
1.2
0 24 48 72 96 120 144
Ct/C
12
0
Hours
b BFA (5 mg/L) + (Br 200 µg/L)
DHAA
THAA
201
Figure 9.4: DHAA and THAA formation fraction at 100 Cl2/mg TOC in the
absence of bromide (a) and at 200 µg/L bromide (b). Ct (concentration measured
at time t), C120 (concentration measured at 120 hours)
0
0.2
0.4
0.6
0.8
1
1.2
0 24 48 72 96 120 144
Ct/C
12
0
a BFA (1 mg/L)
DHAA
THAA
0
0.2
0.4
0.6
0.8
1
1.2
0 24 48 72 96 120 144
Ct/C
12
0
Hours
b BFA (1 mg/ L) + (Br 200 µg/L)
DHAA
THAA
202
The formation rate of THMs was higher than that of HAAs in swimming pools.
Figure 9.5 compares the rate of THM4 and HAA9 formation in synthetic swimming pool
water. THMs were formed almost instantaneously when chlorine reacted with BFs,
whereas HAA formation occurred at a slower rate.
Figure 9.5: THM 4 and HAA9 formation fraction during 5-day incubation (a) and
during the first 24 hours (b) from BFA(G) at TOC 5 mg/L, pH7, and T= 26°C.
0
40
80
120
160
200
0 24 48 72 96 120 144
µg/L
Hours
a HAA9 THM4
0
50
100
150
0.5 1 3 5 7 10 15 24
µg/L
Hours
b
203
Conclusions
Greater than 50% of five-day THM formation occurred during the first five hours
in the presence and absence of bromide for synthetic pool water and BFA(G)
solutions. This indicates that a significant portion of THMs will be formed in the
pool before the water undergoes any possible treatment in addition to sand
filtration.
The Cl2/DOC ratio did not make an impact on the formation rates of THMs
Dilution using the filling water from the distribution system will increase the
overall THM concentration in the pool until the chlorine demand of NOM is met.
However, the rate of THM formation in the pool during this period will be lower
as compared to the no dilution case, where BF components control the formation
rate.
Only 15% to 30% of five-day HAA formation occurred during the first five hours
in the presence and absence of bromide for synthetic pool water and BFA(G)
solutions. HAA formation was below the minimum reporting level or at 1 µg/L in
the absence of bromide. Although the five-day HAA yields were higher than
those of THMs since BFA(G) are more reactive to the formation of HAA than
THM, the slower rate of HAA formation indicates that there is more opportunity
to remove their precursors through treatment processes during water turnover.
The formation of THMs was faster than that of HAAs in swimming pools. THMs
were formed almost instantaneously when chlorine reacted with BFs, whereas
HAA formation occurred at a slower rate.
204
Higher Cl2/DOC ratio suppressed DHAA formation and decreased THAA
formation also. In the presence of bromide this ratio effect is observed to a lesser
degree.
205
CHAPTER TEN
CONCLUSIONS AND RECOMMENDATIONS
Conclusions:
The important conclusions for each objective of this study are summarized below.
Objective (1): Determine the occurrence of THMs, HAAs, HNMs, HANs, and NDMA
in indoor swimming pool water in South Carolina, Georgia, and North Carolina.
DBPs levels in pools are at higher levels than those found in drinking water.
THMs measured in this study were between 26 and 213 µg/L, HANs were in the
range of 5 to 53 µg/L, HNMs fall between 1.4 and 13.3 µg/L, HAAs ranged
between 172-9005 µg/L, and NDMA was between 2 and 83 ng/L.
Brominated DBPs of all classes were higher in pools that generate chlorine
electrochemically in situ using sodium chloride.
There is great variability in the levels of measured DBPs within pools and also
among different pools.
During the sampling period (9 months), DBPs concentration in the same pool was
not the same always, but changed from time to time depending on the time of the
year and on specific pool events and activities on the time of sampling.
Objective (2): Conduct a multipathway risk assessment on disinfection by-products of
swimming pool water
206
Indoor swimming pools are semi-closed systems that expose both swimmers and
other workers attending the pool to the hazardous DBPs especially the volatile
ones through the respiratory system.
Lifetime cancer risk and hazard indices estimated from DBPs in swimming pools
were considerably higher than those from DBPs in drinking water. Lifetime
cancer risk exceeded the negligible 10-6
by a factor of 10-10000. Also hazard
indices were mostly greater than 1 and reached 20 and 26. More risk can be
contributed to swimming in chlorinated water than drinking chlorinated water.
Most of the cancer risk and non-cancer risk estimated was due to chloroform
especially through inhalation route.
Objective (3): Determine the role and contribution of the two main precursors (i.e.,
NOM from the distribution system vs. body fluids from swimmers) to the formation of
trihalomethanes (THMs), haloacetic acid (HAAs), and halonitromethanes (HNMs) in
swimming pools
FP tests demonstrated that BFAs were more reactive toward chlorine than filling
water (i.e., treated drinking water) NOMs.
BFAs formed more HAAs than THMs, while filling water NOMs produced more
THMs than HAAs. On the other hand, both NOMs and BFAs produced similar
amounts of HNMs (chloropicrin), which was much lower compared to THM and
HAA formation.
207
Analysis of individual BFA components demonstrated that citric acid had
significantly higher reactivity toward THM and HAA formation than other
components, which had relatively similar THM and HAA yields.
Filling waters collected from five different treatment plants exhibited comparable
THM formation relatively independent of time and location, whereas HAA yields
exhibited more spatial and time dependent variability.
Temperature (lowest 26°C and highest 40°C) affected THMs, HAAs, and HNMs
formation differently. At 40°C temperature more THMs and HAAs were formed.
THMs formation showed more temperature dependence than did HAAs
formation. The contact time increased both THMs and HAAs. More HAAs
increase was noticed by reaction time increase whereas less THMs increase was
noticed for the same contact time. Chloropicrin tended to decrease by increasing
contact time, although very slightly.
Objective (4): Investigate the impacts of swimming pool operational parameters:
chlorine residual (FAC), pH, bather load (TOC), water bromide content, and
temperature on the formation and speciation of THMs, HAAs, and HNMs
DBPs formation is affected by the chlorine residual maintained in the pool water.
The effect of FAC was more pronounced for HAAs compared to THMs.
Lower pH caused a decrease in the three DBP classes (THMs, HAAs, and
HNMs).
208
TOC increase caused an increase in the three investigated DBP classes although
the yield of DBPs decreased with TOC increase.
Bromide increased the overall THMs and HNMs formation and enhanced the
formation of brominated species of the three DBP classes.
Objective (5): Study the formation kinetics of THMs and, HAAs from the body fluid
precursors in swimming pools, especially at short reaction times.
DBPs formation rate under swimming pool operation conditions is fast. Within
the first three to six hours more than 50% of the total five-day THMs was formed.
A lower rate was noticed for HAAs (only 30% formed within the first three-six
hours)
Recommendations for Pool Operators and Swimmers
Swimming pools operational parameters, regulations and guidelines need to be revised
and issued considering the formation and control of DBPs in swimming pool water and
air. Regulations or guidelines for DBPs in pool water and air are important to maintain
and improve the health conditions and impacts on swimmers and workers in indoor
swimming pools. Recommendations depending on this research results and conclusions
are:
1. DBPs Precursors control:
209
Improving swimmers personal hygienic conditions awareness is an
important factor that may contribute to decrease the DBPs formation in
indoor swimming pools.
Enforcing swimmers showering immediately before swimming can
minimize the organic input from swimmers bodies.
Bathers load for each indoor swimming pool should carefully enforce
during the day and per each working day too.
2. Operational parameters control
The pool water should be diluted according to the daily number of
swimmers. Replacement of well defined water volume by fresh water will
decrease the DBPs and their precursors accumulation in indoor pool
waters.
Aeration and good ventilation of the indoor pools atmosphere should be
considered to decrease the air content of volatile DBPs.
Lowering swimming pool water pH to decrease the THMs, HAAs, and
HNMs. Also the chlorine disinfection efficiency will increase.
Lowering the chlorine residual to 1 mg/L will decrease DBPs.
Avoiding electrochemical generation from sodium chloride that has
bromide impurities.
Recommendations for future research
210
Research on alternative treatment processes or improvement during swimming
pool water recycling and treatment is required. Filtration media and improvement
of filtration via coagulation is an important issue to improve for increasing DBP
precursor removal.
Swimming pool water dilution and the dilution factor is also necessary to
investigate and verify its benefit in decreasing the accumulation of formed DBPs
and their precursors.
Ventilation strategies and ratios required to minimize pool atmosphere content of
DBPs is also another field of research that can improve pool air quality and
decrease the exposure to DBPs.
A risk assessment comparison of biological hazard vs. chemical hazard in
swimming pools is important and crucial to optimize chlorination and other
operational parameters that can give the least chemical hazard while keeping the
biological risk to a minimal level. Outbreaks from swimming pools and their
adverse health impacts should be studied more to evaluate them and allow for a
comparison between biological and chemical hazards in swimming pools.
Combination of more than disinfection methods in swimming pool to reduce
chlorine demand could be tested.
211
APPENDICES
212
Appendix A
Swimming Activity Distribution
Table A.1: swimming activity distribution among different gender and age*
Sex Age (years)
Tota
l **
Sw
imm
ing
Male
Fem
ale
7-1
1
12
-17
18
-24
25
-34
35
-44
45
-54
55
-64
˃65
Particip
an
ts
25340000
31123000
9208000
936000
5841000
8211000
9090000
7348000
3917000
3490000
56,4
63000
* Table adopted from National Sporting Goods Association.
http://www.nsga.org/public/pages/index.cfm?pageid=864 [accessed June 26, 2009]
**Participants engaged in activity six times or more in the year.
213
Appendix B
Guidelines and Regulations of DBPs
Table B.1: US EPA and EU MCL and WHO Guidelines of regulated DBPs (US EPA,
2006; EU Directive 98/83/EC; WHO, 2003)
Disinfection By-Product US EPA MCL
µg/L
EU MCL
µg/L
WHO
guidelines
µg/L
THM4 80 100
Chloroform 300
Bromodichloromethane 60
Dibromochloromethane 100
Bromoform 100
HAA5 60
Monochloroacetic acid 70
Dichloroacetic acid 0 50
Trichloroacetic acid 20 100
MCL (maximum contaminant level), THM4 (sum of four THM species), HAA5
(sum of five HAA species)
214
Appendix C
DBPs Species in Three Monitored Indoor Pools
Table C.2: THM species determined in S16 swimming pool during the study
Date TCM BDCM DBCM TBM TTHM
µg/L µg/L µg/L µg/L µg/L 22/5/2009 59 1 ND ND 60
22/5/2009 56 1 ND ND 57
22/5/2009 57 1 ND ND 57
24/5/2009 53 1 ND ND 54
24/5/2009 51 1 ND ND 52
30/5/2009 52 1 ND ND 53
2/6/2009 55 1 ND ND 56
6/6/2009 47 1 ND ND 48
9/6/2009 39 1 ND ND 40
18/10/2009 78 2 ND ND 81
25/10/2009 37 1 ND ND 38
22/12/2009
10/1/2010 28 0 ND ND 29
17/1/2010 52 2 ND ND 54
17/2/2010 61 2 ND ND 63
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and TBM
(tribromomethane), TTHM (total trihalomethanes)
Table C.3: THM species determined in S17L swimming pool during the study
Date TCM BDCM DBCM TBM TTHM
µg/L µg/L µg/L µg/L µg/L 22/5/2009 71 17 4 ND 92
22/5/2009 68 17 4 ND 89
22/5/2009 67 18 4 ND 88
24/5/2009 63 19 4 ND 86
24/5/2009 66 19 5 ND 91
30/5/2009 65 15 3 ND 83
2/6/2009 63 11 2 ND 77
6/6/2009 67 8 1 ND 77
9/6/2009 70 11 2 ND 84
18/10/2009 75 3 0 ND 79
25/10/2009 76 3 0 ND 79
22/12/2009 50 12 2 ND 64
10/01/2010 24 21 21 6 72
17/01/2010 45 29 14 3 91
17/02/2010 82 11 2 ND 95
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and TBM
(tribromomethane), TTHM (total trihalomethanes)
215
Table C.4: THM species determined in S17T swimming pool during the study
Date TCM BDCM DBCM TBM TTHM
µg/L µg/L µg/L µg/L µg/L
22/5/2009 157 6 <MRL <MRL 163
22/5/2009 154 6 <MRL <MRL 160
22/5/2009 156 6 <MRL <MRL 162
24/5/2009 165 6 1 <MRL 171
24/5/2009 155 6 1 <MRL 161
30/5/2009 166 25 7 1 199
2/6/2009 166 21 4 1 192
6/6/2009 129 7 1 <MRL 137
9/6/2009 144 13 3 <MRL 160
18/10/2009 236 19 3 <MRL 259
25/10/2009 239 9 1 <MRL 249
22/12/2009 172 4 <MRL <MRL 176
10/1/2010 157 20 5 <MRL 182
17/01/2010 179 8 1 <MRL 188
17/02/2010 207 6 <MRL <MRL 213
TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), and TBM
(tribromomethane), TTHM (total trihalomethanes)
Table C.5: HAA species determined in S16 swimming pool during the study
Date BAA DCAA BCAA TCAA DBAA BDCAA DBCAA THAA
µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L 22/5/2009 ND 603 6 1420 <MRL 10 ND 2039
22/5/2009 ND 603 7 1412 <MRL 9 ND 2031
22/5/2009 ND 614 7 1409 <MRL 9 ND 2039
24/5/2009 ND 548 7 1114 1 12 ND 1681
24/5/2009 ND 506 5 1100 <MRL 36 ND 1648
30/5/2009 ND 595 6 1109 1 14 ND 1725
2/6/2009 ND 591 8 1078 1 13 ND 1691
6/6/2009 ND 607 10 1068 3 15 5 1708
9/6/2009 ND 613 9 1031 2 15 3 1674
18/10/2009 ND 280 3 1502 <MRL 19 ND 1804
25/10/2009 ND 291 3 1359 <MRL 20 ND 1673
22/12/2009
10/1/2010 ND 342 8 1090 <MRL 37 ND 1479
17/1/2010 1 458 4 528 2 12 ND 1005
17/2/2010 ND 549 5 568 <MRL 20 1 1143
BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA
(trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA (dibromoacetic acid), TBAA
(tribromoacetic acid), THAA (total HAA)
216
Table C.6: HAA species determined in S17L swimming pool during the study
Date BAA DCAA BCAA TCAA DBAA BDCAA DBCAA THAA
µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L 22/5/2009 <MRL NM NM NM NM NM NM NM
22/5/2009 <MRL NM NM NM NM NM NM NM
22/5/2009 <MRL NM NM NM NM NM NM NM
24/5/2009 <MRL 503 62 860 13 79 15 1531
24/5/2009 <MRL 460 67 813 11 73 13 1437
30/5/2009 <MRL 387 38 863 8 82 15 1392
2/6/2009 <MRL 392 38 853 7 79 10 1377
6/6/2009 <MRL 437 50 860 7 84 15 1434
9/6/2009 <MRL 459 52 855 7 82 14 1470
18/10/2009 <MRL 525 20 576 1 48 5 1174
25/10/2009 <MRL 249 18 564 1 37 0 1169
22/12/2009 <MRL 417 51 420 6 46 14 955
10/1/2010 <MRL 203 75 431 16 47 20 793
17/1/2010 3 271 52 213 11 86 31 667
17/2/2010 5 504 106 288 25 110 32 1070
BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA
(trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA (dibromoacetic acid), TBAA
(tribromoacetic acid), THAA (total HAA)
Table C.7: HAA species determined in S17T swimming pool during the study
Date BAA DCAA BCAA TCAA DBAA BDCAA DBCAA THAA
µg/L µg/L µg/L µg/L µg/L µg/L µg/L µg/L 22/5/2009 <MRL NM NM NM NM NM NM NM
22/5/2009 <MRL NM NM NM NM NM NM NM
22/5/2009 <MRL NM NM NM NM NM NM NM
24/5/2009 <MRL 503 62 860 13 79 15 1531
24/5/2009 <MRL 460 67 813 11 73 13 1437
30/5/2009 <MRL 387 38 863 8 82 15 1392
2/6/2009 <MRL 392 38 853 7 79 10 1377
6/6/2009 <MRL 437 50 860 7 84 15 1434
9/6/2009 <MRL 459 52 855 7 82 14 1470
18/10/2009 <MRL 525 20 576 1 48 5 1174
25/10/2009 <MRL 249 18 564 1 37 0 1169
22/12/2009 <MRL 7547 326 3700 39 75 9 11659
10/1/2010 <MRL 3322 343 3534 32 136 26 7392
17/01/2010 3 4215 169 1747 16 130 11 6291
17/02/2010 4 6787 176 1925 16 93 4 9005
BAA (bromoacetic acid), DCAA (dichloroacetic acid), BCAA (bromochloroacetic acid), TCAA
(trichloroacetic acid), DBAA (dibromoacetic acid), DBCAA (dibromoacetic acid), TBAA
(tribromoacetic acid), THAA (total HAA)
217
Table C.8: HNM species determined in S16 swimming pool during the study
Date TCNM BNM BCNM DBNM THNM
µg/L µg/L µg/L µg/L µg/L 22/5/2009 0.9 <MRL 4.1 <MRL 5.4
22/5/2009 0.8 <MRL 4.6 <MRL 5.8
22/5/2009 0.9 <MRL 4.5 <MRL 5.9
24/5/2009 0.2 <MRL 3.2 <MRL 3.4
24/5/2009 0.2 <MRL 3.4 <MRL 3.5
30/5/2009 0.2 <MRL 3.0 <MRL 3.2
2/6/2009 0.2 <MRL 3.0 <MRL 3.2
6/6/2009 0.5 <MRL 2.4 <MRL 3.1
9/6/2009 0.5 <MRL 2.3 <MRL 3.0
18/10/2009 0.4 <MRL 4.0 <MRL 4.4
25/10/2009 0.2 <MRL 3.1 <MRL 3.4
22/12/2009
10/1/2010 0.8 <MRL 4.1 <MRL 5.0
17/1/2010 0.9 <MRL 3.4 <MRL 4.2
17/02/2010 0.8 <MRL 2.6 <MRL 3.4
TCNM (trichloronitromethane), BNM (bromonitromethane), BCNM
(bromochloronitromethane), THNM (total halonitromethane)
Table C.9: HNM species determined in S17L swimming pool during the study
Date TCNM BNM BCNM DBNM THNM
µg/L µg/L µg/L µg/L µg/L 22/5/2009 <MRL 4.4 4.8 ND 9.7
22/5/2009 <MRL 4.5 4.7 ND 9.7
22/5/2009 <MRL 4.6 4.9 ND 10.1
24/5/2009 <MRL 4.1 4.5 ND 8.7
24/5/2009 <MRL 4.1 4.2 ND 8.5
30/5/2009 <MRL 2.9 4.7 ND 7.8
2/6/2009 <MRL 1.7 4.6 ND 6.6
6/6/2009 <MRL 1.8 5.2 ND 7.5
9/6/2009 <MRL 3.1 5.4 ND 9.0
18/10/2009 <MRL 0.2 5.3 ND 5.8
25/10/2009 <MRL 0.3 5.7 ND 6.4
22/12/2009 <MRL 1.3 3.1 ND 4.7
10/1/2010 <MRL 4.8 2.6 ND 8.1
17/1/2010 <MRL 4.2 4.3 ND 9.2
17/02/2010 0.7 1.6 5.8 ND 8.1
TCNM (trichloronitromethane), BNM (bromonitromethane), BCNM
(bromochloronitromethane), THNM (total halonitromethane)
218
Table C.10: HNM species determined in S17T swimming pool during the study
Date TCNM BNM BCNM DBNM THNM
µg/L µg/L µg/L µg/L µg/L
22/5/2009 1.3 2.4 10.2 ND 13.8
22/5/2009 1.2 2.4 9.0 ND 12.6
22/5/2009 1.2 2.5 9.5 ND 13.2
24/5/2009 0.8 2.3 7.8 ND 10.9
24/5/2009 0.8 2.3 8.2 ND 11.3
30/5/2009 0.8 5.3 8.9 ND 15.0
2/06/2009 0.7 6.5 6.5 ND 13.7
6/06/2009 1.0 3.1 8.2 ND 12.2
9/06/2009 1.0 5.7 7.0 ND 13.7
18/10/2009 0.8 2.2 12 ND 15
25/10/2009 1.3 0.9 20.6 ND 22.9
22/12/2009 1 0.6 7 ND 8.6
10/01/2010 1.3 6 10.9 ND 18.1
17/01/2010 1.8 1.6 13.3 ND 16.7
17/02/2010 1.4 1 6.8 ND 9.2
TCNM (trichloronitromethane), BNM (bromonitromethane), BCNM
(bromochloronitromethane), THNM (total halonitromethane)
219
Appendix D
Exposure Factors and Calculated Doses
Table D.1: Recommended ingestion water volumes during swimming as appeared in:
EXPOSURE FACTORS HANDBOOK: 2009 UPDATE*
Age group Mean
95
th Percentile
mL/eventa mL/hour mL/event mL/hour
Children 37 49
154 205
Adults 16 21
53 71
All NR NR
NR 90
*Source: Dufour et al., 2006 a Event mean time 45 minutes
NR: Not Reported
220
Table D.2: Swimming activity duration as appeared in: EXPOSURE FACTORS
HANDBOOK: 2009 UPDATE*
Age group Mean 95
th Percentile
Minutes Minutes
Children 139 181
Adults 145 181
221
Table D.3: Adult competitive and noncompetitive male swimmers exposure dose calculations in S16 pool
DBP Cw Cair Exposure
Route
Non-competitive male Competitive male
PDR PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
µg/L µg/m
3
mg/event mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM 53 7950
Oral 1.33E-03 1.70E-05 5.58E-06 2.39E-06 6.63E-04 8.48E-06 5.53E-06 1.74E-06
Dermal 9.15E-03 1.17E-04 3.85E-05 1.65E-05 9.15E-03 1.17E-04 7.64E-05 2.40E-05
Inhalation 7.95 0.1 3.35E-02 1.43E-02 25.44 0.33 0.21 6.68E-02
Total 7.96 0.1 3.35E-02 1.44E-02 25.45 0.33 0.21 6.68E-02
BDCM 1 66.7
Oral 2.50E-05 3.20E-07 1.05E-07 4.51E-08 1.25E-05 1.60E-07 1.04E-07 3.28E-08
Dermal 1.13E-04 1.44E-06 4.74E-07 2.03E-07 1.13E-04 1.44E-06 9.39E-07 2.95E-07
Inhalation 6.67E-02 8.54E-04 2.81E-04 1.20E-04 0.21 2.73E-03 1.78E-03 5.60E-04
Total 6.68E-02 8.56E-04 2.81E-04 1.21E-04 0.21 2.73E-03 1.78E-03 5.60E-04
DCAA 532 0.18
Oral 1.33E-02 1.70E-04 5.60E-05 2.40E-05 6.65E-03 8.51E-05 5.55E-05 1.74E-05
Dermal 1.25E-02 1.60E-04 5.26E-05 2.25E-05 1.25E-02 1.60E-04 1.04E-04 3.28E-05
Inhalation 1.82E-04 2.34E-06 7.68E-07 3.29E-07 5.84E-04 7.48E-06 4.88E-06 1.53E-06
Total 2.60E-02 3.33E-04 1.09E-04 4.69E-05 1.97E-02 2.53E-04 1.65E-04 5.18E-05
TCAA 1237 0.68
Oral 3.09E-02 3.96E-04 1.30E-04 5.58E-05 1.55E-02 1.98E-04 1.29E-04 4.06E-05
Dermal 3.48E-02 4.46E-04 1.46E-04 6.28E-05 3.48E-02 4.46E-04 2.91E-04 9.13E-05
Inhalation 6.83E-04 8.74E-06 2.87E-06 1.23E-06 2.19E-03 2.80E-05 1.82E-05 5.73E-06
Total 6.64E-02 8.50E-04 2.80E-04 1.20E-04 5.24E-02 6.72E-04 4.38E-04 1.38E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
222
Table D.4: Adult competitive and noncompetitive female swimmers exposure dose calculations in S16 pool
DBP Cw Cair
Non-competitive female Competitive female
Exposure
route
PDR PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
µg/L µg/m3 mg/event mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM
53 7950
Oral 1.33E-03 2.03E-05 6.66E-06 2.85E-06 6.63E-04 1.01E-05 6.61E-06 2.08E-06
Dermal 7.97E-03 1.22E-04 4.01E-05 1.72E-05 7.97E-03 1.22E-04 7.95E-05 2.50E-05
Inhalation 7.95E+00 1.20E-01 4.00E-02 1.71E-02 2.54E+01 3.90E-01 2.50E-01 7.97E-02
Total 7.96E+00 1.20E-01 4.00E-02 1.71E-02 2.55E+01 3.90E-01 2.50E-01 7.97E-02
BDCM
1 66.7
Oral 2.50E-05 3.82E-07 1.26E-07 5.39E-08 1.25E-05 1.91E-07 1.25E-07 3.92E-08
Dermal 9.80E-05 1.50E-06 4.93E-07 2.11E-07 9.80E-05 1.50E-06 9.77E-07 3.07E-07
Inhalation 6.67E-02 1.02E-03 3.35E-04 1.44E-04 2.10E-01 3.26E-03 2.13E-03 6.69E-04
Total 6.68E-02 1.02E-03 3.36E-04 1.44E-04 2.10E-01 3.26E-03 2.13E-03 6.69E-04
DCAA
532 0.18
Oral 1.33E-02 2.03E-04 6.69E-05 2.87E-05 6.65E-03 1.02E-04 6.63E-05 2.08E-05
Dermal 1.09E-02 1.66E-04 5.47E-05 2.34E-05 1.09E-02 1.66E-04 1.08E-04 3.41E-05
Inhalation 1.82E-04 2.79E-06 9.17E-07 3.93E-07 5.84E-04 8.93E-06 5.82E-06 1.83E-06
Total 2.44E-02 3.72E-04 1.22E-04 5.25E-05 1.81E-02 2.77E-04 1.81E-04 5.68E-05
TCAA
1237 0.68
Oral 3.09E-02 4.73E-04 1.55E-04 6.66E-05 1.55E-02 2.36E-04 1.54E-04 4.85E-05
Dermal 3.03E-02 4.63E-04 1.52E-04 6.53E-05 3.03E-02 4.63E-04 3.02E-04 9.50E-05
Inhalation 6.83E-04 1.04E-05 3.43E-06 1.47E-06 2.19E-03 3.34E-05 2.18E-05 6.85E-06
Total 6.19E-02 9.47E-04 3.11E-04 1.33E-04 4.80E-02 7.33E-04 4.78E-04 1.50E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
223
Table D.5: Child (11-14 years) competitive and noncompetitive swimmers exposure dose calculations in S16 pool
DBP Cw Cair Child (11-14 years) non-competitive Child (11-14 years) competitive
Exposure PDR PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
µg/L µg/m
3 route mg/event mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM 53 7950
Oral 2.65E-03 5.50E-05 1.81E-05 1.03E-06 1.33E-03 2.75E-05 1.42E-05 8.14E-07
Dermal 6.70E-03 1.39E-04 4.57E-05 2.61E-06 6.70E-03 1.39E-04 7.20E-05 4.11E-06
Inhalation 7.95E+00 1.70E-01 5.43E-02 3.10E-03 1.51E+01 3.10E-01 1.60E-01 9.28E-03
Total 7.96E+00 1.70E-01 5.43E-02 3.10E-03 1.51E+01 3.10E-01 1.60E-01 9.28E-03
BDCM
1
66.7
Oral 5.00E-05 1.04E-06 3.41E-07 1.95E-08 2.50E-05 5.19E-07 2.69E-07 1.54E-08
Dermal 8.24E-05 1.71E-06 5.62E-07 3.21E-08 8.24E-05 1.71E-06 8.85E-07 5.06E-08
Inhalation 6.67E-02 1.38E-03 4.55E-04 2.60E-05 1.30E-01 2.63E-03 1.36E-03 7.78E-05
Total 6.68E-02 1.39E-03 4.56E-04 2.61E-05 1.30E-01 2.63E-03 1.36E-03 7.79E-05
DCAA 532 0.18
Oral 7.98E-02 1.66E-03 3.09E-04 1.76E-05 1.33E-02 2.76E-04 1.43E-04 8.17E-06
Dermal 2.74E-02 5.69E-04 1.06E-04 6.06E-06 9.14E-03 1.90E-04 9.83E-05 5.61E-06
Inhalation 5.47E-04 1.14E-05 2.12E-06 1.21E-07 3.47E-04 7.20E-06 3.73E-06 2.13E-07
Total 1.10E-01 2.24E-03 4.17E-04 2.38E-05 2.28E-02 4.73E-04 2.45E-04 1.40E-05
TCAA 1237 0.68
Oral 6.19E-02 1.28E-03 4.22E-04 2.41E-05 3.09E-02 6.42E-04 3.32E-04 1.90E-05
Dermal 2.55E-02 5.29E-04 1.74E-04 9.93E-06 2.55E-02 5.29E-04 2.74E-04 1.56E-05
Inhalation 6.83E-04 1.42E-05 4.66E-06 2.66E-07 1.30E-03 2.69E-05 1.39E-05 7.97E-07
Total 8.80E-02 1.83E-03 6.01E-04 3.43E-05 5.77E-02 1.20E-03 6.20E-04 3.54E-05
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
224
Table D.6: Adult competitive and noncompetitive male swimmers exposure dose calculations in S17L pool
DBP Cw
µg/L Cair
µg/m3
Exposure route
Non-competitive male Competitive male
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
TCM 68 1.02E+04
Oral 1.70E-03 2.18E-05 7.16E-06 3.07E-06 8.50E-04 1.09E-05 7.10E-06 2.23E-06
Dermal 1.17E-02 1.50E-04 4.94E-05 2.12E-05 1.17E-02 1.50E-04 9.80E-05 3.08E-05
Inhalation 1.02E+01 1.30E-01 4.29E-02 1.84E-02 3.26E+01 4.20E-01 2.70E-01 8.56E-02
Total 1.02E+01 1.30E-01 4.30E-02 1.84E-02 3.27E+01 4.20E-01 2.70E-01 8.57E-02
BDCM 13 867.1
Oral 3.25E-04 4.16E-06 1.37E-06 5.86E-07 1.63E-04 2.08E-06 1.36E-06 4.26E-07
Dermal 1.46E-03 1.87E-05 6.16E-06 2.64E-06 1.46E-03 1.87E-05 1.22E-05 3.84E-06
Inhalation 8.70E-01 1.11E-02 3.65E-03 1.56E-03 2.77E+00 3.55E-02 2.32E-02 7.28E-03
Total 8.70E-01 1.11E-02 3.66E-03 1.57E-03 2.78E+00 3.55E-02 2.32E-02 7.29E-03
DBCM 3 96.3
Oral 7.50E-05 9.60E-07 3.16E-07 1.35E-07 3.75E-05 4.80E-07 3.13E-07 9.84E-08
Dermal 2.27E-04 2.91E-06 9.55E-07 4.09E-07 2.27E-04 2.91E-06 1.90E-06 9.84E-08
Inhalation 9.63E-02 1.23E-03 4.05E-04 1.74E-04 3.10E-01 3.95E-03 2.57E-03 8.09E-04
Total 9.66E-02 1.24E-03 4.07E-04 1.74E-04 3.10E-01 3.95E-03 2.58E-03 8.09E-04
DCAA 426 0.15
Oral 1.06E-02 1.36E-04 4.48E-05 1.92E-05 5.32E-03 6.82E-05 4.45E-05 1.40E-05
Dermal 1.00E-02 1.28E-04 4.21E-05 1.80E-05 1.00E-02 1.28E-04 8.35E-05 2.62E-05
Inhalation 1.46E-04 1.87E-06 6.15E-07 2.64E-07 4.68E-04 5.99E-06 3.90E-06 1.23E-06
Total 2.08E-02 2.66E-04 8.75E-05 3.75E-05 1.58E-02 2.02E-04 1.32E-04 4.14E-05
TCAA 1373 0.76
Oral 3.43E-02 4.40E-04 1.44E-04 6.19E-05 1.72E-02 2.20E-04 1.43E-04 4.50E-05
Dermal 3.86E-02 4.95E-04 1.63E-04 6.97E-05 3.86E-02 4.95E-04 3.22E-04 1.01E-04
Inhalation 7.58E-04 9.70E-06 3.19E-06 1.37E-06 2.43E-03 3.11E-05 2.02E-05 6.36E-06
Total 7.37E-02 9.44E-04 3.10E-04 1.33E-04 5.82E-02 7.45E-04 4.86E-04 1.53E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
225
Table D.7: Adult competitive and noncompetitive female swimmers exposure dose calculations in S17L pool
Non-competitive female Competitive female
DBP Cw
µg/L Cair
µg/m3
Exposure route
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
TCM 68 1.02E+04
Oral 1.70E-03 2.60E-05 8.55E-06 3.66E-06 8.50E-04 1.30E-05 8.47E-06 2.66E-06
Dermal 1.02E-02 1.56E-04 5.14E-05 2.20E-05 1.02E-02 1.56E-04 1.02E-04 3.20E-05
Inhalation 1.02E+01 1.60E-01 5.13E-02 2.20E-02 3.26E+01 5.00E-01 3.30E-01 1.00E-01
Total 1.02E+01 1.60E-01 5.13E-02 2.20E-02 3.27E+01 5.00E-01 3.30E-01 1.00E-01
BDCM 13 867.1
Oral 3.25E-04 4.97E-06 1.63E-06 7.00E-07 1.63E-04 2.48E-06 1.62E-06 5.09E-07
Dermal 1.27E-03 1.95E-05 6.41E-06 2.75E-06 1.27E-03 1.95E-05 1.27E-05 3.99E-06
Inhalation 8.70E-01 1.33E-02 4.36E-03 1.87E-03 2.77E+00 4.24E-02 2.77E-02 8.69E-03
Total 8.70E-01 1.33E-02 4.37E-03 1.87E-03 2.78E+00 4.24E-02 2.77E-02 8.70E-03
DBCM 3 96.3
Oral 7.50E-05 1.15E-06 3.77E-07 1.62E-07 3.75E-05 5.73E-07 3.74E-07 1.18E-07
Dermal 1.98E-04 3.02E-06 9.94E-07 4.26E-07 1.98E-04 3.02E-06 1.97E-06 6.20E-07
Inhalation 9.63E-02 1.47E-03 4.84E-04 2.07E-04 3.10E-01 4.71E-03 3.07E-03 9.66E-04
Total 9.66E-02 1.48E-03 4.85E-04 2.08E-04 3.10E-01 4.72E-03 3.07E-03 9.66E-04
DCAA 426 0.15
Oral 1.06E-02 1.63E-04 5.35E-05 2.29E-05 5.32E-03 8.14E-05 5.31E-05 1.67E-05
Dermal 8.71E-03 1.33E-04 4.38E-05 1.88E-05 8.71E-03 1.33E-04 8.69E-05 2.73E-05
Inhalation 1.46E-04 2.23E-06 7.35E-07 3.15E-07 4.68E-04 7.15E-06 4.66E-06 1.47E-06
Total 1.95E-02 2.98E-04 9.81E-05 4.20E-05 1.45E-02 2.22E-04 1.45E-04 4.54E-05
TCAA 1373 0.76
Oral 3.43E-02 5.25E-04 1.73E-04 7.40E-05 1.72E-02 2.62E-04 1.71E-04 5.38E-05
Dermal 3.36E-02 5.14E-04 1.69E-04 7.25E-05 3.36E-02 5.14E-04 3.35E-04 1.05E-04
Inhalation 7.58E-04 1.16E-05 3.81E-06 1.63E-06 2.43E-03 3.71E-05 2.42E-05 7.60E-06
Total 6.87E-02 1.05E-03 3.45E-04 1.48E-04 5.32E-02 8.14E-04 5.31E-04 1.67E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
226
Table D.8: Children (11-14) competitive and noncompetitive swimmers exposure dose calculations in S17L pool
Child (11-14 years) non-competitive Child (11-14 years) competitive
DBP Cw
µg/L Cair
µg/m3
Exposure route
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
TCM 68 1.02E+04
Oral 3.40E-03 7.06E-05 2.32E-05 1.33E-06 1.70E-03 3.53E-05 1.83E-05 1.04E-06
Dermal 8.59E-03 1.78E-04 5.87E-05 3.35E-06 8.59E-03 1.78E-04 9.24E-05 5.28E-06
Inhalation 1.02E+01 2.10E-01 6.96E-02 3.98E-03 1.94E+01 4.00E-01 2.10E-01 1.19E-02
Total 1.02E+01 2.10E-01 6.97E-02 3.98E-03 1.94E+01 4.00E-01 2.10E-01 1.19E-02
BDCM 13 867.1
Oral 6.50E-04 1.35E-05 4.44E-06 2.54E-07 3.25E-04 6.75E-06 3.49E-06 2.00E-07
Dermal 1.07E-03 2.22E-05 7.31E-06 4.18E-07 1.07E-03 2.22E-05 1.15E-05 6.58E-07
Inhalation 8.70E-01 1.80E-02 5.92E-03 3.38E-04 1.65E+00 3.42E-02 1.77E-02 1.01E-03
Total 8.70E-01 1.80E-02 5.93E-03 3.39E-04 1.65E+00 3.42E-02 1.77E-02 1.01E-03
DBCM 3 96.3
Oral 1.50E-04 3.11E-06 1.02E-06 5.85E-08 7.50E-05 1.56E-06 8.06E-07 4.61E-08
Dermal 1.66E-04 3.45E-06 1.13E-06 6.48E-08 1.66E-04 3.45E-06 1.79E-06 1.02E-07
Inhalation 9.63E-02 2.00E-03 6.57E-04 3.76E-05 1.80E-01 3.80E-03 1.97E-03 1.12E-04
Total 9.66E-02 2.01E-03 6.59E-04 3.77E-05 1.80E-01 3.80E-03 1.97E-03 1.13E-04
DCAA 426 0.15
Oral 6.39E-02 1.33E-03 2.47E-04 1.41E-05 1.06E-02 2.21E-04 1.14E-04 6.54E-06
Dermal 2.20E-02 4.56E-04 8.49E-05 4.85E-06 7.32E-03 1.52E-04 7.87E-05 4.50E-06
Inhalation 4.38E-04 9.10E-06 1.70E-06 9.69E-08 2.78E-04 5.76E-06 2.98E-06 1.71E-07
Total 8.63E-02 1.79E-03 3.34E-04 1.91E-05 1.82E-02 3.79E-04 1.96E-04 1.12E-05
TCAA 1373 0.76
Oral 6.87E-02 1.43E-03 4.69E-04 2.68E-05 3.43E-02 7.13E-04 3.69E-04 2.11E-05
Dermal 2.83E-02 5.87E-04 1.93E-04 1.10E-05 2.83E-02 5.87E-04 3.04E-04 1.74E-05
Inhalation 7.58E-04 1.57E-05 5.17E-06 2.96E-07 1.44E-03 2.99E-05 1.55E-05 8.85E-07
Total 9.77E-02 2.03E-03 6.67E-04 3.81E-05 6.40E-02 1.33E-03 6.88E-04 3.93E-05
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
227
Table D.9: Adult competitive and noncompetitive male swimmers exposure dose calculations in S17W pool
Non-competitive male Competitive male
DBP Cw
µg/L Cair
µg/m3
Exposure route
PDR mg/event
PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM 170 2.55E+04
Oral 4.25E-03 5.44E-05 1.79E-05 7.67E-06 2.13E-03 2.72E-05 1.77E-05 5.58E-06
Dermal 2.94E-02 3.76E-04 1.24E-04 5.30E-05 2.94E-02 3.76E-04 2.45E-04 7.70E-05
Inhalation 2.55E+01 3.30E-01 1.10E-01 4.60E-02 8.16E+01 1.04E+00 6.80E-01 2.10E-01
Total 2.55E+01 3.30E-01 1.10E-01 4.61E-02 8.16E+01 1.05E+00 6.80E-01 2.10E-01
BDCM 11 733.7
Oral 2.75E-04 3.52E-06 1.16E-06 4.96E-07 1.38E-04 1.76E-06 1.15E-06 3.61E-07
Dermal 1.24E-03 1.58E-05 5.21E-06 2.23E-06 1.24E-03 1.58E-05 1.03E-05 3.25E-06
Inhalation 7.30E-01 9.39E-03 3.09E-03 1.32E-03 2.35E+00 3.01E-02 1.96E-02 6.16E-03
Total 7.40E-01 9.41E-03 3.09E-03 1.33E-03 2.35E+00 3.01E-02 1.96E-02 6.16E-03
DBCM 2 64.2
Oral 5.00E-05 6.40E-07 2.10E-07 9.02E-08 2.50E-05 3.20E-07 2.09E-07 6.56E-08
Dermal 1.51E-04 1.94E-06 6.37E-07 2.73E-07 1.51E-04 1.94E-06 1.26E-06 3.97E-07
Inhalation 6.42E-02 8.22E-04 2.70E-04 1.16E-04 2.10E-01 2.63E-03 1.72E-03 5.39E-04
Total 6.44E-02 8.25E-04 2.71E-04 1.16E-04 2.10E-01 2.63E-03 1.72E-03 5.40E-04
DCAA 2030 0.7
Oral 5.08E-02 6.50E-04 2.14E-04 9.16E-05 2.54E-02 3.25E-04 2.12E-04 6.66E-05
Dermal 4.77E-02 6.10E-04 2.01E-04 8.60E-05 4.77E-02 6.10E-04 3.98E-04 6.66E-05
Inhalation 6.96E-04 8.92E-06 2.93E-06 1.26E-06 2.23E-03 2.85E-05 1.86E-05 5.85E-06
Total 9.91E-02 1.27E-03 4.17E-04 1.79E-04 7.53E-02 9.64E-04 6.28E-04 1.97E-04
TCAA 4201 2.32
Oral 1.10E-01 1.34E-03 4.42E-04 1.89E-04 5.25E-02 6.72E-04 4.38E-04 1.38E-04
Dermal 1.20E-01 1.51E-03 4.97E-04 2.13E-04 1.20E-01 1.51E-03 9.87E-04 3.10E-04
Inhalation 2.32E-03 2.97E-05 9.76E-06 4.18E-06 7.42E-03 9.50E-05 6.20E-05 1.95E-05
Total 2.30E-01 2.89E-03 9.49E-04 4.07E-04 1.80E-01 2.28E-03 1.49E-03 4.67E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
228
Table D.10: Adult competitive and noncompetitive female swimmers exposure dose calculations in S17W pool
Non-competitive female Competitive female
DBP Cw Cair Exposure PDR PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
µg/L µg/m3 route mg/event mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM 170 2.55E+04
Oral 4.25E-03 6.50E-05 2.14E-05 9.16E-06 2.13E-03 3.25E-05 2.12E-05 6.66E-06
Dermal 2.56E-02 3.91E-04 1.29E-04 5.51E-05 2.56E-02 3.91E-04 2.55E-04 8.01E-05
Inhalation 2.55E+01 3.90E-01 1.30E-01 5.49E-02 8.16E+01 1.25E+00 8.10E-01 2.60E-01
Total 2.55E+01 3.90E-01 1.30E-01 5.50E-02 8.16E+01 1.25E+00 8.10E-01 2.60E-01
BDCM 11 733.7
Oral 2.75E-04 4.20E-06 1.38E-06 5.92E-07 1.38E-04 2.10E-06 1.37E-06 4.31E-07
Dermal 1.08E-03 1.65E-05 5.42E-06 2.32E-06 1.08E-03 1.65E-05 1.08E-05 3.38E-06
Inhalation 7.30E-01 1.12E-02 3.69E-03 1.58E-03 2.35E+00 3.59E-02 2.34E-02 7.36E-03
Total 7.40E-01 1.12E-02 3.70E-03 1.58E-03 2.35E+00 3.59E-02 2.34E-02 7.36E-03
DBCM 2 64.2
Oral 5.00E-05 7.65E-07 2.51E-07 1.08E-07 2.50E-05 3.82E-07 2.49E-07 7.83E-08
Dermal 1.32E-04 2.02E-06 6.63E-07 2.84E-07 1.32E-04 2.02E-06 1.31E-06 4.13E-07
Inhalation 6.42E-02 9.82E-04 3.23E-04 1.38E-04 2.10E-01 3.14E-03 2.05E-03 6.44E-04
Total 6.44E-02 9.84E-04 3.24E-04 1.39E-04 2.10E-01 3.14E-03 2.05E-03 6.44E-04
DCAA 2030 0.7
Oral 5.08E-02 7.76E-04 2.55E-04 1.09E-04 2.54E-02 3.88E-04 2.53E-04 7.95E-05
Dermal 4.15E-02 6.35E-04 2.09E-04 8.94E-05 4.15E-02 6.35E-04 4.14E-04 1.30E-04
Inhalation 6.96E-04 1.06E-05 3.50E-06 1.50E-06 2.23E-03 3.41E-05 2.22E-05 6.98E-06
Total 9.30E-02 1.42E-03 4.67E-04 2.00E-04 6.91E-02 1.06E-03 6.89E-04 2.17E-04
TCAA 4201 2.32
Oral 1.10E-01 1.61E-03 5.28E-04 2.26E-04 5.25E-02 8.03E-04 5.24E-04 1.65E-04
Dermal 1.00E-01 1.57E-03 5.18E-04 2.22E-04 1.00E-01 1.57E-03 1.03E-03 3.23E-04
Inhalation 2.32E-03 3.55E-05 1.17E-05 5.00E-06 7.42E-03 1.13E-04 7.40E-05 2.33E-05
Total 2.10E-01 3.22E-03 1.06E-03 4.53E-04 1.60E-01 2.49E-03 1.62E-03 5.10E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
229
Table D.11: Children (11-14) competitive and noncompetitive swimmers exposure dose calculations in S17W pool
Child (11-14 years) non-competitive Child (11-14 years) competitive
DBP Cw Cair Exposure PDR PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
µg/L µg/m3 route mg/event mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM 170 2.55E+04
Oral 8.50E-03 1.76E-04 5.80E-05 3.32E-06 4.25E-03 8.82E-05 4.57E-05 2.61E-06
Dermal 2.15E-02 4.46E-04 1.47E-04 8.38E-06 2.15E-02 4.46E-04 2.31E-04 1.32E-05
Inhalation 2.55E+01 5.30E-01 1.70E-01 9.95E-03 4.85E+01 1.01E+00 5.20E-01 2.98E-02
Total 2.55E+01 5.30E-01 1.70E-01 9.96E-03 4.85E+01 1.01E+00 5.20E-01 2.98E-02
BDCM 11 733.7
Oral 5.50E-04 1.14E-05 3.75E-06 2.15E-07 2.75E-04 5.71E-06 2.96E-06 1.69E-07
Dermal 9.06E-04 1.88E-05 6.18E-06 3.53E-07 9.06E-04 1.88E-05 9.74E-06 5.56E-07
Inhalation 7.30E-01 1.52E-02 5.01E-03 2.86E-04 1.39E+00 2.89E-02 1.50E-02 8.56E-04
Total 7.40E-01 1.53E-02 5.02E-03 2.87E-04 1.40E+00 2.90E-02 1.50E-02 8.57E-04
DBCM 2 64.2
Oral 1.00E-04 2.08E-06 6.83E-07 3.90E-08 5.00E-05 1.04E-06 5.37E-07 3.07E-08
Dermal 1.11E-04 2.30E-06 7.56E-07 4.32E-08 1.11E-04 2.30E-06 1.19E-06 6.80E-08
Inhalation 6.42E-02 1.33E-03 4.38E-04 2.50E-05 1.20E-01 2.53E-03 1.31E-03 7.49E-05
Total 6.44E-02 1.34E-03 4.40E-04 2.51E-05 1.20E-01 2.54E-03 1.31E-03 7.50E-05
DCAA 2030 0.7
Oral 3.00E-01 6.32E-03 1.18E-03 6.73E-05 5.08E-02 1.05E-03 5.46E-04 3.12E-05
Dermal 1.00E-01 2.17E-03 4.05E-04 2.31E-05 3.49E-02 7.24E-04 3.75E-04 2.14E-05
Inhalation 2.09E-03 4.34E-05 8.08E-06 4.62E-07 1.32E-03 2.75E-05 1.42E-05 8.13E-07
Total 4.10E-01 8.54E-03 1.59E-03 9.09E-05 8.70E-02 1.81E-03 9.35E-04 5.34E-05
TCAA 4201 2.32
Oral 2.10E-01 4.36E-03 1.43E-03 8.19E-05 1.10E-01 2.18E-03 1.13E-03 6.45E-05
Dermal 8.65E-02 1.80E-03 5.90E-04 3.37E-05 8.65E-02 1.80E-03 9.30E-04 5.31E-05
Inhalation 2.32E-03 4.81E-05 1.58E-05 9.04E-07 4.41E-03 9.15E-05 4.74E-05 2.71E-06
Total 3.00E-01 6.20E-03 2.04E-03 1.17E-04 2.00E-01 4.07E-03 2.11E-03 1.20E-04
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
230
Table D.12: Lifeguard male and female exposure dose calculations in S16 pool
DBP Cw Cair
Male lifeguard Female lifeguard
Exposure
route
PDR PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
µg/L µg/m3 mg/event mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM
53 7950
Oral
Dermal
Inhalation 2.39E+01 3.10E-01 1.10E-01 1.55E-02 2.39E+01 3.60E-01 1.30E-01 1.86E-02
Total 2.39E+01 3.10E-01 1.10E-01 1.55E-02 2.39E+01 3.60E-01 1.30E-01 1.86E-02
BDCM
1 66.7
Oral
Dermal
Inhalation 2.00E-01 2.56E-03 9.13E-04 1.30E-04 2.00E-01 3.06E-03 1.09E-03 1.56E-04
Total 2.00E-01 2.56E-03 9.13E-04 1.30E-04 2.00E-01 3.06E-03 1.09E-03 1.56E-04
DCAA
532 0.18
Oral
Dermal
Inhalation 5.47E-04 7.01E-06 2.50E-06 3.57E-07 5.47E-04 8.37E-06 2.98E-06 4.26E-07
Total 5.47E-04 7.01E-06 2.50E-06 3.57E-07 5.47E-04 8.37E-06 2.98E-06 4.26E-07
TCAA
1237 0.68
Oral
Dermal
Inhalation 8.81E-04 1.13E-05 4.02E-06 5.74E-07 8.81E-04 1.35E-05 4.80E-06 6.85E-07
Total 8.81E-04 1.13E-05 4.02E-06 5.74E-07 8.81E-04 1.35E-05 4.80E-06 6.85E-07
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
231
Table D.13: Lifeguard male and female exposure dose calculations in S17L pool
DBP Cw
µg/L Cair
µg/m3
Exposure route
Male lifeguard Female lifeguard
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
PDR mg/event
PDRnormalized mg/kg/event
ADD mg/kg/day
LADD mg/kg/day
TCM 68 1.02E+04
Oral Dermal Inhalation 3.06E+01 3.90E-01 1.40E-01 1.99E-02 3.06E+01 4.70E-01 1.70E-01 2.38E-02
Total 3.06E+01 3.90E-01 1.40E-01 1.99E-02 3.06E+01 4.70E-01 1.70E-01 2.38E-02
BDCM 13 867.1
Oral Dermal Inhalation 2.60E+00 3.33E-02 1.19E-02 1.69E-03 2.60E+00 3.98E-02 1.42E-02 2.02E-03
Total 2.60E+00 3.33E-02 1.19E-02 1.69E-03 2.60E+00 3.98E-02 1.42E-02 2.02E-03
DBCM 3 96.3
Oral Dermal Inhalation 2.90E-01 3.70E-03 1.32E-03 1.88E-04 2.90E-01 4.42E-03 1.57E-03 2.25E-04
Total 2.90E-01 3.70E-03 1.32E-03 1.88E-04 2.90E-01 4.42E-03 1.57E-03 2.25E-04
DCAA 426 0.15
Oral Dermal Inhalation 4.38E-04 5.61E-06 2.00E-06 2.86E-07 4.38E-04 6.70E-06 2.39E-06 3.41E-07
Total 4.38E-04 5.61E-06 2.00E-06 2.86E-07 4.38E-04 6.70E-06 2.39E-06 3.41E-07
TCAA 1373 0.76
Oral Dermal Inhalation 2.27E-03 2.91E-05 1.04E-05 1.48E-06 2.27E-03 3.48E-05 1.24E-05 1.77E-06
Total 2.27E-03 2.91E-05 1.04E-05 1.48E-06 2.27E-03 3.48E-05 1.24E-05 1.77E-06
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
232
Table D.14: Lifeguard male and female exposure dose calculations in S17T pool
Lifeguard male Lifeguard female
DBP Cw
µg/L Cair
µg/m3
Exposure route
PDR mg/event
PDRnormalized ADD LADD PDR PDRnormalized ADD LADD
mg/kg/event mg/kg/day mg/kg/day mg/event mg/kg/event mg/kg/day mg/kg/day
TCM 170 2.55E+04
Oral Dermal Inhalation 7.65E+01 9.80E-01 3.50E-01 4.98E-02 7.65E+01 1.17E+00 4.20E-01 5.95E-02
Total 7.65E+01 9.80E-01 3.50E-01 4.98E-02 7.65E+01 1.17E+00 4.20E-01 5.95E-02
BDCM 11 733.7
Oral Dermal Inhalation 2.20E+00 2.82E-02 1.00E-02 1.43E-03 2.20E+00 3.37E-02 1.20E-02 1.71E-03
Total 2.20E+00 2.82E-02 1.00E-02 1.43E-03 2.20E+00 3.37E-02 1.20E-02 1.71E-03
DBCM 2 64.2
Oral Dermal Inhalation 1.90E-01 2.47E-03 8.78E-04 1.25E-04 1.90E-01 2.94E-03 1.05E-03 1.50E-04
Total 1.90E-01 2.47E-03 8.78E-04 1.25E-04 1.90E-01 2.94E-03 1.05E-03 1.50E-04
DCAA 2030 0.7
Oral Dermal Inhalation 2.09E-03 2.67E-05 9.53E-06 1.36E-06 2.09E-03 3.19E-05 1.14E-05 1.63E-06
Total 2.09E-03 2.67E-05 9.53E-06 1.36E-06 2.09E-03 3.19E-05 1.14E-05 1.63E-06
TCAA 4201 2.32
Oral Dermal Inhalation 6.96E-03 8.91E-05 3.17E-05 4.53E-06 6.96E-03 1.06E-04 3.79E-05 5.41E-06
Total 6.96E-03 8.91E-05 3.17E-05 4.53E-06 6.96E-03 1.06E-04 3.79E-05 5.41E-06
Cw (concentration in water), Ca (calculated concentration in air, PDR (potential dose rate), ADD (average daily dose), LADD
(life average daily dose), TCM (chloroform), BDCM (bromdichloromethane), DBCM (dibromochloromethane), DCAA
(dichloroacetic acid), TCAA (trichloroacetic acid)
233
REFERENCES
ACC, American Chemistry Council. 2002. An Analysis of the Training Patterns and
Practices of Competitive Swimmers. Prepared by Richard Reiss, Sciences
International Inc. December 19, 2002.
Adin, A.; Katzhendler, J.; Alkaslassy, D.; Rav-Acha, C. 1991. Trihalomethane formation
in chlorinated drinking water: A kinetic model. Water Research, 25 (7): 797-805.
Afghan, B. K., Leung, R., Ryan, J. F. 1974. Automated fluorometric method for
determination of citric acid in sewage and sewage effluents. Water Research, 8:
789-795.
Aggazzotti, G.; Fantuzzi, G.; Righi, E.; Predieri G. 1995. Environmental and biological
monitoring of chloroform in indoor swimming pools. Journal of Chromatography,
710: 181–190.
Aggazzotti, G.; Fantuzzi, G.; Righi, E.; Tartoni, PL.; Cassinadri, T.; Predieri, G. 1993.
Chloroform in alveolar air of individuals attending indoor swimming pools.
Archives of Environmental Health, 48: 250–254.
Aggazzotti, G.; Fantuzzi, G.; Tartoni, P. L.; Predieri, G. 1990. Plasma chloroform
concentrations in swimmers using indoor swimming pools. Archives of
Environmental Health, 45: 175–179.
Aggazzotti, G.; Predieri, G. 1986. Survey of volatile halogenated organics (VHO)inItaly.
Levels of VHO in drinking waters, surface waters and swimming pools. Water
Research, 20: 959-63.
Aggazzottiu, G.; Fantuzzi, G.; Righi, E.; Predieri, G. 1998. Blood and breath analyses as
biological indicators of exposure to trihalomethanes in indoor swimming pools. The
Science of the Total Environment, 217: 155-163.
Al-Omari, A.; Fayyad, M.; Qader, A. 2004. Modeling trihalomethane formation for Jabal
Amman water supply system in Jordan. Environmental Modeling and Assessment;
9: 245–52.
Althaus, H.; Pacik, D. 1981. Anthropogenic load substances in hot whirlpools. Archiv des
Badewesens, (34). (In German)
American Chemistry Council (ACC). 2002. An Analysis of the Training Patterns and
Practices of Competitive Swimmers. Prepared by Richard Reiss, Sciences
International Inc. December 19, 2002.
234
Ames, B. N.; McCann, J.; Yamasaki, E. 1975 Methods for detecting carcinogens and
mutagens with Salmonella mammalian microsome mutagenicity test. Mutation
Research, 31:347-364.
Amy, G., Siddiqui, M., Zhai, W., Bebroux, J. Odem. W. 1994. Survey of Bromide in
Drinking Water and Impacts on DBP Formation. American Water Works
Association Research Foundation, Denver, Colorado. 150 pages.
Andrzejewski, P.; Kasprzyk-Hordern, B.; Nawrocki, J. 2005. The hazard of N-
nitrosodimethylamine (NDMA) formation during water disinfection with strong
oxidants. Desalination, 176 (1-3): 37-45.
Anipsitakis, G. P.; Tufano, T. P.; Dionysiou, D. D. 2008. Chemical and microbial
decontamination of pool water using activated potassium peroxymonosulfate. Water
Research, 42: 2899-2910.
Armstrong, D.W., and Golden, T. 1986. Determination of distribution and concentration
of trihalomethanes in aquatic recreational and therapeutic facilities by electron-
capture GC,‖ LC-GC Mag. Liquid Gas Chromatography, 4 (7): 652-655.
Ashley, D.; Blount, B.; Singer, P.; Depaz, E.; Wilkes, C.; Gordon, S.; Lyu, C.; Masters, J.
2005. Changes in blood trihalomethane concentrations resulting from differences in
water quality and water use activities. Archives of Environmental and Occupational
Health, 60 (1): 7-15.
ATSDR. 1999. ToxFAQs - N-Nitrosodimethylamine. Atlanta, Georgia: U.S. Department
of Health and Human Services, Public Health Service.
AWWA. 2005. Water Treatment Plant Design. 4th edition. New York, McGraw-Hill, US.
AWWA.1990. Water Quality and Treatment: A Handbook of Community Water
Supplies. 4th
edition. New York, McGraw-Hill, US.
Barbot, E.; Moulin, P. 2008. Swimming pool water treatment by ultrafiltration–
adsorption process. Journal of Membrane Science, 314: 50-57.
Batjer, K.; Cetinkaya, M.; Duszeln, J. V.; Gabel, B.; Lahl, U.; Stachel, B.; Thiemann, W.
1980. Chloroform emission into urban atmosphere. Chemosphere, 9: 311-316.
Beech, J. A.; Diaz, R.; Ordaz, C.; Palomeque, B. 1980. Nitrates, chlorates and
trihalomethanes in swimming pool water. American Journal of Public Health, 70:
79–82.
235
Benoit, F. M. and Jackson. 1987. Trihalomethane Formation in Whirlpool Spas. Water
Research, 21 (3): 353-357.
Bernard, A., Carbonnelle, S., Michel, O., Higuet, S., de Burbure, C., Buchet, J.-P.,
Hermans, C., Dumont, X., Doyle, I., 2003. Lung hyperpermeability and asthma
prevalence in schoolchildren: Unexpected associations with the attendance at indoor
chlorinated swimming pools. Occupational and Environmental Medicine, 60: 385–
394.
Bernard, A.; Carbonnelle, S.; Nickmilder, M.; de Burbure, C. 2005. Non-invasive
biomarkers of pulmonary damage and inflammation: Application to children
exposed to ozone and trichloramine. Toxicology and Applied Pharmacology, 206:
185- 190.
Benner, T. C. 2004. Brief survey of EPA standard-setting and health assessment.
Environmental Science and Technology, 38 (13): 3457-3464.
Bisted, O. 2002. Activated carbon and UV for pool water treatment. Presentation at the
school of water sciences, 1 day conference on swimming pool water quality and
treatment. Cranfield University, ISBN 1861940203.
Biziuk, M.; Czerwinski, J.; Kozlowski, E. 1993. Identification and determination of
organohalogen compounds in swimming pool water. International Journal of
Environmental Analytical Chemistry, 46: 109–115.
Bjork, R. G. 1975. GLC determination of PPB levels of citrate by conversion to
bromoform. Analytical Biochemistry, 63: 80-86.
Black and Vetch Corporation. 2010. White’s Handbook of Chlorination and Alternative
Disinfectants. 5th edition. John Wiley and Sons, Inc. Hoboken, New Jersy.
Blatchley, E. R., III; Johnson, R. W.; Alleman, J. E.; McCoy, W. F. 1992. Effective
Henry’s constants for free chlorine and free bromine. Water Research, 26: 99-106.
Boccelli, D. L.; Tryby, M. E.; Uber, J, G.; and Summers, R. S. 2003. A reactive species
model for chlorine decay and THM formation under rechlorination conditions.
Water Research, 37: 2654–2666.
Bond, T.; Henriet, O.; Goslan, E. H.; Parsons, S. A.; Jefferson, B. 2009. Disinfection
byproduct formation and fractionation behavior of natural organic matter
surrogates. Environmental Science and Technology, 43: 5982-5989.
236
Boorman, G., Dellarco, V., Dunnic, J. K., Chapin, R., Hunter, S., Hauchman, F., Gardner,
H., Cox, M., Sills, R. 1999. Drinking water disinfection by-products: review and
approach to toxicity evaluation. Environmental Health Perspective, 107, 207 – 217.
Borgmann-Strahsen, R. 2003. Comparative assessment of different biocides in swimming
pool water. International Biodeterioration and Biodegradation, 51: 291-297.
Borneff, J. 1979. Hygiene. Verlag, Stuttgart. (in German)
Borsanyi, M. 1998. THMs in Hungarian swimming pool waters. Budapest, National
Institute of Environmental Health, Department of Water Hygiene.
Bove, F. J.; Fulcomer, M. C.; Klotz, J. B.; Esmart, J.; Dufficy E. M.; Savrin, J. E. 1995.
Public drinking water contamination birth outcome. American Journal of
Epidemiology, 141: 850–862.
Bove, F.; Shim, Y.; Zeitz, P. 2002. Drinking water contaminants and adverse pregnancy
outcomes: A review. Environmental Health Perspectives, 110 (1): 61–74.
Bradley, P.M., Carr, S.A.; Baird, R.B.; Chappelle, F.H. 2005. Biodegradation of N-
nitrosodimethylamine in soil from a water reclamation facility. Bioremediation
Journal, 9: 115-120.
Bryant, E. A., Fulton, G. P., Budd, G. C. 1992. Disinfection Alternatives for Safe
Drinking Water. Hazen and Sawyer. Von Nostrand Reinhold: New York.
Bull, R. J.; Birnbaum, L. S.; Cantor, K. P.; Rose, J. B.; Butterworth, B. E.; Pegram, R.;
Tuomisto, J. 1995 Water chlorination: Essential process or cancer hazard.
Fundamental and Applied Toxicology, 28 (2): 155-166.
Bull, R. J.; Sanchez, I. M.; Nelson, M. A. Larson, J. L.; Lansing, A. J. 1990. Liver tumor
induction in B6C3F1 mice by dichloacetate and trichloroacetate. Toxicology, 63:
341-359.
Cammann, K.; Hubner, K. 1995. Trihalomethane concentrations in swimmers’ and bath
attendants’ blood and urine after swimming or working in indoor swimming pools.
Archives of Environmental Health, 50: 61–65.
Cantor, K. P.; 1997. Drinking water and cancer. Cancer Causes Control, 8: 292–308.
Cantor, K. P.; Hoover, R.; Hartge, P. 1987. Bladder cancer, drinking water sources, and
tap water consumption: A case control study. Journal of the National Cancer
Institute, 79: 1269–1279.
237
Cantor, K. P.; Hoover, R.; Mason, T. J.; McCabe, L. J. 1978. Association of cancer
mortality with halomethanes in drinking water. Journal of the National Cancer
Institute Inst, 61: 979–985.
Cantor, K. P.; Lynch, C. F.; Hildesheim, M. E.; Dosemeci, M.; Lubin, J.; Alavanja, M.;
Craun, G. 1998. Drinking water source and chlorination byproducts I Risk of
bladder cancer. Epidemiology, 9: 21–28.
Carbonnelle, S.; Francaux, M.; Doyle, I.; Dumont, X.; de Burbure, C.; Morel, G.; Michel,
O.; Bernard, A. 2002. Changes in serum pneumoproteins caused by short-term
exposures to nitrogen trichloride in indoor chlorinated swimming pools.
Biomarkers, 7: 464-478.
Caro, J. Gallego, M. 2008. Alveolar air and urine analyses as biomarkers of exposure to
trihalomethanes in an indoor swimming pool. Environmental Science and
Technology, 42: 5002-5007.
Caro, J.; Gallego, M. 2007. Assessment of exposure of workers and swimmers to
trihalomethanes in an indoor swimming pool. Environmental Science and
Technology, 41: 4793-4798.
Cassan, D.; Mercier, B.; Castex, F. Rambaud, A. 2006. Effects of medium-pressure UV
lamps radiation on water quality in a chlorinated indoor swimming pool.
Chemosphere 62: 1507–1513.
CDC, Center for Disease Control and Prevention. 2008. Surveillance for waterborne
disease and outbreaks associated with recreational water use and other aquatic
facility-associated health events-United States. 2005-2006. Surveillance summaries,
MMWR; 57 (SS-9).
CDHS, California Department of Health Services. 2009. California Drinking Water:
Activities Related to NDMA and other Nitrosamines.
http://www.dhs.ca.gov/ps/ddwem/chemicals/NDMA/NDMAindex. htm [Accessed
Dec, 2009].
CDHS, California Department of Health Services; NDMA in California Drinking Water;
March 15. 2002, http://www.dhs.ca.gov/ps/ddwem/chemicals/NDMA/history.htm.
Charrois, J.W.A., Boyd, J.M.; Froese, K.L.; Hrudey, S.E. 2007. Occurrence of N-
nitrosamines in Alberta public drinking-water distribution systems. Journal of
Environmental Engineering and Science, 6(1): 103-114.
238
Chellam, S.2000. Effects of Nanofiltration on Trihalomethane and Haloacetic Acid
Precursor Removal and Speciation in Waters Containing Low Concentrations of
Bromide Ion. Environmental Science and Technology, 34:1813-1820.
Chen, P. H.; Richardson, S. D.; Krasner, S. W.; Majetich, G.; Glish, G. L. 2002.
Hydrogen abstraction and decomposition of bromopicrin and other trihalogenated
disinfection byproducts by GC/MS. Environmental Science and Technology, 36
(15): 3362-3371.
Chen, W.H.; Young, T.M. 2008. NDMA formation during chlorination and
chloramination of aqueous diuron solutions. Environmental Science and
Technology, 42(4): 1072-1077.
Choi, J.H., Valentine, R.L., 2003. N-nitrosodimethylamine formation by free-chlorine-
enhanced nitrosation of dimethylamine. Environmental Science and Technology, 37
(21): 4871-4876.
Choi, J.H.; Valentine, R.L. 2002. Formation of N-nitrosodimethylamine (NDMA) from
reaction of monochloramine: a new disinfection by-product. Water Research, 36(4):
817-824.
Chrostowski, P. C. 2004. Swimming pool shock treatment. Journal of Environmental
Health, 66 (9): 26-27.
Chu, H.; Nieuwenhuijsen, M. J. 2002. Distribution and determinants of trihalomethanes
concentrations in indoor swimming pools. Occupational and Environmental
Medicine, 59: 243-247.
Clark, M.; Sivaganesan, M. 2002. Predicting chlorine residuals in drinking water: Second
order model. Journal of Water Resources Planning and Management, 128 (2): 152-
161.
CNN, (By Madison Park). 2009. Tinkling in the pool causes disgust and discomfort.
http://www.cnn.com/2009/HEALTH/05/22/pools.urinate.hygiene/index.htm?iref=m
pstoryview. [Accessed May 22, 2009].
Corley, R. A.; Gordon, S. M.; Wallace, L. A. 2000 Physiologically based
pharmacokinetic modeling of the temperature-dependent dermal absorption of
chloroform by humans following bath water exposures. Toxicological Science, 53:
13–23.
Cowman, G. A.; Singer, P. C. 1996. Effect of bromide ion on haloacetic acid speciation
resulting from chlorination and chloramination of aquatic humic substances.
Environmental Science and Technology, 30 (1): 16-24.
239
De Angelo, A. B.; Danial, F.B.; Stober, J. A.; Olson, G.R. 1991. The Carcinogenicity of
dichloroacetic acid in the male B6C3F1 mouse. Fundamental and Applied
Toxicology, 16: 337-347.
Deborde, M.; Gunten, U. 2008. Reactions of chlorine with inorganic and organic
compounds during water treatment-Kinetics and mechanisms: A critical review.
Water Research, 42: 13-51
Doyle, T. J.; Zheng, W.; Cerhan, J. R.; Hong, C. P.; Sellers, T, A.; Kushi, L. H.; Polsom,
A. R. 1997. The association of drinking water source and chlorination by-products
with cancer incidence among postmenopausal women in Iowa: A prospective
cohort study. American Journal of Public Health, 87: 1168–1176.
Dufour, A. P.; Evans, O.; Behymer, T. D.; Cantu, R. 2006. Water ingestion during
swimming activities in a pool: A pilot study. Journal of Water and Health, 4 (4):
425-430.
Duirk, S. and Valentine, R. 2007. Bromide Oxidation and Formation of Dihaloacetic
Acids in Chloraminated Water. Environmental Science and Technology, 41: 7047-
7053.
DWI, 2008. Guidance on the Water Supply (Water Quality) Regulations 2000a specific
to N-nitrosodimethylamine (NDMA) concentrations in drinking water
http://www.dwi.gov.uk/guidance/NDMA%20guidance.pdf. [acessesed January,
2010]
Egorov, A. I.; Tereschenko, A. A.; Altshul, L. M.; Vartiainen, T.; Samsonov, D.;
LaBrecque, B.;Ma¨ki-Paakkanen, J.; Drizhd, N. L.; Ford, T. E. 2003. Exposures to
drinking water chlorination by-products in a Russian city. International Journal of
Hygiene and Environmental Health, 206: 539-551.
Eichelsdorfer, D.; Jandic, J.; Weil, W. 1980. Organohalogen compounds in swimming
pool water. Mitteilung: Modellversuche zur Biung Leichtfluchtiger
Halogenkohlenwasserstoffe. Z. Wasser Abwasser Forshung. 13 (5): 5 (In German).
Eichelsdorfer, D.; Jandik, J. W. 1981. Formation and occurrence of organic halocarbons
in swimming pool water. A.B. Archiv des Badewesens. 34, 167-172.
Erdinger L.; Kirsch, F.; Sonntag H-G. 1997. Potassium as an indicator of anthropogenic
contamination of swimming pool water. Zentralblatt für Hygiene und
Umweltmedizin, 200(4): 297-308 (in German).
Erdinger, L.; Klaus K.; Gabrio, T. 2005. Formation of trihalomethanes in swimming pool
water-identification of precursors and kinetics of formation, International
240
Conference on Health and Water Quality Aspects of the Man Made Recreational
Water Environment, Margitsziget, Budapest.
Erdinger, L.; Kuhn, K. P.; Kirsch, F.; Feldhues, R.; Frobel, T.; Nohynek, B.; and Gabrio,
T. 2004. Pathways of trihalomethane uptake in swimming pools. International
Journal of Hygiene and Environmental Health, 207: 571-575.
EU Directive 98/83/EC of 3 November 1998.
Ewers, H.; Hajimiragha, H.; Fischer, U.; Bottger, A.; Ante, R. 1987. Organic halogenated
compounds in swimming pool waters. Forum Stadte-Hygiene, 38: 77-79.
Fantuzzi, G.; Righi, E.; Predieri, G.; Ceppelli, G.; Gobba, F.; Aggazzotti, G. 2001.
Occupational exposure to trihalomethanes in indoor swimming pools. Science of
the Total Environment, 264: 257-265.
Fantuzzi, G.; Righi, E.; Predieri, G.; Giacobazzi, P.; Aggazzotti, G. 2007. Haloacetic
acids (HAAs), bromated, chlorite, chlorate, and trihalomethanes (THMs)
determination in indoor swimming pools. Abstracts Pools and Spa Conference,
Germany.
Gallagher, M. D.; Nuckols, J. R.; Stallones, L.; Savitz, D. A. 1998. Exposure to
trihalomethanes and adverse pregnancy outcomes. Epidemiology, 9: 484-489.
Gallard, H.; Gunten U. 2002. Chlorination of natural organic matter: Kinetics of
chlorination and of THM formation. Water Research, 36: 65–74.
Garcia-Villanova, R. J.; Garcia, C.; Cesar, Gomez, J. A.; Garcia, M. P.; Ardanuy, R.
1997. Formation, evolution and modeling of trihalomethanes in the drinking water
of a town: II. In the distribution system. Water Research, 31 (6): 1405-1413.
German standard DIN 19643. Treatment of water of swimming- pools and baths. Part 1:
General requirements (1997). Part 2: —Combination of process: adsorption—
flocculation— filtration—chlorination (1997). Part 3: Combination of process:
flocculation—filtration—ozonisation—adsorbing filtration—chlorination (1997).
Part 4: Combination of process: flocculation ozonisation—multilayer filtration—
chlorination (1999). Part 5: Combination of process: flocculation—filtration—
adsorption at granular activated carbon—chlorination (2000). Normausschuss
Wasserwesen (NAW) im DIN Deutsches Institut fűr Normung e.V., Beuth Verlag
GmbH, Berlin (in German).
Glauner, T.; Frimmel F. H.; and Zwiener C. 2004. Swimming pool water- the required
quality and what can be done technologically. GWF Wasser Abwasser. 145, 706-
713 (in German).
241
Glauner, T.; Waldmann, P.; Frimmel, F. H.; and Zwiener, C. 2005. Swimming pool
water-fractionation and genotoxicological characterization of organic constituents.
Water Research, 39: 4494-4502.
Goeres, D. M.; Palys, T.; Sandel, B. B.; and Geiger, J. 2004. Evaluation of disinfectant
efficacy against biofilm and suspended bacteria in a laboratory swimming pool
model. Water Research, 38: 3103-3109.
Gordon, S. M.; Brinkman, M. C.; Ashley, D. L.; Blount, B. C.; Lyu, C.; Masters, J.;
Singer, P. C. 2006. Changes in breath trihalomethane levels resulting from
household water-use activities. Environmental Health Perspectives, 114: 514-21.
Gordon, S. M.; Wallace, L. A.; Callahan, P. J.; Kenny, D. V.; and Brinkman, M. C. 1998.
Effect of water temperature on dermal exposure to chloroform. Environmental
Health Perspectives, 106: 337-345.
Gould, J.P., Fitchorn, L.E., Urheim, E., 1983. Formation of brominated trihalomethane:
Extent and kinetics. In: Jolley, R.L. (Ed.), Water Chlorination: Environmental
Impact and Health Effects, Chemistry and Water Treatment, vol. 4. Ann Arbor
Science, Ann Arbor, MI, pp. 297–310.
Government of Ontario. Safe Drinking Water Act 2002. Ontario Regulation 169/03,
Schedule 2. http://www.ene.gov.on.ca/envision/ water/sdwa/legislation.htm
[Accessed December, 2009].
Graves, C. G.; Matanoski, G. M.; Tardiff, R. G. 2001. Weight of evidence for an
association between adverse reproductive and developmental effects and exposure
to disinfection by-products: A critical review. Regulatory Toxicology and
Pharmacology, 34: 103-124.
Griffiths T. 2003. The Complete Swimming Pool Reference. 2nd edition, Sagamore
Publishing. ISBN: 1-57167-523-x.
Gunkel, K.; Jessen, H. J.; 1988. The problem of urea in bathing water. Zeitschrift für die
Gesamte Hygiene, 34: 248–250 (in German).
Gunnison, D., M.E. Zappi, C. Teeter, J.C. Pennington, and R. Bajpai, 2000. Attenuation
mechanisms of N-nitrosodimethylamine at an operating intercept and treat
groundwater remediation system. Journal of Hazardous Materials, 73(2): 179-197.
Guy, L. L.; Beniot, F. M.; Williams, D.T. 1997. A One-Year Survey of Halogenated
Disinfection By-Products in the Distribution System of Treatment Plants Using
Three Different Disinfection Processes. Chemosphere, 34 (11): 2301-2317.
242
Hagen, K. Abstracts of the Workshop on Pool Water Chemistry and Health, University of
Karlsruhe, Germany, Sept. 22-24, 2003; http://www.wasserchemie.uni-
karlsruhe.de/. [Accessed January, 2009].
Hailin, G. E., Wallace, G. G. and O’Halloran, R. A. J. 1990. Determination of trace
amounts of chloramines by liquid chromatographic separation and amperometric
detection. Analytica Chimica Acta, 237: 149-153.
Hallenbeck, W. H. 1993. Quantitative Risk Assessment for Environmental and
Occupational Health. 2nd edition. Lewis, Chelsea, MI.
Hery, M.; Hecht,G.; Gerber,J. M.; Gendre, J. C.; Hubert, G.; RebuffaudI, J. 1995.
Exposure to Chloramines in the Atmosphere of Indoor Swimming Pools. Analytical
Occupational Hygiene 39 (4): 427-439.
Holzwarth, G.; Balmer, R. G.; Soni, L. 1984. The fate of chlorine and chloramines in
cooling towers: Henry’s law constants for flash off. Water Research, 18: 1421-
1427.
Honer, W. G.; Ashwood-Smith, M. J.; Warby, C. 1980. Mutagenic activity of swimming-
pool water. Mutation Research, 78 (2): 137-144.
Hong, H. C.; Wong, M. H.; and Liang, Y. 2008. Amino acids as precursors of
trihalomethanes and haloacetic acids formation during chlorination. Archives of
Environmental Contamination and Toxicology, DOI 10.1007/s00244-008-9216-4.
HSDB, Hazardous Substance Data Bank (HSDB). 2007. Information generated for N-
Nitrosodimethylamine on January 23. http://toxnet.nlm.nih.gov.
Hsu, C.; Jeng, W.; Chang, R.; Chien, L.; Han, B. 2001. Estimation of potential lifetime
cancer risks for trihalomethanes from consuming chlorinated drinking water in
Taiwan. Environmental Research, 85: 77-82.
Hsu, H. T.; M. J. Chen, M. J.; Lin, C. H.; Chou, W. S. and. Chen, J. H. 2009.
Chloroform in indoor swimming-pool air: Monitoring and modeling coupled with
the effects of environmental conditions and occupant activities. Water Research, 43:
3693-3704.
Hu, J. 2009. Exploring formation and distribution of halonitromethanes in drinking
waters. PhD dissertation. Clemson University, Clemson, SC.
243
Hua, G. and Reckhow, D. A. 2007. Characterization of disinfection byproduct precursors
based on hydrophobicity and molecular size. Environmental Science and
Technology, 41: 3309-3315.
Hua, G.; and Reckhow, D. A. 2008. DBP formation during chlorination: Effect of
reaction time, pH, dosage, and temperature. Journal of American Water Works
Association, 100(8): 82-89.
Huang, W.; and Yeh, H. 1997.The effect of organic characteristics and bromide on
disinfection by-products formation by chlorination. Journal of Environmental
Science and Health, A32: 2311-2336.
Hureiki, L.; Croue, J. P.; and Legube, B. 1994. Chlorination studies of free and combined
amino acids. Water Research, 28 (12): 2521-2531.
IAF, International Aquatic Water Foundation, 2005, Water treatment information
bulletins. The Association of Pool and Spa Professionals.
http://www.apsp.org/clientresources/documents/2005-06%20IBs.pdf.[Accessed
April 7, 2009].
Icihashi, K.; Teranishi, K.; and Ichimura, A. 1999. Brominated trihalomethanes
formation in halogenations of humic acid in the coexistence of hypochlorite and
hypobromite ions. Water Research, 33 (2), 477-483.
IRIS, Integrated Risk Information System. United States Environmental Protection
Agency (EPA), Office of Research and Development (ORD).
http://www.epa.gov/subst/0045.htm [Accessed December, 2009].
Jo, W. K.; Weisel, C. P.; and Lioy, P. J. 1990. Chloroform exposure and the health risk
associated with multiple uses of chlorinated tap water. Risk Analysis, 10: 581-585.
Jobb, D.B., R.B. Hunsinger, O. Meresz, and V. Taguchi. 1994. Removal of N-
nitrosodimethylamine from the Ohsweken (Six Nations) water supply final report.
Ontario Ministry of Environment and Energy, Queen’s Printer for Ontario.
Judd, S. J.; and Black, S. H. 2000. Disinfection by-products formation in swimming pool
waters: A simple mass balance. Water Research, 34 (5): 1611-1619.
Judd, S. J.; and Bullock G. 2003. The fate of chlorine and organic materials in swimming
pools. Chemosphere, 5 (19): 869-879.
Judd, S. J.; and Jeffrey, J. A. 1995. Trihalomethane formation during swimming pool
water disinfection using hypobromous and hypochlorous acids. Water Research, 29
(4): 1203-1206.
244
Kaas, P.; and Rudiengaard, P. 1987. Toxicologic and epidemiologic aspects of
organochlorine compounds in bathing water. Paper presented to the 3rd Symposium
on ―Problems of swimming pool water hygiene‖, Reinhardsbrunn.
Karagas, M. R.; Villanueva, C. M.; Nieuwenhuijsen M.; Weisel, C. P.; Cantor, K. P.;
Kogevinas, M. 2008. Disinfection byproducts in drinking water and skin cancer? A
hypothesis. Cancer Causes Control, 19: 547-548.
Karanfil, T., Krasner, S. W., Westerhoff, P., and Xie, Y. 2008. Recent advances in
disinfection byproduct formation, occurrence, control, health effects, and
regulations. In: Disinfection By-Products in Drinking Water: Occurrence,
Formation, Health Effects, and Control. Karanfil, T., S. W. Krasner, P. Westerhoff,
Y. Xie eds. American Chemical Society: Washington, D. C.
Kim, H. 1997. Human exposure to dichloroacetic acid and trchloroacetic acid from
chlorinated water during household use and swimming. PhD Dissertation.
University of Medicine and Dentistry of New Jersey. New Brunswick, NJ.
Kim, H.; Shim, J.; and Lee, S. 2002. Formation of disinfection by-products in chlorinated
swimming pool water. Chemosphere, 46: 123-130.
King, W. D.; Dodds, L.; Armson, B. A.; Allen, A. C.; Fell, D. B.; Nimrod, C. 2004.
Exposure assessment in epidemiologic studies of adverse pregnancy outcomes and
disinfection byproducts. Journal of Exposure and Analytical Environmental
Epidemiology, 14:14466-14472.
King, W. D.; Marrett, L. D. 1996. Case-control study of bladder cancer and chlorination
by- products in treated water (Ontario, Canada). Cancer Causes Control, 7: 596-
604.
Kitis, M.; Karanfil, T.; Wigton, A.; Kilduff, J. E. 2002. Probing reactivity of dissolved
organic matter for disinfection by-product formation using XAD-8 resin adsorption
and ultrafiltration fractionation. Water Research, 36: 3834-3848.
Korich, D. G.; Mead, J. R.; Madore, M. S.; Sinclair, N. A.; and Stirling, C. R. 1990.
Effects of ozone, chlorine dioxide, chlorine and monochloramine on
cryptosporidium oocyst viability. Applied and Environmental Microbiology, 56 (5):
1423-1428.
Koski, T. A. Stuart, L. S. Ortenzio, L. F.1966. Comparison of Chlorine, Bromine, and
Iodine as Disinfectants for Swimming Pool Water. Applied Microbiology, 14,
(2):276-279.
245
Kozlowska, K.; Polkowska, Z.; Namiesnik, J. 2006. Effect of treated swimming pool
water on the levels of trihalomethanes in swimmer's urine. Toxicological and
Environmental Chemistry, 88 (2): 259-272.
Kramer, M. D.; Lynch, C. F.; Isacson, P.; Hanson, J. W. 1992. The association of
waterborne chloroform with intrauterine growth retardation. Epidemiology, 3: 407-
413.
Lagerkvist, J. B.; Bernard, A.; Blomberg, A.; Bergstrom, E.; Forsberg, B.; Holmstrom,
K.; Karp, K.; Lundstrom, N.; Segerstedt, B.; Svensson, M.; Nordberg, G. 2004.
Pulmonary epithelial integrity in children: Relationship to ambient ozone exposure
and swimming pool. Environmental Health Perspectives, 112: 1768- 1771.
Lahl, U.; Batjer, K.; Duszeln, J. V.; Gabel, B.; Stachel, B.; and Thiemann, W. 1981.
Distribution and balance of volatile halogenated hydrocarbons in the water and air
of covered swimming pools using chlorine for water disinfection. Water Research,
15:803-814.
Larson, R. A.; and Rockwell A. L. 1978. Citric zcid: Potential precursor of chloroform in
water chlorination. Naturwissnschaften, 65: 490.
Larson, R. A.; and Rockwell A. L. 1979. Chloroform and chlorophenol production by
decarboxylation of natural acids during aqueous chlorination. Environmental
Science and Technology, 13 (3):325-329.
Lee, J.; Ha, K.; Zoh, K. 2009. Characteristics of trihalomethane (THM) production and
associated health risk assessment in swimming pool waters treated with different
disinfection methods. Science of the Total Environment, 407: 1990-1997.
Lee, S. C.; Guo, H.; Lam, S.; Lau, S. 2004. Multipathway risk assessment on disinfection
by-products of drinking water in Hong Kong. Environmental Research, 94: 47-56.
Levesque, B.; Ayotte, P.; LeBlanc, A.; Dewailly, E.; Prud'Homme, D.; Lavoie, R.;
Allaire, S. Levallois, P. 1994. Evaluation of dermal and respiratory chloroform
exposure in humans. Environmental Health Perspectives, 102 (12): 1082-1087.
Levesque, B.; Ayotte, P.; Tardif, R.; Charest-Tardif, G.; Dewailly, E.; Prud’Homme, D.;
Gingras, G.; Allaire, S. 2000. Evaluation of the health risk associated with exposure
to chloroform in indoor swimming pools. Journal of Toxicology and Environmental
Health, Part A, 61: 225-243.
Li, J., Blatchley III, E. R., 2007. Volatile disinfection byproduct formation resulting from
chlorination of organic-nitrogen precursors in swimming pools. Environmental
Science and Technology 41 (19): 6732-6739.
246
Liang, L.; Singer, P. C. 2003. Factors influencing the formation and relative distribution
of haloacetic acids and trihalomethanes in drinking water. Environmental Science
and Technology, 37: 2920-2928.
Lindstrom, A. B.; Pleil, J. D.; and Berkoff, D. C. 1997. Alveolar breath sampling and
analysis to assess trihalomethane exposures during competitive swimming training.
Environmental Health Perspective, 105: 636–642.
Loos, R.; and Barcelo D. 2001. Determination of haloacetic acids in aqueous
environments by solid-phase extraction followed by ion-pair liquid
chromatography-electroscopy ionization mass spectrometric detection.
Chromatography A, 938: 45-55.
Mabey, W., and Mill, T. 1978. Critical review of hydrolysis of organic compounds in
water under environmental conditions. Journal of Physical and Chemical Reference
Data, 7 (2): 383-415.
Mallika, P.; Sarisak, S.; Pongsri, P. 2008. Cancer risk assessment from exposure to
trihalomethanes in tap water and swimming pool water. Journal of Environmental
Sciences, 20: 372-378.
Mannschott, P.; Erdinger, L.; and Sonntag, H. P. 1995. Determination of halogenated
organic compounds in swimming pool water. Zentralblatt für Hygiene und
Umweltmedizin, 197: 516-533.
Marina, L. S.; Ibarluzea, J.; Basterrechea, M.; Goñi, F.; Ulibarrena, E.; Artieda, J.;
Orruño, I. 2009. Indoor air and bathing water pollution in indoor swimming pools
in Guipúzcoa (Spain). Gaceta Sanitaria, 23 (2): 115-120. (in Spanish).
Martin, B.; Charest-Tardif, G; Krishnan, K. 2001. Blood: air partitioning coefficients of
individual and mixtures of THMs. Cheospher, 44: 377-381.
Massin, N.; Bohadana, A. B.; Wild,P.; Hery, M.; Toamain, J. P.; Hubert, G. 1998.
Respiratory symptoms and bronchial responsiveness in lifeguards exposed to
nitrogen trichloride in indoor swimming pools. Occupational and Environmental
Medicine, 55: 258–263.
Michael, L. T.; Rlchard A. Y.; and Carl J. M. 1986. Chlorination byproducts of amino
acids in natural waters. Environmental Science and Technology, 20 (11): 1117-
1122.
247
Miles, A. M.; Singer, P. C.; Ashley, D. L.; Lynberg, M. C.; Mendola, P.; Langlois, P. H.;
Nuckols, J. R. 2002. Comparison of trihalomethanes in tap water and blood.
Environmental Science and Technology, 36: 1692-1698.
Miller, J. W.; and Uden P. C. 1983. Characterization of nonvolatile aqueous chlorination
products of humic substances. Environmental Science and Technology, 17 (3): 150-
157.
Mitch, W.A. and Sedlak, D.L. 2002. Formation of N-nitrosodimethylamine (NDMA)
from dimethylamine during chlorination. Environmental Science and Technology,
36(4): 588-595.
Mitch, W.A., Krasner, S.W.; Westerhoff, P.; and Dotson, A. 2009. Occurrence and
formation of nitrogenous disinfection by-products. Project report for Water
Research Foundation: Denver, CO.
Mitch, W.A., Sharp, J.O.; Trussell, R.R.; Valentine, R.L.; Alvarez-Cohen, L.; and Sedlak,
D.L. 2003. N-nitrosodimethylamine (NDMA) as a drinking water contaminant: A
review. Environmental Engineering Science, 20(5): 389-404.
Morris, J. C.; Ram, N. M.; Baum, B.; Wajon, E. 1980. Formation and Significance of N-
Chloro Compounds in Water Supplies; U.S. Government Printing Office:
Washington, DC, EPA 600/2-80-031.
Morris, R. D.; Audet, A. M.; Angelillo, I. F.; Chalmers, T. C.; Mosteller F. 1992.
Chlorination, chlorination by-products, and cancer: A meta-analysis. American
Journal of Public Health, 82: 955-963.
Najm, I. and Trussell, R.R. 2001. NDMA formation in water and wastewater. Journal of
American Water Works Association, 93(2): 92-99.
National Sporting Goods Association, Mt. Prospect, IL. Sports Participation in 2006:
Series I and Series II (copyright). http://www.nsga.org/public/pages/index.cfm?
pageid=864[Accessed June 26, 2009].
Nieuwenhuijsen, M. J.; Toledano, M. B.; Eaton, N.; Fawell, J.; Elliott, P. 2000.
Chlorination disinfection byproducts in water and their association with adverse
reproductive outcomes: A review. Occupational and Environmental Medicine, 57:
73-85.
Nikolaou, A. D.; Lekkas, T. D.; Golfinopoulos, S. K. 2004. Kinetics of the formation and
decomposition of chlorination by-products in surface waters. Chemical Engineering
Journal, 100: 139-148.
248
NRC, National Research Council, 1983. Risk Assessment in the Federal Government:
Managing the Process, Committee on the Institutional Means for Assessment of
Risks to Public Health, Commission on Life Sciences, NRC, Washington, DC,
National Academy Press.
NRC, National Research Council. 1994. Science and Judgment in Risk Assessment.
Washington, DC: National Academy Press.
NSPF, 2006. Certified Pool-Spa Operator Handbook. National Swimming Pool
Foundation, Colorado Springs, CO.
Nuckols, J. R.; Ashley, D. L.; Lyu, C.; Gordon S. M.; Hinckley, A. F.; Singer, P. 2005.
Influence of tap water quality and household water use activities on indoor air and
internal dose levels of trihalomethanes. Environmental Health Perspective, 113:
863-870.
Obolensky, A.; and Singer, P. C. (2005) Halogen substitution patterns among disinfection
byproducts in the information collection rule database. Environmental Science and
Technology, 39 (8): 2719-273.
Page, T.; Harris, R. H.; Epstein, S. S. 1976. Drinking water and cancer mortality in
Louisiana. Science, 193: 55-57.
Pehlivanoglu-Mantas, E., Hawley, E.L., Deeb, R.A., Sedlak, D.L., 2006. Formation of
nitrosodimethylamine (NDMA) during chlorine disinfection of wastewater effluents
prior to use in irrigation systems. Water Research, 40 (2): 341-347.
Planas, C.; Palacios, S.; Ventura, F.; Rivera, J.; Caixacha, J. 2008. Analysis of
nitrosamines in water by automated SPE and isotope dilution GC/HRMS
Occurrence in the different steps of a drinking water treatment plant, and in
chlorinated samples from a reservoir and a sewage treatment plant effluent. Talanta,
76: 906-913.
Plewa, M. J.; Muellner, M. G.; Richardson, S. D.; Francesca Fasano, Buettner, K. M.;
Woo, Y.; McKague, A. B.; and Elizabeth D. Wagner, E. D. 2008a. Occurrence,
synthesis, and mammalian cell cytotoxicity and genotoxicity of haloacetamides, an
emerging class of nitrogenous drinking water disinfection byproducts.
Environmental and Science and Technology, 42: 955-961.
Plewa, M. J.; Wagner, E.; Muellner, M.; Hsu, K.; Richardson, S. 2008b. Chapter 3:
Comparative mammalian cell toxicity of nitrogen containing disinfection by-
products and carbonaceous disinfection by-products. In: Occurrence, Formation,
Health Effects and Control of Disinfection By-Products in Drinking Water.
249
Karanfil, T; Krasner, S.; Westerhoff, P.; and Xie, Y. American Chemical Society
Symposium series 995.
Pool Operation Management. 2009. www.pooloperationmanagement.com/regulations.
htm. [accessed February,14 2009].
Puchert, W. 1994. Determination of volatile halogenated hydrocarbons in different
environmental compartments as basis for the estimation of a possible pollution in
West Pommerania. Dissertation. Bremen, University of Bremen (in German).
Puchert, W.; Prosch, J.; Koppe, F. G.; and Wagner, H. 1989. Occurrence of volatile
halogenated hydrocarbons in bathing water. Acta Hydrochimica et Hydrobiologica,
17: 201-205.
Putnam, D. F. 1971. Composition and concentrative properties of human urine. NASA
Contractor Report CR-1802.
PWTAG, Pool Water Treatment Advisory Group. 1999. Swimming pool water treatment
and quality standards. BC Publications, UK.
RAIS, Risk Assessment Information System. 2009.
http://rais.ornl.gov/homepage/rap_docs.shtml.
Reckhow, D. 2008. Can treatment and occurrence research keep up with the CCL
process? The case of DBPs (and PPCPs). Research Committee Seminar on CCL3
VA section AWWA.
Reiss, R.; Schoenig, G.; and Wright, G. 2006. Development of factors for estimating
swimmers’ exposures to chemicals in swimming pools. Human and Ecological Risk
Assessment, 12: 139-156.
Richardson S. D.; Simmons J. E.; Rice G. 2002. Disinfection byproducts: The next
generation, Environmental Science and Technology, 36: 198A-205A.
Richardson, S. D. 2003. Disinfection by-products and other emerging contaminants in
drinking Water. Trends in Analytical Chemistry, 22 (10): 666-684.
Richardson, S. D.; Plewa, M. J.; Wagner E. D.; Schoeny R.; and DeMarini D. M. 2007.
Occurrence, genotoxicity, and carcinogenicity of regulated and emerging
disinfection by-products in drinking water: A review and roadmap for research.
Mutation Research, 636: 178-242.
Richardson, S. D.; Thruston, A. D.; Caughran, T. V.; Chen, P. H.; Collette, T. W.; Floyd,
T. L. 1999. Identification of new drinking water disinfection by products formed in
250
the presence of bromide. Environmental Science and Technology, 33 (19): 3378-
3383.
Rodriguez, M. J.; Serodesb, J.; Royc, D. 2007. Formation and fate of haloacetic acids
(HAAs) within the water treatment plant. Water Research, 41: 4222-4232.
Rogozen, M. B.; Rich, H. E.; Guttman, M. A.; Grosjean, D.; Williams, E. L.; 1988.
Sources and Concentrations of Chloroform Emissions in the South Coast Air Basin.
Final Report to the State of California Air Resources Board. Science Applications
International Corporation, Contract A4-115-32.
Rook, J. J. 1974. Formation of haloforms during chlorination of natural waters. Journal
of Water Treatment and Examination, 23: 234-243.
Rook, J. J. 1976. Haloforms in drinking water. Journal of American Water Works
Association, 68: 168-172.
Sandel, B. B. 1990. Disinfection by-products in swimming pools and spas. Olin
Corporation Research Center (Report CNHC-RR-90-154) (available from Arch
Chemical, Charleston, NC).
Sarrion, M. N.; Santos, F. J.; and Galceran, M. T. 2000. In situ derivatization/solid-phase
microextraction for the determination of haloacetic acids in water. Analytical
Chemistry, 72: 4865-4873.
Savitz, D. A.; Singer, P. C.; Hartmann, K. E.; Herring, A. H.; Weinberg, H. S.;
Makarushka, C.; Hoffman, C.; Chan, R.; Maclehose, R. 2005. Drinking Water
Disinfection By-products and Pregnancy Outcome, American Water Works
Association Research Foundation, Report, Denver, CO.
SBI. Specialist In Business Information, 2007. U.S. market for swimming pool
equipment and maintenance products.
www.marketresearch.com/map/prod/1461666.html. Published by: SBI, May. 1,
2007 (142 Pages) [accessed September,21 2008].
SC DHEC, South Carolina Department of Health and Environmental Control. 2007. R.
61-51 Public Swimming Pools. Bureau of Water.
Scholer, H. F.; Schopp, D. 1984. Volatile halogenated hydrocarbons in swimming pool
waters. Forum Stadte-Hygiene, 35: 109–112 (in German).
Schreiber, I.M., Mitch, W.A., 2006. Nitrosamine formation pathway revisited: the
importance of chloramine speciation and dissolved oxygen. Environmental Science
and Technology, 40 (19): 6007-6014.
251
Schreiber, I.M., Mitch, W.A., 2007. Enhanced nitrogenous disinfection byproduct
formation near the breakpoint: Implications for nitrification control. Environmental
Science and Technology, 41(20): 7039-7046.
Scully, F. E.; Howell, G. D.; Kravltz, R.; Jewel, J. T. 1988. Proteins in natural waters and
their relation to the formation of chlorinated organics during water disinfection.
Environmental Science and Technology, 22 (5): 537-542.
Sedlak, D.L., Deeb, R.A., Hawley, E.L., Mitch, W.A., Durbin, T.D., Mowbray, S., Carr,
S., 2005. Sources and fate of nitrosodimethylamine and its precursors in municipal
wastewater treatment plants. Water Environmental Research, 77 (1): 32-39.
Seux, R., 1988. Evolution de la pollution apportée par les baigneurs dans les eaux de
piscines sous l’action du chlore. Journal Francais d'Hydrologie, 19: 151-168. (in
French).
Simard, S. 2009. Occurrence des sous-produits de la désinfection dans l’eau des piscines
publiques de la ville de Québec. [Occurrence of disinfection by-products in water of
public swimming pools of Quebec]. Master thesis. Faculty of Graduate Studies at
the University Lavaldans le cadre du programme de maîtrise en génie civil under
the master's program in civil engineering. (in French).
Singer, P. C.; Winberg, H. S.; Brophy, K.; Liang, L.; Roberts, M.; Grissted, I.; Krasner,
S.; Baribeau, H.; Arora, H.; and Najm, I. 2002. Relative Dominance of Haloacetic
Acids and Trihalomethanes in Treated Drinking Water. American Water Works
Association Research Foundation, Report, Denver, CO.
Stack, M. A.; Fitzgerald, G.; OConnell, S.; and James, K. J. 2000. Measurement of
trihalomethanes in potable and recreational waters using solid phase micro
extraction with gas chromatography-mass spectrometry. Chemosphere, 41: 1821-
1826.
Standard Methods for the Examination of Water and Wastewater. 1995.19th ed. APHA,
AWWA, and WEF, Washington.
Stottmeister, E. 1998. Disinfection by-products in German swimming pool waters. Paper
presented to 2nd International Conference on Pool Water Quality and Treatment, 4
March 1998, School of Water Sciences, Cranfield University, Cranfield, UK.
Stottmeister, E. 1999. Occurrence of disinfection by-products in swimming pool waters.
Umweltmedizinischer Informationsdienst, 2: 21–29 (in German).
252
Stottmeister, E.; Naglitsch, F. 1996. Human exposure to other disinfection by-products
than trihalomethanes in swimming pools. Annual report of the Federal
Environmental Agency, Berlin, Germany.
Suslow, T. 2001. Water disinfection: A practical approach to calculating dose values for
preharvest and postharvest applications. University of California, Agriculture and
Natural Resources. Publication 7256.
Tachikawa, M; Aburada,T.; Tezuka, M.; Sawamura, R. 2005. Occurrence and production
of chloramines in the chlorination of creatinine in aqueous solution. Water
Research, 39: 371–379.
Thacker, N. P.; and Nitnaware, V. 2003. Factors influencing formation of
trihalomethanes in swimming pool water. Bulletin of Environmental Contamination
and Toxicology, 71: 633-640.
Thickett, K.M., McCoach, J.S., Gerber, J.M., Sadhra, S., Burge, P.S., 2002. Occupational
asthma caused by chloramines in indoor swimming-pool air. European Respiratory
Journal 19 (5): 827 832.
Tintometer GmbH. 2006. The Lovibond Handbook of Swimming Pool and Spa Water
Treatment. 2nd edition.
www.tintometer.de/wordpress/other/handbook_gb_print.pdf [accessed Aug. 25,
2008].
Tokmak, B.; Capar, G.; Dilek, F.; Yetis, U. 2004. Trihalomethanes and associated
potential cancer risks in the water. Environmental Research, 96: 345-352.
Trehy, M. L.; Yost,R. A.; Miles, C. J. 1986. Chlorination Byproducts of Amino Acids in
Natural Waters. Envlronmental Scence and Technology, 20, 1117-1122.
Uhl, W. 2007. Pool water treatment and disinfection: current practice and new
developments, 2nd International Conference on Health and Water Quality Aspects
of the Man Made Recreational Water Environment, March 14-16, Munich,
Germany.
Uhl, W.; and Hartmann, C. 2005. Disinfection by-products and microbial contamination
in the treatment of pool water with granular activated carbon. Water Science and
Technology, 52 (8): 71-76.
US Census Bureau. 2009 Statistical Abstract of the United States. Recreation and leisure
activities: participation in selected sports activities 2006. Available at
http://www.census.gov/compendia/statab/Tables/09s1209.pdf. [Accessed June, 26
2009].
253
US EPA. 1989. Risk Assessment Guidance for Superfund, Volume 1, Human Health
Evaluation Manual (Part A). Office of Emergency and Remedial Response.
EPA/540/1-89/002. Washington, DC.
US EPA. 1991. Risk Assessment Guidance for superfund—Vol. I, Part B. Washington,
DC: US Environmental Protection Agency; EPA/540/R 92/003.
US EPA. 1993. Reference Dose (RfD): Description and Use in Health Risk Assessments,
Background Document 1A March 15, 1993. http://www.epa.gov/iris/rfd.htm.
[accessed March, 2010]
US EPA. 1997. Exposure Factors Handbook Revised. EPA/600/P-95/002F.
Environmental Protection Agency, Washington, DC.
US EPA. 1999. Guidelines for carcinogen risk assessment. Risk assessment forum U.S.
Environmental Protection Agency, Washington, DC; NCEA-F-0644.
US EPA. 2003a. User's manual swimmer exposure assessment model (SWIMODEL)
Version 3.0. U.S. Environmental Protection Agency Office of Pesticide Programs
Antimicrobials Division.
US EPA. 2003b. Swimmer exposure assessment model, www.epa.gov/
oppad001/swimodel.htm
US EPA. 2004. Method 521: Determination of Nitrosamines in Drinking Water by Solid
Phase Extraction and Capillary Column Gas Chromotography with Large Volume
Injection and Chemical Ionization Tandem Mass Spectrometry (MSMS). Vesion
1.0. EPA Document #: EPA/600/R-05/054.
US EPA. 2005. Guidelines for Carcinogen Risk Assessment. Risk Assessment Forum
U.S. Environmental Protection Agency, Washington, DC; EPA/630/P/03/001F.
US EPA. 2005. Unregulated Contaminant Monitoring Regulation (UCMR) for Public
Water Systems Revisions. Fed. Regist. 70 (161). August 22, 2005.
US EPA. 2006. National Primary Drinking Water Regulations: Stage 2 Disinfectants and
Disinfection Byproducts Rule; Final Rule. http://www.epa.gov/fedrgstr/EPA-
WATER/2006/January/Day-04/w03.pdf.
US EPA. 2009a. Integrated Risk Information System (electronic data base). U.S.
Environmental Protection Agency, Washington DC. Available at:
http://www.epa.gov/iris [Accessed June, 2009].
254
US EPA. 2009b. Exposure Factors Handbook: 2009 update. EPA/600/R-09/052a.
Environmental Protection Agency, Washington, DC.
Villanueva, C. M.; Cantor K. P.; Grimalt J. O.; Castano-Vinyals G.; Malats, N.;
Silverman, D.; Tardon, A.; Garcia-Closas R.; Serra C.; Carrato A. 2006.
Assessment of lifetime exposure to trihalomethanes through different routes,
Occupational and Environmental Medicine, 63: 273-277.
Villanueva, C. M.; Cantor, K. P.; Cordier, S.; Jaakkola, J. J.; King, W. D.; Lynch, C.F.;
Porru, S.; Kogevinas, M. 2004. Disinfection byproducts and bladder cancer: A
pooled analysis. Epidemiology, 15 (3): 357-367.
Villanueva, C. M.; Cantor, K. P.; Grimalt, J. O.; Malats, N.; Silverman, D.; Tardon, A;
Garcia C, R.; Serra, C.; Carrato, A.; Castano-Vinyals, G.; Marcos, R.; Rothman, N.;
Real, F. X.; Dosemeci, M.; and Kogevinas, M. 2007a. Bladder cancer and exposure
to water disinfection by products through ingestion, bathing, showering and
swimming in pools. American Journal of Epidemiology, 165: 148-156.
Villanueva, C. M.; Gagniere, B.; Monfort, C.; Nieuwenhuijsen, M. J.; and Cordier, S.
2007b. Sources of variability in levels and exposure to trihalomethanes.
Environmental Research, 103: 211-220.
Wachter, J. K.; and Andelman, J. B. 1984. Organohalide Formation on Chlorination of
Algal Extracellular Products. Envlronmental Science and Technology, 18 (11): 811-
817
Waller, K.; Swan, S. H.; DeLorenze, G.; Hopkins, B. 1998. Trihalomethanes in drinking
water and spontaneous abortion. Epidemiology 9:134–140.
Walse, S.; and Mitch W. 2008. Nitrosamine carcinogens also swim in chlorinated pools.
Environmental Science and Technology, 42: 1032-1037.
Wang, G.; Deng, Y.; Lin, T. 2007. Cancer risk assessment from trihalomethanes in
drinking water. Science of the Total Environment, 387: 86-95.
Weaver, W. W.; Li, J.; Wen, Y.; Johnston, J.; Blatchley, M. R.; Blatchley III, E. R.
2009.Volatile disinfection by-product analysis from chlorinated indoor swimming
pools. Water Research, 43: 3308-3318.
Weisel, C. P; Chen, W. J. 1994. Exposure to chlorination byproducts from hot water use.
Risk Analysis, 14 (1):101–106.
Westerhoff, P.; Chao, P.; Mash, H. 2004. Reactivity of natural organic matter with
aqueous chlorine and bromine. Water Research, 38: 1502-1513.
255
Whitaker, H.; Nieuwenhuijsen, M. J.; Best, N. 2003. The relationship between water
concentrations and individual uptake of chloroform: A simulation study.
Environmental Health Perspective, 111: 688-94.
White, G. C. 1999. Handbook of Chlorination and Alternative Disinfectants, 4th edition.
Wiley, New York, 213-219.
WHO (World Health Organization). 2004. Guidelines for Drinking-water Quality, 3rd
edition, Volume 1, Recommendations, World Health Organization, Geneva.
WHO. (World Health Organization). 2000. Environmental health criteria: Disinfectants
and disinfectant by-products. World Health Organization, Geneva.
WHO. (World Health Organization). 2006. Guidelines for Safe Recreational Water
Environments, volume 2: swimming pools and similar environments. Geneva.
Wilczak, A.; Assadi-Rad, A.; Lai, H.H.; Hoover, L.L.; Smith, J.F.; Berger, R.; Rodigari,
F.; Beland, J.W.; Lazzelle, L.J.; Kinicannon, E.G.; Baker, H.; and Heaney, C.T.
2003. Formation of NDMA in chloraminated water coagulated with DADMAC
cationic polymer. Journal of American Water Works Association, 95(9): 94-106.
Xu, X.; Mariano, T. M.; Laskin, J. D.; Weisel C. P. 2002. Percutaneous absorption of
trihalomethanes, haloacetic acids, and haloketones. Toxicology and Applied
Pharmacology, 184: 19-26.
Xu, X.; Weisel, C. P. 2005. Human respiratory uptake of chloroform and haloketones
during showering. Journal of Exposure and Analytical Environmental
Epidemiology, 15: 6–16.
Yang, C. Y.; Cheng, B. H.; Tsai, S. S.; Wu, T. N.; Lin, M. C.; Lin, K. C. 2000.
Association between chlorination of drinking water and adverse pregnancy outcome
in Taiwan. Environmental Health Perspective, 108: 765-768.
Yang, C. Y.; Chiu, H. F.; Cheng, M. F.; Tsai, S. S. 1998. Chlorination of drinking water
and cancer mortality in Taiwan. Environmental Research, 78: 1-6.
Yang, C. Y.; Chiu, J. F.; Chiu, H. F.; Wang, T. N.; Lee, C. H.; Ko, Y. C. 1996.
Relationship between water hardness and coronary mortality in Taiwan. Journal of
Toxicology and Environmental Health, 49: 1-9.
Zhang, X. and. Minear, R. A. Decomposition of trihaloacetic acids and formation of the
corresponding trihalomethanes in drinking water. Water Research, 36: 3665–3673.
256
Zhao, Y.-Y., Boyd, J.M., Woodbeck, M., Andrews, R.C., Qin, F., Hrudey, S.E., Li, X.-F.,
2008. Formation of N-nitrosamines from eleven disinfection treatments of seven
different surface waters. Environmental Science and Technology, 42 (13): 4857-
4862.
Zhuo, C.; Chengyong, Y.; Junhe, L.; Huixian, Z.; Jinqi, Z. 2001. Factors on the formation
by-products MX, DCA and TCA by chlorination of fulvic acid from lake sediments.
Chemosphere, 45: 379-385.
Zwiener, C. 2007. Disinfection by-products- precursors, Reaction processes, products,
and prevention. Proceedings of World Aquatic Health Conference, National
Swimming Pool Foundation, October 2-4, 2007, Cincinnati, OH.Zwiener, C.;
Richardson S. D.; De Marini D. M.; Grummt T.; Glauner T. and Frimmel F. H.
2007. Drowning in disinfection byproducts: assessing swimming pool water.
Environmental Science and Technology, 41 (2): 363-372.
Zwiener, C.; Richardson S. D.; De Marini D. M.; Grummt T.; Glauner T. and Frimmel F.
H. 2007. Drowning in disinfection byproducts: assessing swimming pool water.
Environmental Science and Technology, 41 (2): 363-372.
