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SR301230
TCN 4204RI REPORTREV. II
30/SEPT/91
aR30!23i
TCN 4204RI REPORTREV. #1
30/SEPT/91
AR30I232
TETRA TECH INC. - BORING LOG SHEET: 1 OF
PROJECT: Butz Landfill PROJECT NO. T4204-03BORING DESIGNATION; Failed T5 Borings (3) DATE(S) DRILLED: 12/06/90DRILLING CONTRACTOR; Walton Drill ing Corp. DRILLING METHOD: Hollow-Stem AugerBORING DIAMETER: 8" SAMPLING INTERVAL: NASAMPLING METHOD; Cuttings TOTAL DEPTH:LOGGED BY: R. H. BoedekerGROUT TYPE: NA GROUT METHOD: NASTATIC WATER DEPTH: REFERENCE:DATE:REMARKS: Four borings were driTiled in an attempt to install well "T5" downgradient from
well T2. The first 3 borings were not used because no ground water was encounteredor because of the shallow depth to bedrock.
LITHOL06ICINTERVAL
SAMPLEINTERVAL SPOOK BLOWS RECOVERY
CLASSIFICATIONOF MATERIAL
Boring 10.0-6.0 Water level
9 1.0'Auger refusal @ 6.0* (fine sandstone bedrock, trace shales);moved to new location
Boring 20.0-6.5 No water
encounteredAuger refusal 9 6.5' (brown andgray shales laying over fine sandstones); moved to new location
Boring 30.0-7.2 No water
encounteredAuger refusal 9 7.2'
flR30i233
TETRA TECH INC. - HELL DRILLING LOG
PROJECT: Butz LandfillWELL DESIGNATION: T5DRILLING CONTRACTOR: Walton CorporationBORING DIAMETER: 8"SAMPLING INTERVAL: NA
PERMIT NO.SHEET: 1 OF 1PROJECT NO. T4204-03 ^DATE(S) DRILLED: 12/07/90 P|DRILLING METHOD: Hollow-Stem AugerSAMPLING METHOD: CuttingsTOTAL DEPTH: 17'
LOGGED BY: R. H. BoedekerSCREENED SIZEAND MATERIAL: 4" PVC 0.010" SlotCASING SIZE AND MATERIAL: 4" PVCGRAVEL PACK SIZE: #2 Morie sandGROUT TYPE: Type I cementGROUTING METHOD: GravityDEVELOPMENT MechanicalMETHOD: Surging/Pumping TIME:STATIC WATER DEPTH: 10.49' DATE: 12/13/90
REMARKS:
LITHOLOGICINTERVAL
0.0-8.58.5-16.0
16.0-17.0
17.0
SCREENED INTERVAL: 17-8. 5 'CASED INTERVAL: 8.5-0'PACKED INTERVAL: 17-7.0'GROUTED INTERVAL: 5.4'-0BENTONITE SEAL: 7.0-5.4"ESTIMATEDYIELD: <1 gpmREFERENCE: top of casing
SAMPLEINTERVAL SPOOK BLOWS RECOVERY
CLASSIFICATIONOF MATERIAL
Clayey silt: reddish brownSandstone: light green; weatheredShale: redAUGER REFUSAL - END OF BORING
II
——— 4~HR3QI23U
TCN 4204RI REPORT
REV. #130/SEPT/91
WELL SAMPLING DATA
SR301236
WELL/SAMPLE DESIGNATION: , R1S
DEPTH TO WATER 12.70 ft WELL VOLUME " 131 gala
TOTAL DEPTH 103.0 ft PURGE METHOD Pump
WELL DIAMETER 6 inches DATE PURGED 10/30/90
TIME pH TEMP CONDUCTIVITY1000 -_____ - 200 umhos1020 6.14 - 2301040 6.34 - 240
NOTES: Temp, probe not operating correctly. Purged at 10 gpmfor approximately 40 minutes or total of 400 gals.
WELL/SAMPLE DESIGNATIONS TlAi
DEPTH TO WATER 11.52 ft WELL VOLUME 1.14 gals
TOTAL DEPTH 17.7 ft PURGE METHOD Pumo
WELL DIAMETER 2 inches DATE PURGED 10-30-90
TIME pH TEMP CONDUCTIVITY1038 6.32 - 2601046 6.34 - 260
NOTES: Temp, probe not working. Pumped 1.5 gpm for 11 minutesor total volume of 16.5 gals.
•• ' -<'• '•••• •••" ••''^ • '•:""::
DEPTH TO WATER 11.16 ft WELL VOLUME 2.28 gals
TOTAL DEPTH 21.0 ft PURGE METHOD Pump
WELL DIAMETER 2 inches DATE PURGED 10-30-90
TIME pH TEMP CONDUCTIVITY1347 6.32 _r_____ 901352 6.41 _r_____ 2401354 6.38 _r_____ 1801359 6.33 _j:_____ 280
NOTES: Temp, probe not working. Purged 1.5 gpm for 15 minutesor total of 22.5 gals.
5R30I237
iDEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME
WELL/SAMPLE
20.27 ft
244 ft
6 inches
pH
DESIGNATION: RID
WELL
PURGE
DATE
TEMP
VOLUME 337 qals
METHOD Pump
PURGED 10-30-90
CONDUCTIVITY
NOTES: Pumped at 5 gpm through carbon cannister on and off allday. Low yield prevented constant pumping. Pumped approximately337 gals.
WELL/SAMPLE DESIGNATIONS Rl.lB
DEPTH TO WATER ____12.99 ft WELL VOLUME 254 aals
TOTAL DEPTH _____184.5 ft PURGE METHOD Pump
WELL DIAMETER 6 inches DATE PURGED 10/31/90
TIME pH TEMP CONDUCTIVITY- 6.29 -___ 190 umhoa- 6.02 - 100- 5.92 - 65
_____ 5.89 - 75
NOTES: Temp, probe not operating correctly. Purged at 8 gpmuntil dry or total of approximately 250 gals.
WELL7SAMg£B BESIGHaglOB:: TI. IS
DEPTH TO WATER 12.20 ft WELL VOLUME 0.37 aals
TOTAL DEPTH 14.5 ft PURGE METHOD Pump
WELL DIAMETER 2 inches DATE PURGED 10-31-90
TIME pH TEMP CONDUCTIVITY0911 5.46 - 300930 5.80 - 500943 5.87 - 50
NOTES: Temp, probe not working. Pumped total of 7.5 gals,
| : WELS/SAMPLE DESIGNATION* Rl.lA ||
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME12551400
22.76 ft WELL VOLUME 266 qals
204 ft PURGE METHOD Pump
6 inches DATE PURGED 10-31-90
pH TEMP CONDUCTIVITY7.13 11 C 1065.76 - 120
NOTES : Purged580 gals.
10 gpm for 58 minutes or until dry for total of
j - WELL/SAMPLE DESIGNATION* Tl. 1A ; |
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME
13.55 ft WELL VOLUME 1.25 qals
15.45 ft PURGE METHOD Bailer
4 inches DATE PURGED 10/31/90
pH TEMP CONDUCTIVITY
NOTES : Bailed well until dry. Removed total of 1.25 gals.
P "-••': ' •• '• • : *ji ' ' ' v?" ••<• 1
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME1350141314301455
10.0 ft WELL VOLUME 185 aals
136.5 ft PURGE METHOD Pump
6 inches DATE PURGED 10-31-90
pH TEMP CONDUCTIVITY6.50 11 C 958.75 10.5 1456.38 11.0 1426.61 11.0 153
NOTES: Pumped between 6.6 and 9 gpm for total of 595 gals.Pumped water through carbon cannister.
DEPTH TO WATER
TOTAL DEPTH
WE'LL DIAMETER
TIME
WELL/ SAMPLE
3.2 ft
19.3 ft
2 inches
pH5.90
DESIGNATION: T2
WELL VOLUME 2.6 qals
PURGE METHOD Pump
DATE PURGED 10-31-90
TEMP CONDUCTIVITY13 C 209
NOTES : Purged
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME084509151035
2 gpm for for 7
WELL/SAMPLE
47.51 ft
243 ft
6 inches
PH7.577.477.38
minutes for total of 14 gals.
DESIGNATION: R3D ||
WELL VOLUME 285 aals
PURGE METHOD Pump
DATE PURGED 11-01-90
TEMP CONDUCTIVITY11 C 12110.5 10711.0 112
NOTES : Pumped
1DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME09350950
7.5 gpm for 110 minutes for total of 825 gals.
WELL/SAMPLE
28.65 ft
118 ft
6 inches
pH9.9310.44
DESIGNATIONS R3S
WELL VOLUME 129 qals
PURGE METHOD Pump
DATE PURGED 11-01-90
TEMP CONDUCTIVITY10.5 C 12711 127
NOTES: Pumped one well volume (129 gals) until dry.
\ WELL/SAMPLE DESIGNATION: T3 ||
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME
19.08 ft WELL VOLUME 6 aals
28 ft PURGE METHOD Pump
4 inches DATE PURGED 11-01-90
pH TEMP CONDUCTIVITY5.94 11 C 1165.67 12 104
NOTES : Purgeduntil dry.
1.25 gpm for 7 minutes for total of 8.75 gals
| WELL/SAMPLE DESIGNATION: T4 ||
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME133413411355
10.50 ft WELL VOLUME 6 qals
21.5 ft PURGE METHOD Pump
4 inches DATE PURGED 11-01-90
pH TEMP CONDUCTIVITY5.53 12 C 1124.99 12 1035.10 12 90
NOTES : Pumped 1 gpm for 21 minutes for total of 21 gals.
f '• '. ' •••'•• ;l: i' -;: WEIiIi/SAKPLB/' DESIGNATION '' ' |
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME145615301555
15.50 ft WELL VOLUME 187 aals
150 ft PURGE METHOD Pump
6 inches DATE PURGED 11-01-90
pH TEMP CONDUCTIVITY6.51 10.5 C 1505.92 11 836.17 11 85
NOTES: Pumped at 10 gpm for 59 minutes of total of 590 gals,
AR30I2M
| WELL/SAMPLE DESIGNATION: R6
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME
—
14.50 ft
248 ft
6 inches
pH7.395.88
WELL
PURGE
DATE
TEMP10 C11
VOLUME 335 aals
METHOD Pump
PURGED 11-02-90
CONDUCTIVITY11274
NOTES: Pumped at average of 8.5 gpm for 41 minutes for total of348.5 gals. Well was pumped dry.
f WELL/SAMPLE DESIGNATION i R5
DEPTH
TOTAL
WELL
TO WATER
DEPTH
DIAMETER
TIME1140 •12071220
9.76 ft
250 ft
6 inches
pH6.176.206.21
WELL
PURGE
DATE
TEMP11 C1111
VOLUME 353 aals
METHOD Pump
PURGED 11-02-90
CONDUCTIVITY747574
NOTES: Pumped at 10 gpm for 106 minutes of total of 1060 gals.
WELL SAMPLING DATA
AR30l2if3
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME132913491410
NOTES : Purged410 gals.
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME135514001405
NOTES : Bailed
f, ::,,:,,,.,;DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME143214411448
WELL/SAMPLE DESIGNATIONS R1S |
12.96 ft WELL VOLUME 131 aals
103.0 ft PURGE METHOD Pump
6 inches DATE PURGED 12/03/90
pH TEMP CONDUCTIVITY6.62 9 3406.58 11 440
11 430
at 10 gpm for approximately 41 minutes or total of
WELL/SAMPLE DESIGNATION* • tfi&'& .y;---' • '.. ||
11.90 ft WELL VOLUME 1.14 qals
17.7 ft PURGE METHOD Bailer
2 inches DATE PURGED 12-03-90
pH TEMP CONDUCTIVITY6.56 10 4104.95 11 - 4155.00 11 413
total of 4 gals.
':& ''WBM,/S&Wjy:i:! BBS GNATIOIJ ^ ' ' ; f
11.85 ft WELL VOLUME 1.50 qals
21..0 ft PURGE METHOD Bailer
2 inches DATE PURGED 12-03-90
pH TEMP CONDUCTIVITY10 1059 1709 110
NOTES: pH meter wet, not working. Bailed total of 4 gals,
| WELL/SAMPLE DESIGNATION: RID ||
WELL/SAMPLE DESIGNATION RID
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME
"20 ft WELL VOLUME
244 ft PURGE METHOD Pump
6 inches DATE PURGED 12
pH TEMP CONDUCTIVITY
NOTES: After 1 HP pump lost in well R1.1A, only 1/2 HP could beused in this well. Pump could only be set to 100' depth,Purging not continuous.
1 WELL/SAMPLE DESIGNATION: R1.1B ||
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME094810191049
13.93 ft
184.5 ft
6 inches
pH5.565.605.90
WELL VOLUME 254 aals
PURGE METHOD Pump
DATE PURGED 12-03-90
TEMP CONDUCTIVITY10 11011 9010 92
NOTES : PurgedPump was lost
1DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME103610401048
at 6.5 gpm for 61 minutes for total of 396.5 gals.in well after purging complete-no sample collected.
WELL/ SAMPLE
12.25 ft
14.5 ft
2 inches
pH5.575.475.46
DESIGNATIONS Tl. IB
WELL VOLUME 0.37 aals
PURGE METHOD Bailer
DATE PURGED 12-03-90
TEMP CONDUCTIVITY9 6510 6510 60
NOTES: Bailed total of 1.5 gals.
WELL/SAMPLE DESIGNATIONS R1.1A
DEPTH TO WATER _________ WELL VOLUME
TOTAL DEPTH 204 ft PURGE METHOD.
WELL DIAMETER 6 inches DATE PURGED
TIME pH TEMP CONDUCTIVITY
NOTES: Pump stuck in well. Abandoned after numerous attempts toremove it. No sample collected.
| WELL/SAMPLE DESIGNATION? Tl»IA ||
DEPTH TO WATER 13.60 ft WELL VOLUME 1.25 gala
TOTAL DEPTH 15.45 ft PURGE METHOD Bailer
WELL DIAMETER 4 inches DATE PURGED 12-03-90
TIME pH TEMP CONDUCTIVITY1508 - 9 120
NOTES: Bailed well until dry. Removed total of 0.75 gals.pH meter not working.
'" : ; "'"'-'-' :':v:' ;'WBLI»ySftMP -;y— -• • • -• — _u .... • * -—————————-r—-_—-—.-! _ ._ -
DEPTH TO WATER 9.04 ft WELL VOLUME 185 gals
TOTAL DEPTH 136.5 ft PURGE METHOD Pump
WELL DIAMETER 6 inches DATE PURGED 12-04-90
TIME pH TEMP CONDUCTIVITY1517 9.26 7 C 1401602 8.30 8 1401630 8.56 10.5 140
NOTES: Pumped 7 gpm for 73 minutes for total of 511 gals. Pumpedthrough carbon cannister. Readings taken of filtered water.
DEPTH TO WATER
TOTAL DEPTH
rfELL DIAMETER
TIME132913341339
WELL/ SAMPLE
3.2 ft
19.3 ft
2 inches
pH6.586.626.47
DESIGNATION: T2 |
WELL VOLUME 2.6 qals
PURGE METHOD Bailer
DATE PURGED 12-04-90
TEMP CONDUCTIVITY10 C 2509.5 25510.5 260
NOTES : Purged
IDEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME105612451440
1 gpm for for 10 minutes for total of 10 gals.
WELL/SAMPLE
47.85 ft
243 ft
6 inches
pH7.198.848.86
DESIGNATION: R3D
WELL VOLUME 285 aals
PURGE METHOD Pump
DATE PURGED 12-04-90
TEMP CONDUCTIVITY10 C10.210.4
NOTES : Pumped806.4 gals.
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME12351307
average of 3.6
WELL/SAMPLE
30.00 ft
118 ft
6 inches
pH9.9310.44
gpm for 224 minutes for total of
DESIGNATIONS R3S r 1 i; ||
WELL VOLUME 129 aals
PURGE METHOD Pump
DATE PURGED 12-04-90
TEMP CONDUCTIVITY10.5 C 18411 206
NOTES: Pumped 165 gals until dry.
t - • '" : : : • • ' ;'• ':•• • :-.' • '|,
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME114011471157
WELL/SAMPLE
19.20 ft
28 ft
4 inches
pH7.316.206.02
DESIGNATIONS T3 |J
WELL VOLUME 6 aals
PURGE METHOD Pump
DATE PURGED 12-04-90
TEMP CONDUCTIVITY10.9 14611.8 15812.2 142
NOTES : Purgeddry.
[:'• ':; ;'••"• •.'•••V ' '•'•:>
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME122512371250
1.5 gpm for 8 minutes for total of 12 gals until
WELL/SAMPLE
10.50 ft
21.5 ft
4 inches
pH5.425.405.25
DESIGNATIONS T4 |
WELL VOLUME 6 gals
PURGE METHOD Pump
DATE PURGED 12-04-90
TEMP CONDUCTIVITY11 C 7311 7011 68
NOTES : Pumped 1 gpm for 25 minutes for total of 25 gals.
[•-•••'••• •
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME102011251140
18.50 ft
150 ft
6 inches
pH5.706.406.43
WELL VOLUME 187 gals
PURGE METHOD Pump
DATE PURGED 12-04-90
TEMP CONDUCTIVITY10 C 6010 6510 65
NOTES: Pumped at 7 gpm for 80 minutes of total of 560 gals.
ARSONS
[ WELL/SAMPLE DESIGNATION: R6 ||
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME0910
9.10 ft WELL VOLUME 335 aals
248 ft PURGE METHOD Pump
6 inches DATE PURGED 12-05-90
pH TEMP CONDUCTIVITY8.35 9 C 546.80 9 606.31 10 60
1550 6.26 9 60
NOTES: Pumped total of 233 gals. Used 1/2 HP pump. Cord onpump only 100 long. Could not set pump > 115 ft w/ Ext. Cord.
| WELL/SAMPLE DESIGNATION: R5 |]
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME090309401010
8.53 ft WELL VOLUME 353 aals
250 ft PURGE METHOD Pump
6 inches DATE PURGED 12-04-90
pH TEMP CONDUCTIVITY8.91 10 C6.90 9.7 2806.94 10.1 150
NOTES: Pumped at 10 gpm for 107 minutes of total of 1070 gals.
| WEUk/SAMPLE DESIGNATION: T5
DEPTH TO WATER
TOTAL DEPTH
WELL DIAMETER
TIME08550930
11.52 ft WELL VOLUME 4.55 aals
18.49 ft PURGE METHOD Pump
6 inches DATE PURGED 12-13-90
pH TEMP CONDUCTIVITY5.55 11.2 2406.50 9.7 240
NOTES: Pumped dry twice for total of 9 gals.
TCN 4204RI REPORTREV. #1
30/SEPT/91
8R3Q/250
|, , - : >.:';.'••.-....- - '.'•'•• WELL DATA SHEET j
Date: 12/12/90 Residence: Helen Shaffer Samole #: 05Address: Box 53. Tannersville. PA 18372Directions: corner of 715 and Camel back Road
Phone: (717) 629-0382 Owner? Yes x NoWell Construction: Drilled x Duo SoringDepth: Unknown Date Installed: ~1950Well Casing: Plastic Steel x Unknown
Other:Other:
Driller's Name: UnknownOther:
Household Plumbing: Copper x Plastic __ Cast Iron ___ Lead ___Water Treatment: Particulate Filter __ Neutralizer __ Softener __ Carbon FilterComments: ___no filter • _________________________________________Sketch location of house, wells, septic, and other features:
Complaints: T0.S0
Previous AnalyComments:
^ DRIVEWAY \ j&h-•K
o VX
SHAFFERRESIDENCE
CHURCH
WELL
C A M E L B A C K R O A D
1
istesiortainsther
sis: By:Bacteria
nonenonenone
unknown Date: 1988- none detected
SAMPLING INFORMATION
Samole 1: BL-RW-Shaffer Time: 1230Water Purging:Sample Drawn FComments:
Began Unti 1 : From Where?rom: kitchen sink
WELL DATA SHEET
Date: 12/10/90_______ Residence: Best Western________ Sample #: 02Address: Ramesh Patel. Best Western Hill Motor Lodge. Tannersvllle. PA 18372______Directions: on Route 715. across from Exxon Station____________________
Phone: (717) 629-1667_____ Owner? Yes x No ___ Other: _____________Well Construction: Drilled x Dug ___ Spring ___ Other: ____________Depth: "200' Date Installed: "1963______ Driller's Name: not knownWell Casing: Plastic ___ Steel x Unknown ___ Other: ____________Household Plumbing: Copper x Plastic __ Cast Iron ___ Lead ___Water Treatment: Particulate Filter __ Neutralizer __ Softener __ Carbon FilterComments: no filters_________________________________________Sketch location of house, wells, septic, and other features:
WELL 111
ROOMS |
O SEPTIC
ROOMS 1 WELL
D SEPTIC RPST ufpsTmu
°ROOMS* 1 HILL MOTOR LODGECH SEPTIC
R O U T E 715
c
2nd building has well 1n front at end of building.1st and 3rd building served by well at top of hill.
Complaints: Tastes noneOdor noneStains noneOther _____
Previous Analysis: By: Hess Environmental Labs____________ Date: November 1990Comments: microbiological testing___________________________________
SAMPLING INFORMATION
Sample f: BL-RW-WESTERN_______________ Time: 1145Water Purging: BeganSample Drawn From:
Until:kitchen sink in hotel office
From Where?
Comments:
Source of Information: Robert Paul
WELL DATA SHEET
Date: 12/10/90______ Residence: ____Mobile Gas Station Sample #: 03Address: Owner; Lloyd No! an____Box.31.1. Stroudsburq. PA 18360______________Directions: On Route 715 across from access ramp to Interstate 80______________
Phone; (717) 421-1800 Owner? Yes x No Other;Well Construction: Drilled ___ Dug ___ Spring ___ Other: ________________Depth: ______ Date Installed: __________ Driller's Name: __________Well Casing: Plastic ___ Steel ___ Unknown ___ Other: _____________Household Plumbing: Copper _____ Plastic __ Cast Iron ___ Lead _____Water Treatment: Particulate Filter _ Neutral1zer _ Softener _ Carbon Filter _ NoneComments: Owner contacted but has not provided any information on well_________Sketch location of house, wells, septic, and other features:
ROCK WALL
9 WELL
PUMPS MOBILSTATION
R O U T E 715
Complaints: Tastes NoOdor NoStains NoOther No
Previous Analysis: By: ________________________________ Date:Comments: Answers provided by employees of station ____________
SAMPLING INFORMATION
Sample *: _______________________ Time: 1410Water Purging: Began ________ Until: _______ From Where?Sample Drawn From: ___Sink in back room_______________________Comments: _____________ __
WELL DATA SHEET
Date: 12/10/90______ Residence: Thirsty Camel Restaurant Sample #: 01Address: Co-owner; Keith Kempinsld RRll. Box II. Tannersville. PA 18372______Directions: Approximately 1/4 mile from Route 715 on Camelback Road__________
Phone: (717) 629-5182 Owner? Yes x No ___ Other: _Well Construction: Drilled ___ Dug ___ Spring ___ Other: _Depth: ______ Date Installed: __________ Driller's Name:Well Casing: Plastic ___ Steel ___ Unknown ___ Other: _Household Plumbing: Copper ___ Plastic __ Cast Iron ___ Lead ___Water Treatment: Particulate Filter _ Neutralizer _ Softener _ Carbon Filter _ NoneComments: Did not have any information on well_________________________Sketch location of house, wells, septic, and other features:
& WELL
THIRSTYCAMEL
RESTAURANT
PARKING
AREA
APARTMENTBLDQ.
C A M E L B A C K R O A D
Note: Both apartment building and restaurant served by same well.
Complaints: Tastes NoOdor NoStains NoOther No
Previous Analysis: By: ______________________________ Date:Comments: ______________ ___ ___ _________
SAMPLING INFORMATION
Sample I: BL-RW-CAMEL_________________ Time: 1130Water Purging: Began ________ Until: _______ From Where?Sample Drawn From: Sink behind bar____________________Comments: ______________________
L W E L L DATA SHEETU—— -—-—.— , ——
Date: 12/10/90________ Residence: Robert C. Riday______ Sample f: 04Address: RD 3. Box 3327. Stroudsburq. PA 18360__________Directions: approximately 1/8 mile east of Butz Landfill site on North Road. Reeders. PA
Phone; (717) 629-5178 Owner? Yes x No Other;Well Construction: Drilled x Dug ___ Spring ___ Other: ____________________Depth: 125' Date Installed: 1965_____ Driller's Name: Unknown ________Well Casing: Plastic x Steel ___ Unknown ___ Other: ________________Household Plumbing: Copper x Plastic __ Cast Iron ___ Lead ___Water Treatment: Particulate Filter __ Neutralizer __ Softener __ Carbon FilterComments: no filter___________________________________________Sketch location of house, wells, septic, and other features:
R O U T E 715
DRIVEWAY
RIOAYRESIDENCE
SEPTIC|——[TANK
Complaints: Tastes noneOdor noneStains noneOther none
Previous Analysis: By: EPA________________________ Date: Hay 1987Comments: No TCE detected____________________________________
SAMPLING INFORMATION
SaMple #: BL-RN-RIDAY_________________ Time: 1630Water Purging: Began ________ Until: _______ From Where?Sample Drawn From: kitchen sink________________________Comments: _______________________________________________
TCN 4204RI REPORT
REV. #130/SEPT/91
TCN 4204RI REPORT
REV. #130/SEPT/91
58301257
DEPTH LITHOLOGYffeet below top of casing) _______
0-20 Overburden (Cased Off)20-34 Sandstone34-50 Shale50-59 Sandstone59-71 Shale71-92 Sfltstone92-100 -Sandstone
Casing Stickup * 4.3'
Kelt KM
DEPTH LITHOLOGY(feet below top of casing) ______
0-105 Overburden (Cased Off)105-116 Sandstone116-144 Siltstone144-149 Sandstone149-175 Siltstone175-184 Sandstone184-204 Siltstone204-208 Sandstone208-244 Siltstone
Casing Stickup = 1.4'
AR301258
Well R1.1A
DEPTH(feet below too of
0-2020-2828-4848-5858-8080-8585-106106-118118-125125-136136-158158-166166-184184-196
LITHOLOGYcasino)
Overburden (CasedShale
SiltstoneInterbedded Shale and
ShaleSandstoneShale
'SiltstoneShale
SandstoneShale
SiltstoneShale
SandstoneCasing Stickup = 2'
Off)
Siltstone
| Well R1.1B
DEPTH(feet below top of
0-2020-3434-4444-5860-7474-114114-132132-182
LITHOLOGYcasinq)
Overburden (CasedShale
SiltstoneShale
SandstoneShale
SandstoneShale
Casing Stickup = 4.3'
Off)
: .. j -- . ii :0 --iiriFiB?- .,,;r;::;-::-::,r,V: . : "'- • |DEPTH
(feet below top of0-2020-114114-134
LITHOLOGYcasinq)
Overburden (CasedShale
SiltstoneOff)
Casing Stickup - 1.8'
5R3QJ259
l' \:'?1-: :; :A:.--°'::- '' -'^•••:-' ; • wen. RSS ':•••.. . v-; -V;: --- ;•-••' ••
DEPTH(feet below too of
0-4242-103
LITHOLOGYcasinq)
Overburden (Cased Off)Shale
Casing Stickup = 0.8'
••. :> : • * ' . . ' " '' :' : • '•:: ''•••'•' " <"•'•. ; ' ' • Wel 1: R3B ' '• ;;;:/ •• •/ : '. . :*:'f r^ • • • - , : . •
DEPTHCfeet below top of
0-107107-134134-166166-175175-184184-208208-216216-226226-243
LITHOLOGYcasino)
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Casing Stickup = 2.8'
i-«i.-..'-" ..:::.r.v:;;:i":::''-:-:;' it?iMiiM!i3l*V & \;• • • • • • . . . • • .;• , • •;.;•••: :j-:: :---;-;-¥->;::j:;K-: ',:••• -i;-:-:1-. '!••:. V-V'' Wfl'.P-. WfS*f;.. : ':••• :. :.:.w-:v.;..;:-..':.:-:«j;. . y.. ...:?:-:':::.;;;:-.?-". '•• • ••••.• :•.•••• .••••:• : |
DEPTHffeet below too of
0-2020-2424-3232-4444-7272-102102-110110-138138-149
LITHOLOGYcasino)
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SiltstoneShale
Casing Stickup - 1.31
| Well R5
DEPTH(feet below top of
0-2020-4545-6060-8484-9090-114114-122122-188188-194194-208208-216216-226226-243
LITHOLOGYcasinq)
Overburden (Cased Off)SiltstoneSandstoneShale
SiltstoneShale
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SandstoneShale
SandstoneShale
Siltstone
Casing Stickup =1.1'
|| Hell R6 |
DEPTH(feet below top of
0-2020-3838-5454-9292-110110-128128-138138-168168-192192-207207-244
LITHOLOGYcasinq)
Overburden (Cased Off)Shale
SandstoneShale
SiltstoneShale
SandstoneShale
Si 1 tstone/SandstoneShale
Siltstone
Casing Stickup =1.6'
3R30I26!
TCN 4204RI REPORT
REV. #130/SEPT/91
AR30I263
GLOSSARY OF DATA QUALIFIER CODES
CODES RELATING TO IDENTIFICATION(confidence concerning presence or absence of compounds):
U - Not detected. The associated number indicates approximatesample concentration necessary to be detected.
(NO CODE) - Confirmed identification.
B = Not detected substantially above the level reported inlaboratory or field blanks.
R * Unreliable result, Analyte may or may not be present in thesample. Supporting data necessary to confirm result.
N * Tentative identification. Consider present. Special methodsmay be needed to confirm its present or absence in futuresampling efforts.
CODES RELATED TO QUANTITATION(can be used for both positive results and sample quantitatlon limits):
J = Analyte present. Reported value may not be accurate orprecise.
K = Analyte present. Reported value may be biased high. Actualvalue is expected to be lower.
L = Analyte present. Reported value may be biased low. Actualvalue is expected to be higher.
UJ 3 Not detected, quantitatlon may be inaccurate or imprecise.UL = Not detected, quantitatlon limit is probably higher.
OTHER CODES
Q > No analytical result.D = Compound Identified In an analysis at a secondary dilution
factor.X * Additional flags defined separately.
flR3QI263
TCN 4204RI REPORT
REV. #130/SEPT/91
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TCN 4204RI REPORTREV. #1
30/SEPT/91
TOXICITY PROFILE FOR ARSENIC
GENERAL DESCRIPTION:
Chemical Properties: Inorganic arsenic is a component of sulfitic ores, ofcopper, cobalt, and nickel. Arsenic trioxide (white arsenic) is releasedas a yapor during air roasting of these ores. Inorganic arsenic appearsas a silver-gray to white, brittle, crystalline, metallic-looking,odorless, and tasteless substance. The molecular weight of arsenic is74.92 g/mol (Weast 1988).
Molecular Formula: As
Absorption: Many factors govern the uptake and amount of arsenic absorbedby the gastrointestinal and respiratory tracts including the chemical formof the element being absorbed, the physical characteristics, and the doselevel. Net absorption of arsenic through the gastrointestinal andrespiratory tracts is estimated to be > 30% of the total ingested orinhaled amount (USEPA 1984).
Fate: Industrial sources are primary contributors of arsenic into theatmosphere. Vapor of arsenic trioxide forms readily at high temperaturesand rapidly adheres to particulate matter. Wet and dry deposition playmajor roles in transferring arsenic to surface waters and soils. Insoils, arsenic binds to clay particles. Leaching of arsenic intogroundwater may also occur. The mobility of the pertinent form is afunction of soil pH, phosphate levels, iron, aluminum content, and soiltype. Reduction and methylation of inorganic arsenic occurs only to alimited extent in soils, reportedly 1-2% over a period of months (USEPA1984).
CARCINOGENIC EFFECTS:
Studies performed on occupational smelter workers found a correlation between theexposure to arsenic and lung cancer mortality (Enterline and Marsh 1982; Lee-Feldstein 1983; Axelson et al. 1978; Tokudome and Kurdtsene 1976; Rencher et al.
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1977). Chronic oral exposure results in severe gastrointestinal damage andincludes a sequence of changes in skin epithelium, proceeding fromhyperpigmentation to hyperkeratosis characterized as keratin proliferation of averrucose nature (USEPA 1984). This may lead in some cases to late onset skincancers. The skin cancers can be histopathologically characterized as eithersquamous carcinomas in the keratotic areas or basal cell carcinomas, with alatency period of 6-50 yrs. (USEPA 1984). Arsenic is classified as a Group Acarcinogen (i.e., human carcinogen) (USEPA 1991). The oral slope factor forarsenic, 1.70 (mg/kg/day)"1 (USEPA 1991), is based on large scale epidemiologicstudies of arsenic-contaminated drinking water (Tseng 1977). The studiesinvolved the population living in Taiwan where the arsenic-contaminated drinkingwater supply was endemic. Results showed significant increases in mortalityrates for cancer of the bladder, lung, liver, kidney, skin, and colon. Cancerof various internal organs has been found in several case reports involving theingestion of arsenic (Tseng 1977).
NONCARCIMOGEN1C EFFECTS:
Central nervous system (CNS) effects, gastrointestinal effects and peripheralcardiovascular effects have been documented following accidental ingestion ofarsenic (USEPA 1984). A reversible anemia has been observed after chronicexposure via arsenic-contaminated well water (USEPA 1984). An epidemiologicalstudy performed on a Taiwanese population with protracted exposure to arsenicingestion showed an increase in the incidence of Blackfoot disease (peripheralvasculopathy), although direct causation is considered questionable. A chronicoral RfD for arsenic of l.OE-3 mg/kg/day in drinking water has been calculatedusing an uncertainty factor of 1 based on the Taiwan study (USEPA 1990, Tseng1977). An USEPA work group is currently reevaluating the RfD for arsenic (USEPA1991).
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Oral Slope Factor: 1.70 (mg/kg/day)"1Weight of Evidence: A
Noncarcinogenic Toxicity:Oral Reference Dose: l.OE-3 mg/kg/dayOral Uncertainty Factor: 1Critical Effect: Keratosis and hyperpigmentation
M30I305
REFERENCES:
Axelson, O.E. Dahlgren, C.D. Jansson and S.O. Rehnlund. 1978. Arsenic exposureand mortality: A case referent study from a Swedish copper smelter. Br.i in/4 MoH -?[;• Q.II;J. Ind. Med. 35: 8-15.
Enter!ine, P.E. and G.M. Marsh. Mortality among workers exposed to arsenic andother substances in a copper smelter. Am. J. Epidemiol. 116; 895-910,1982.
Lee-Feldstein, A. 1983. Arsenic and respiratory cancer in man: Follow-up of anoccupational study. In: Arsenic: Industrial, Biomedical, andEnvironmental Perspectives, W. Lederer and R. Fensterheim, Ed. VanNostrand Reinhold, New York.
Rencher, A.C., M.W. Carter and D.W. McKee. 1978. A retrospective epidemiologicalstudy of mortality at a large western copper smelter. J. Occup. Med. 19:754-758.
Tokudome, S. and M. Kuratsune. 1976. A cohort study on mortality from cancer andother causes among workers at a metal refinery. Int. J. Cancer. 17: 310-317.
Tseng, W.P. 1977. Effects and dose-response relationships of skin cancer andblackfoot disease with arsenic. Environmental Health Perspectives.19:109-119.
U.S. Environmental Protection Agency (USEPA). 1984. Health Assessment Documentfor Arsenic. USEPA Report No. 600/8-83-021F. Office of Health andAssessment, USEPA, Washington, D.C.
U.S. Environmental Protection Agency (USEPA). 1990. Health Effects AssessmentSummary Tables (HEAST). Fourth Quarter FY-1990. OSWER, USEPA.
U.S.. Environmental Protection Agency (USEPA). 1991. Integrated RiskInformation System (IRIS). Toxic Profile for Arsenic. Online, March1991. Office of Health and Environmental Assessment. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.
Weast, R.C. 1988. Handbook of chemistry and physics. 69th ed. Boca Raton, FL:CRC Press, B-8, B-72 to B-73.
3R3QI306
TOXICITY PROFILE FOR BERYLLIUM
GENERAL DESCRIPTION:Chemical Properties: Beryllium is a gray metallic element that belongs toGroup IIA of the periodic table and has an oxidation state of +2. It hasa molecular weight of 9.01 g/mol and in pure form is composed of hexagonalcrystals (Weast 1983). Average estimates of the abundance of beryllium inthe earth's crust range from 2-10 ppm. Beryllium occurs as a component ofmore than 40 minerals (USEPA, 1986). Although elemental beryllium isinsoluble, many of its compounds are highly soluble in water.
Molecular Formula: Be
Absorption: Several studies show varying results concerning theabsorption of beryllium. Rats that were administered a dose of berylliumvia a stomach tube absorbed <0.2% (Crowley et al. 1949). Furchner et al.,(1973) and Hyslop et al. (1943), using rodents, dogs, and monkeys, wereable to demonstrate only <1% absorption of beryllium ingested. However,Reeves (1965), in a study involving rats provided beryllium in theirdrinking water for several weeks, concluded that 10-40% of berylliumingested could be absorbed in the stomach due to the lower pH maintainingberyllium salts in their ionized and soluble form.
Fate: Most beryllium in the atmosphere is produced by coal combustion;therefore, its most common form is probably beryllium oxide. Wet and drydeposition are routes of removal of beryllium from the atmosphere (USEPA1987). Particles from stack emissions are thought to stay aloft -10 days.The average concentration of beryllium in rain or snow is expected to be0.01 ng/g (USEPA 1986). After reaching soils and sediments, it is thoughtto be retained as beryllium oxide (USEPA 1986). Beryllium will mostlikely be very persistent in this form (Fishbein 1981).
CARCINOGENIC EFFECTS:
The oral slope factor of 4.3 (mg/kg/day)"1 was derived based on results of twochronic oral laboratory studies (USEPA 1987). In the Schroeder and Mitchener
SR3QI307
(1975a,b) studies, rats and mice were given 5 ppm beryllium sulfate in theirdrinking water. Male rats had an increase of grossly observed tumors and femaleshad a small increase of lymphoma leukemias. One epidemiological study (Berg andBurbank 1972) found a positive correlation between beryllium concentration inwater and cancer death rate in a human population, but the cause and effectrelationship could not be proven (USEPA 1986). Beryllium is considered aprobable human carcinogen (Group B2).
NONCARCINOGENIC EFFECTS:
Several early studies showed a form of rickets was produced in young animalsfollowing ingestion of beryllium because of its propensity to bind with phosphateand thus deplete phosphate levels in the body (Guyatt et al. 1933, Jacobson 1933,Kay and Skill 1934). A later chronic study of beryllium toxicity (Schroeder andMitchener 1975b) showed glucose levels to increase and body weight to decreaseespecially in young animals. There was also some evidence of teratogeniceffects. Based on this study, USEPA (1991) adopted an oral reference dose of 5E-3 (mg/kg/day) because this dosage produced the most significant decrease in bodyweight (Schroeder and Mitchener 1975b). An uncertainty factor of 100 was usedto account for interspecies and intraspecies variability (USEPA 1991).
SUMMARY OF TOXICITY CRITERIA
Carcinogenic Toxicity:Oral Slope Factor: 4.3 (mg/kg/day)"1Weight of Evidence: B2
Noncarcinogenic Toxicity:Oral Reference Dose: 5E-3 mg/kg/dayOral Uncertainty Factor: 100Critical Effect: none observed
REFERENCES:
Berg, J.W. and F. Burbank. 1972. Correlations between carcinogenic tracemetals in water supply and cancer mortality. Ann. N.Y Acad. Sci. 199:249-261.
Crowley, J.F., J.G. Hamilton and K. J. Scott. 1949. The metabolism of Carrier-free radioberyllium in the rat. J. Biol. Chem. 177: 975-984.
AR30I308
Fishbein, L. 1981. Sources, transport and alterations of metal compounds: Anoverview. 1. Arsenic, beryllium, cadmium, chromium, and nickel. Environ.Health Perspect. 40: 43-64.
Furchner, J.E., C.R. Richmond, and J.E. London. 1973. Comparative metabolism ofradionuclides in mammals: VI. Retention of beryllium in the mouse, rat,monkey and dog. Health Phys. 24: 292-300.
Guyatt, B.L, H.D. Ray, and H.D. Branion. 1933. Beryllium rickets. J. Nutr.6:313-324.
Hyslop, F., E.D. Palmes, W.C. Aford , A.R. Monaco and L.T. Fairhall. 1943. Thetoxicity of beryllium. Allied Institutes of Health, Washington, D.C. NIHBull No. 181.
Jacobson, S.A. 1933. Bone lesions in rats produced by the substitution ofberyllium for calcium in diets. Arch. Pathol. 15:18-26.
Kay, H.D. and D.L. Skill. 1934. Prevention and cure of beryllium rickets.Biochem J 28:1222-1229.
Reeves, A.L. 1965. The absorption of beryllium from the gastrointestinal tract.Arch. Environ. Health. 11:209-214.
Schroeder, H.A. and M. Mitchener. 1975a. Life-term studies in rats: Effects ofaluminum, barium, beryllium, and tungsten. J. Nutr. 105(4): 421-427.
Schroeder, H.A. and M. Mitchener. 1975b. Life-term effects of mercury, methylmercury, and nine other trace metals on mice. J. Nutr. 105(4): 452-458.
U.S. Environmental Protection Agency (USEPA). 1986. Health Assessment Documentfor Beryllium. Prepared by the Office of Health and EnvironmentalAssessment, Research Triangle Park, NC.
U.S. Environmental Protection Agency (USEPA). 1987. Health Effects Assessmentfor Beryllium and Compounds. Environmental Criteria and AssessmentOffice, Cincinnati OH.
U.S. Environmental Protection Agency (USEPA). 1991. Integrated RiskInformation System (IRIS). Toxic Profile for Beryllium. Online, March1991. Office of Health and Environmental Assessment. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.
Weast, R.C. Ed. 1983. Handbook of Chemistry and Physics., 64th ed. CRC PressInc., Boca Raton, FL. p. B-74.
AR30I309
TOXICITY PROFILE FOR 1,2-DICHLOROETHANE
GENERAL DESCRIPTION:Chemical Properties: 1,2-Dichloroethane is a member of the halogenatedaliphatic hydrocarbon (purgeable halocarbon) chemical class of compounds.
• 1,2,-Dichloroethane has a molecular weight of 98.96 g/mol (Weast 1981).
CARCINOGENIC EFFECTS:
Fifty male and 50 female Osborne-Wendel rats and B6C3F1 mice were administered1,2-dichloroethane in corn oil by gavage. The study ran 78 weeks followed by anadditional observation period for both the rats and the mice. Dosages for ratswere 47 and 95 mg/kg/day, for male mice 97 and 195 mg/kg/day, and for female mice149 and 299 mg/kg/day. All high dose female rats died after 15 weeks, and after23 weeks all high dose male rats died. Results for male rats exposed to 1,2-dichloroethane included increased incidence of forestomach squamous-cellcarcinomas and hemangiosarcomas. There were significant increases in theincidence of mammary adenocarcinoma in female rats and mice. Female mice alsoexperienced endometrial stromal polyps and sarcomas. Male mice developedhepatocellular carcinomas. Both sexes of mice showed effects of alveolaradenomas and branchiolar adenomas (NCI, 1978). From the above study, an oralslope factor of 9.1xlO'2 (mg/kg/day)'1 was calculated (USEPA 1991).
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Oral Slope Factor: 9.1E-2 (mg/kg/day)"1Inhalation Slope Factor: NDWeight of Evidence: B2
Noncarcinogenic Toxicity: ND
REFERENCES:
NCI (National Cancer Institute). 1978. Bioassay for ,2,-Dichloroethane forPossible Carcinogenicity. NCI Carcinogenic Technical Report Series No.55. DHEW Publ. No. (NIH) 78-1361, Washington, D.C.
U.S.. Environmental Protection Agency (USEPA). 1991. Integrated RiskInformation System (IRIS). Toxicity Profile for 1,2-Dichloroethane.Online March 1991. Office of Health and Environmental Assessment.Environmental Criteria and Assessment Office, Cincinnati, OH.
SR30I3IO
Weast, R.C. 1981 Handbook of Chemistry and Physics. 61st edition. Boca Raton,FI: CRC Press.
flR3G13l I
TOXICITY PROFILE FOR 1,1-DICHLOROETHENE
GENERAL DESCRIPTION:
Chemical Properties: 1,1-Dichloroethene is a highly volatile, colorlessliquid having a molecular weight of 96.95 g/mol. 1,1-Dichloroethene is amember of the halogenated aliphatic hydrocarbon (purgeable halocarbon)chemical class of compounds (USEPA 1989). 1,1-Dichloroethene with asolubility of 4 x 10"2 mg/L is practically insoluble in water (Merck 1983).
Molecular Formula: C2H2C12
Absorption: Lab animal studies show rapid absorption of 1,1-dichloroethene both orally and through inhalation (Dallas et al. 1983;McKenna et al. 1978; Jones and Hathaway 1978).
Fate: Most 1,1-dichloroethene is released to the atmosphere. Majorcontributors of 1,1-dichloroethene are industrial and hazardous wastesites. Most of the 1,1-dichloroethene found in surface waters and soilwill quickly evaporate into the atmosphere. 1,1-Dichloroethene doses notadsorb to particulate matter readily; therefore, most 1,1-dichloroethenefound in subsurface soils will leach into groundwater (USEPA 1989).
CARCINOGENIC EFFECTS:
Inhalation: Maltoni et al. (1985) presently is the one study positively linkinganimals inhaling 1,1-dichloroethene to the formation of tumors. Rats exposed to100 ppm of 1,1-dichloroethene for 7 hours/day, 5 days/week showed increasedincidence of malignant and nonmalignant tumors and leukemias in rats. From theseresults an inhalation slope factor of 1.2 (mg/kg/day)'1 was derived (USEPA 1991).
Oral: NTP (1982) performed a study from which the most conservative slopefactor, 6E-1 (mg/kg/day)'1 was derived. Effects such as a significant increaseof adrenal tumors in males were noted at this dose level. Two other studies(Quast et al. 1983; and Maltoni et al. 1985) verified a slope factor of 2E-1
A R 3 Q 1 3 I 2
(mg/kg/day)"1, but USEPA (1991) has adopted the higher estimate.
NONCARCINOGENIC EFFECTS:
Inhalation: Humans inhaling 1,1-dichloroethene for a short period of time mayencounter neurotoxicity (Henschler et al. 1970; Tierney et al. 1979). Chronicexposure to 1,1-dichloroethene may be associated with hepatotoxicity andnephrotoxicity (Tierney et al. 1979). Tierney et al. (1979) observed in humansinhaling 1,1-dichloroethene (approximately 4,000 ppm) caused central nervoussystem depression and symptoms of inebriation progressing to convulsions andunconsciousness. Laboratory animals chronically exposed to 1,1-dichloroetheneexhibit toxic effects of the central nervous system, liver, kidney and lungs(USEPA 1989). One study performed on rats exposed by inhaling 24 ppm of 1,1-dichloroethene for 6 hours/day, 5 days/week for 18 months showed fatty changesin the liver (Quast et al. 1986). An inhalation reference dose is under reviewby an USEPA work group (USEPA 1991).
Oral: Laboratory animals orally exposed show the main targets of 1,1-dichloroethene toxicity to be the liver and kidney (USEPA 1989). Several studieshave noted in fasted rats that a single dose of 50 mg of 1,1-dichloroethene/kgbody weight or higher caused a significant increase in serum enzyme marker ofliver dysfunction and an increase in liver weight. The nutritional status of theanimals and the dosing vehicle influence the hepatotoxicity of orallyadministered 1,1-dichloroethene (Andersen and Jenkins 1977; Andersen et al. 1980;Chieco et al. 1981; Jenkins and Andersen 1978).
Quast et al. (1983) administered 50, 100, or 200 ppm in drinking water of ratsfor 2 years. Hepatic lesions were noted. In the same study, beagle dogs alsoshowed liver sensitivity to 1,1-dichloroethene in the diet. A LOAEL of 9mg/kg/day was established based on this study. From this an oral RfD of 9E-3mg/kg/day was established taking a 1000-fold uncertainty factor into account forinter- and intraspecies variation and because no NOAEL was established (USEPA,1991).
HR30I3I3
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Oral Slope Factor: 6.0E-1 (mg/kg/day)"1Inhalation Slope Factor: 1.2 (mg/kg/day)"1Weight of Evidence: C
Noncarcinogenic Toxicity:Oral Reference Dose: 9.0E-3 mg/kg/dayOral Uncertainty Factor: 1000
REFERENCES:
Andersen, M.E., J. Jenkins. 1977. Oral tpxicity of 1,1-dichloroethylene in therat: Effects of sex, age, and fasting. Environ Health Perspect 21: 157-163.
Andersen, M.E., O.E. Thomas, M.L. Gargas, et al. 1980. The significance ofmultiple detoxification pathways for reactive metabolites in the toxicityof 1,1-dichloroethylene. Toxicol Appl Pharmacol 52: 422-432.
Chieco, P., M.T. Moslen, E.S. Reynolds. 1981. Effects of administrativevehicle on oral 1,1-dichloroethylene toxicity. Tox Appl Pharmacol 57:146-155.
Dallas, C.E., F.W. Weir, S. Feldman, et al. 1983. The uptake and dispositionof 1,1-dichloroethylene in rats during inhalation exposure. Toxicol ApplPharmacol 68: 140-151.
Henschler, D., F. Broser, H.C. Hopf. 1970. Polyneuritis cranialis followingpoisoning with chlorinated acetylene while handling vinylidene chloridecopolymers. Arch Toxicol 26: 62-75.
Jenkins, L.J., M.E. Andersen. 1978. 1,1-Dichloroethylene nephrotoxicity in therat. Toxicol Appl Pharmacol 46: 131-141.
Jones, B.K., D.E. Hathway. 1978. Differences in metabolism of vinylidenechloride between mice and rats. Br J Cancer 37: 411-417.
Maltoni, C., P. Lefemine, Cotti et al. ed. 1985. Experimental research onvinylidene chloride carcinogenesis. Archives of Research on IndustrialCarcinogenesis. Vol. 3, Princeton, NJ: Princeton Scientific Publishers.
McKenna, M.J., J.A. Zempel, E.O. Madrid, et al. 1978. The pharmacokinetics of[14C] vinylidene chloride in rats following inhalation exposure. ToxicolAppl Pharmacol 45: 599-610.
Merck. 1983. The Merck Index. In: Windholz M. ed. 10th ed. New Jersey:Merck and Co., Inc. 1430.
Quast, J.F., Huniston C.G., Wade C.E., et al., 1983. A chronic toxicity andoncogenicity study in rats and subchronic toxicity study in dogs oningested vinyldene chloride. Fundan. Appl. Toxicol. 3(1): 55-62.
/JR30I3II*
Quast, J.F., M.J. McKenna, L.W. Rampy, et al. 1986. Chronic toxicity andoncogenicity study on inhaled vinylidene chloride in rats. Fund ApplToxicol 6: 105-144.
Tierney, D.R., T.R. Mackwood, M.R. Piana. 1979. status assessment of toxicchemicals: vinyldene chloride. Cincinnati, Ohio: US EnvironmentalProtection Agency. USEPA 600/2-79-2100 (PB80-146442).
U.S. Environmental Protection Agency (USEPA). 1989. lexicological Profile for1,1-Dichloroethene. U.S. Environmental Protection Agency, Washington, DC.December 1989.
U.S. Environmental Protection Agency (USEPA). 1991. Integrated RiskInformation System (IRIS). Office of Health and Environmental Assessment.Cincinnati, OH.
SR30I3I5
TOXICITY PROFILE FOR 1,2-DICHLOROETHENE (TOTAL)
GENERAL DESCRIPTION:
Chemical Properties: 1,2-Dichloroethene exists in cis- and trans-isomerswhich have a molecular weight of 96.94 g/mol (Weast, 1983). Both formsexist as colorless liquids (Hawley 1981). The trans- form has a watersolubility of 6,260 mg/L at 25°C, while the cis- form has a solubility of3,500 mg/L (Horvath 1982). Both forms are also soluble in organicsolvents such as ether, alcohol, benzenes, acetone, and chloroform. Thevapor pressures at 25°C vary from 336 mm Hg for the trans- form to 215 mmHg for the cis- form (Stevens 1979).
Molecular Formula: C2H2C2
Absorption: No studies were found that quantified the rate or extent towhich cis- or trans- 1,2-dichloroethene were absorbed following oralexposure. Sato and Nakajima (1979) reported a blood/air partitioncoefficient for the cis- isomer of 9.2 and for the trans- isomer, 5.8.Exposure to 1,2-dichloroethene by inhalation resulted in equilibrium withthe whole animal and the inspired 1,2-dichloroethene within 1.4-2 hours(Filser and Bolt, 1979). Lehmann and Schmidt-Kehl (1936) reported that72-75% absorption of 1,2-dichloroethene occurred by the lungs in humans.
Fate: Using rainwater samples, Kawamura and Kaplan (1983) indicated that1,2-dichloroethene is removed from the atmosphere via precipitation.However, most of the 1,2-dichloroethene removed in this manner is likelyto reenter the atmosphere by volatilization. Due to the vapor pressuresof both isomers, neither form is expected to partition from the vaporphase to participates in the atmosphere. Experimental results haveconfirmed the volatilization half-lives of 5.0 hours for the cis- isomerand 6.2 hours for the trans- isomer from a body of water 1 m deep (Billing1977).
Adsorption of 1,2-dichloroethene isomers to soil and sediment in water isnot a significant fate process, based on the adsorption coefficients of 32
HR3QI3I6
- 49 estimated from Lyman (1982). This information suggests that leachinginto groundwater is highly likely, and the dichloroethenes are often foundin groundwater (Barber 1988).
CARCINOGENIC TOXICITY:
No data for humans or animals suggest that 1,2-dichloroethene has carcinogenicpotency. In addition, microbiological assays have had negative results formutagenicity (USEPA 1991).
NONCARCIMOGEN1C TOXICITY:
In a 90-day study by Barnes et al. (1985), 24 male and 24 female mice were giventrans- 1,2 dichloroethene in their drinking water at levels of 0.1, 1.0 or 2.0mg/mL. Therefore, based on fluid consumption, the doses for males were 17, 175or 387 mg/kg/day and 23, 224 or 452 mg/kg/day for females. At the end of theexperiment, there were no changes in terminal body weight or gross pathologycaused by any dosage of trans- 1,2,-dichloroethene. In male mice, there weresignificant increases in serum alkaline phosphatase levels at the two higherdoses. Also in males at the highest dose, liver glutathiane concentrations weredecreased. In females, thymus weight and lung weight were depressed at thehigher doses. The level of 17 mg/kg/day was used as a NOAEL. From this an oralRfD of 2E-2 mg/kg/day was calculated using an uncertainty factor of 1000 toaccount for inter- and intraspecies variation and extrapolation from subchronicto chronic exposure (USEPA 1991).
Other bioassays have also shown toxic effects of 1,2-dichloroethene. Dose levelsexceeding 1000 mg/kg are lethal in rats and mice. Symptoms at these levelsinclude severe pulmonary hyperemia and aleolar septal distension, ataxia,depressed respiration and central nervous system depression (Barnes et al. 1985;Freundt et al. 1977, Hayes et. 1987). Effects noted at lower dose levels includeliver pathology (Freundt et al. 1977) and biochemical changes in the liver(Jenkins et al. 1972).
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity: NO
Noncarcinogenic Toxicity:Oral Reference Dose: 2E-2 mg/kg/dayOral Uncertainty Factor: 1000Inhalation Reference Dose: ND
REFERENCES:
Barber, L.B., II, E.M. Thurman, M.P. Schroeder, et al. 1988. Long-term fate oforganic micropollutants in sewage-contaminated groundwater. Environ SciTechnol 22: 205-211.
Barnes, E.W., W.M. Sanders, K.L. White, Jr., et al. 1985. Toxicology of trans-1,2-dichloroethylene in the mouse. Drug Chem. Toxicol. 8: 373-392.
Billing, W.L. 1977. Interphase transfer processes II. Evaporation rates ofchloroethanes, ethanes, ethylenes, propanes, and propylenes from diluteaqueous solutions. Comparison with theoretical predictions. Environ SciTechnol. 11: 405-409.
Drilling WL. 1977. Interphase transfer processes. II. Evaporation rates ofchloromethanes, ethanes, ethylenes, propanes, and propylenes from diluteaqueous solutions. Comparisons with theoretical predictions. Environ.Sci. Technol. 11: 405-409.
Filser, J.G., H.M. Bolt. 1979. Pharmacokinetics of halogenated ethylenes inrats. Arch Toxicol 42: 123-136.
Freundt KJ, Liebaldt GP, Liberwirth E. 1977. Toxicity studies on trans- 1,2-dichloroethene. Toxicity 7: 141-153.
Gossett, J.M. 1987. Measurements of Henry's Law constant for Cl and C2chlorinated hydrocarbons. Environ Sci Tech 21: 202-206.
Hawley GG. 1981. The condensed chemical dictionary. 10th ed. New York, NY:Van Nostrand Reinhold Co., 335.
Hayes JR, Condie LW Jr., Egle JL Jr., et al. 1987. The acute and subchronictoxicity in rats of trans- 1,2-dichloroethene in drinking water. J AmColl Toxcicol 6: 471-478.
Horvath AL. 1982. Halogenated hydrocarbons solubility. - miscibility withwater. New York, NY: Marcel Dekker Inc., 496-496.
Jenkins LJ Jr., Trabulus MJ, Murphy SD. 1972. Biochemical effects of 1,1-dichloroethylene in rats: Comparison with carbon tetrachloride and 1,2-dichloroethylene. Toxicol Appl Pharmacol 23: 501-510.
Kawamura, K., I.R. Kaplan. 1983. Organic compounds in the rainwater of LosAngeles. Environ Sci Tech 17: 497-501.
Lyman WJ. 1982. Adsorption coefficient for soils and sediments. In: Handbookfor chemical property estimation methods. Lyman WJ. Reehl WF, RosenblattDH, eds. New York, NY: McGraw Hill Book Co., Chapter 4.
Sato A, Nakajima T. 1979. A structure-activity relationship of somechlorinated hydrocarbons. Arch Environ Health 34: 69-75.
Stevens VI. 1979. 1,2-Dichloroethylene. In: Kirk-Othmer encyclopedia ofchemical technology, 3rd ed. Vol 5. Grayson M, Eskroth D, eds. New York,NY: John Wiley and Sons, 742-745.
U.S. Environmental Protection Agency (USEPA). 1991. Integrated RiskInformation System (IRIS). Updated March 1991.
flR30)3j9
TOXICITY PROFILE FOR MANGANESE
GENERAL DESCRIPTION:
Chemical Properties: Manganese is a reddish-grey or silvery, brittlemetal having a molecular weight of 54.9 g/mol (Sax 1984) and belonging tothe first transition series of the periodic table. Manganese exists in 11oxidation states from -3 to +7. The most common form includes Mn 4+because of the important oxide Mn02; the +2 form which is stable in acids;and, the +7 valence which is found only in oxy-compounds (USEPA 1984).Most forms are soluble in dilute acids and react slowly in hot or coldwater (Weast 1980).
Molecular Formula: Mn
Absorption: Variable amounts of manganese are absorbed via thegastrointestinal tract, but averages around 3-5% (Davidson et al. 1988,1989; Mena et al. 1969). Low levels of iron in the diet appear to actsynergistically with magnesium uptake in the gastrointestinal system,possibly because these two elements are absorbed by the same transportsystem in the gut (Mena et al. 1969).
Fate: The fate of manganese in aquatic systems may be determined by itsability to undergo chemical and microbiological reactions. In mostnatural aquatic systems, manganese is expected to be present predominantlyin the suspended particulates and sediments as Mn02 and/or Mn304. A smallamount of manganese may remain as soluble Mn+2. By analogy with aquaticiron (USEPA 1981), the residence time of aquatic manganese may be a fewhundred years.
Both chemical and microbiological interactions may cause speciation ofmanganese in soils. Both soil pH and oxidation-reduction potential ofsoil may influence the speciation process. It has been suggested that inacid water-logged soils, manganese passes freely into solution and mayleach into groundwater. Manganese can be readily leached from wasteburial sites and from other natural soils into groundwater (USEPA 1982).
flR30i320
Manganese aerosol may be removed from the air environment through dry orwet precipitation. It has been estimated that the atmospheric residencetime for manganese due to such physical removal processes is about 7 days(Cutpitt 1980).
CARCINOGENIC EFFECTS:
No carcinogen slope factor was derived for oral and inhalation exposure formanganese because there was no significant increase in the incidence of cancerassociated with manganese administration (USEPA 1984). Using the criteria forevaluating the overall weight of evidence for carcinogenicity in humans proposedby the Carcinogen Assessment Group of the USEPA (Federal Register 1984),manganese is best designated a Group D, not classified, substance (ERA 1984).
NONCARCINOGENIC EFFECTS:
Excess manganese in the diet of animals depressed hemoglobin formation (Matrone,et al. 1959), interfered with hemoglobin regeneration (Hartman et al. 1955) andwas associated with decreased blood pressure and elevated serotonin blood levels(Kimura et al. 1978). When excess manganese was put in the drinking water of labanimals, there were ultrastructural changes in the liver. In monkey inhalationstudies, animals exposed to manganese for five months had mild tremors offingers, decreased pinch force and reduced dexterity of upper limbs that wereconsidered to be evidence of neurological damage analogous to humans sufferingform chronic manganese toxicity (Nishiyama et al. 1975).
Epidemiological studies have shown that very high doses (>11.5 mg/kg/day) ofmanganese dissolved in drinking water will cause problems with the centralnervous system (USEPA 1991). These toxic effects are thought to be intensifiedby increased water acidity and by the presence of iron. Chronic exposure tomanganese in drinking water resulted in extra-pyramidal dysfunction symptoms suchas lethargy, increased muscle tonus and spasms, and tremors and mentaldisturbances in 16 people (Kawamura et al. 1941). Elderly people seemed to bemost severely affected and children were least affected. Autopsy of one caseshowed atrophy of the globus palladium, disappearance of its neurons, moderatecongestion of the brain, spinal cord and meninges and meningeal edema (Kawamura
flR30!32l
et al. 1941). Kawamura et al. (1941) reported the case of water consumption fromwells contaminated by manganese from dry cell batteries buried nearby. After theoutbreak of chronic manganese intoxication, water from the wells was tested andfound to contain 14.3 mg/1 of manganese. Over a period of 6 weeks, theconcentration was reported to decrease to 4.2 mg/1.
Oral exposure of humans to manganese has been associated with impotency (Penalver1955, Mena et al. 1967). In animals fed dietary manganese chronically,testicular and sex accessory organ weights were significantly decreased comparedto control mice.
The oral RfD of IxlO'1 mg/kg/day was computed using a NOAEL of 0.14 mg/kg/day forchronic human consumption of manganese. The uncertainty factor and modifyingfactor were assumed to be 1. This RfD was calculated considering a total dietaryintake of manganese. Because manganese from drinking water alone is morebioavailable, this level may not be acceptable in that case. Manganese is anessential human nutrient and the reported problems occurred at levels above 9mg/day (USEPA 1991, WHO 1973, Schroeder at al 1966, NRC 1989).
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Weight-of-evidence: D; not classified as a human carcinogen.
Noncarcinogenic Toxicity:Oral Reference Dose: IE-1 mg/kg/dayOral Uncertainty Factor: 1Critical Effect: central nervous system effects
REFERENCES:
Cutpitt, L.T. 1980. Fate of Toxic and Hazardous Materials in the AirEnvironment. U.S. EPA, ESRL, ORD, Environmental Sciences Research,Research Triangle Park, NC.
Davidson, L., Cederblad, A, Hagebo E, et al. 1988. Intrinsic and extrinsiclabeling for studies of manganese absorption in humans. J Nutr 118:1517-1524.
Davidsson, L, Cederblad, A, Lonnerdal, B, et al. 1989. Manganese retention inman: A method for estimating manganese absorption and man. Am J ClinNutr 49:170-179.
Federal Register. 1984. USEPA. Proposed Guidelines for Carcinogenic RiskAssessment. Federal Register 49:46294-46299.
Hartman, R.H., G. Matrone and G.H. Wise. 1955. Effect of high dietarymanganese on hemoglobin formation. J. Nutr. 57:429-439.
Kawamura, R., H. Ikuta, S. Fukuzumi, et al. 1941. Intoxication by Manganese in-Well Water. Kitasato Arch. Exp. Med. 18:145-169.
Kimura, M., N. Yagi and Y. Itokawa. 1978. Effect of subacute manganese feedingon serotonin metabolism in the rat. J. Toxicol. Environ. Health. 4:701-707.
Matrone, G., R.H. Hartman and A.J. Clawson. 1959. Studies of a manganese ironantagonism in the nutrition of rabbits and baby pigs. J. Nutr. 67:309-317.
Mena, I., 0. Marin, S. Fuenzalida and G.C. Cotzias. 1967. Chronic ManganesePoisoning: Clinical Picture and Manganese Turnover. Neurology. 17:128-136.
Mena, I., K. Horiuchi, K. Burke et al. 1969. Chronic manganese poisoning:Individual susceptibility and absorption of iron. Neurology 19:1000-1006.
Nishiyama, K., Y. Suzuki, N. Fujii, H. Yano, T. Miyai and K. Ohmishi. 1975.Effect of Long-Term Inhalation of Manganese Dusts. II. ContinuousObservation of the Respiratory Organs in Monkeys and Mice. Jap. J. Hyg.30:117.
NRC (National Research Council). 1989. Recommended Dietary Allowances, 10th ed.Food and Nutrition Board, National Research Council, National AcademyPress, Washington, DC. p. 230-235.
Penalver, R. 1955. Manganese Poisoning. The 1954 Ramazzini Oration. Ind. Med.Surg. 24:1-7.
Sax, Irving N. 1984. Dangerous Properties of Industrial Chemicals. New York:Van Nostrand Reinhold Company.
Schroeder, HA, DD Balessa and IH Tipton. 1966. Essential trace metals in man:Manganese, a study in homeostasis. J. Chron. Dis. 19: 545-571.
U.S. Environmental Protection Agency (USEPA). 1981. Multimedia Criteria forIron and Compounds. Environmental Criteria Assessment Office, Cincinnati,OH.
U.S. Environmental Protection Agency (USEPA). 1982. Ambient Air QualityCriteria Document for Manganese. Environmental Criteria and AssessmentOffice, Cincinnati, OH.
3R30I323
U.S. Environmental Protection Agency (USEPA). 1984. Health Effects Assessmentfor Manganese (and Compounds). Prepared by the Office of Health andEnvironmental Assessment, Environmental Criteria and Assessment Office,Cincinnati, OH, and Office of Solid Waste and Emergency Response,Washington, DC.
U.S. Environmental Protection Agency (USEPA). 1991 Integrated Risk InformationSystem (IRIS). Health Criteria and Assessment Office, Washington, DC.Revised March 1991.
Weast, R.C. 1980. Handbook of Chemistry and Physics, 61st ed. The ChemicalRubber Co., Cleveland, OH. p.824-25, B117, F24.
WHO (World Health Organization). 1973. Trace elements in human nutrition:Manganese. Report of a WHO Expert Committee. Technical Report Service,532 WHO, Geneva, Switzerland, p.34-36.
AR30I321*
TOXICITY PROFILE FOR MERCURY
GENERAL DESCRIPTION:
Chemical Properties: Inorganic mercury is a silvery white metal whichoccurs as a liquid at room temperature (Weast 1981). It has a molecularweight of 200.59 g/mol, a vapor presence of 2 x 10"3, and a watersolubility of 0.056 mg/L at 25°C (Windholz 1983). USEPA (1980) hasestablished an MCL for mercury of 0.002 mg/1.
Fate: The speciation of mercury, its pH, redox conditions, and presenceof complexing ions are all factors influencing the environmental fate ofmercury (Rubin 1976). In acidic conditions, it will exist in compoundssuch as HgCl2 and under basic conditions as Hg (OH)2. Mercury is readilysorbed to soil organic matter, clays, and hydrous metal oxides.Bioaccumulation in aquatic organisms is also a significant fate process.BCF values for inorganic mercury range from 1,800 to 5,000 (USEPA 1985,USEPA 1990a). Mercury is biologically methylated and may volatilize fromsoils in small amounts (Lyman et al. 1987).
CARCINOGENIC EFFECTS:
Mercury has not been show to cause cancer in humans. Bioassays involving ratshave demonstrated that local tumors do develop at the point of injection ofmetallic mercury (USEPA, 1984).
NONCARCINOGENIC EFFECTS:
Several studies on the toxic effects of ingestion of mercury have been performedon rats (Druet at al., 1978, Bernaudin et al., 1981, Andres, 1984, and USEPA,1987). The effects of concern include neurotoxicity and kidney effects. USEPA(1990b) has derived an oral reference dose of 3E-4 mg/kg/day based on dataobtained from these studies and using an uncertainty factor of 1000. Mercury hasalso been shown to have severe reproductive effects such as delaying nerve celldevelopment and mental retardation (Marsh 1987). A wide range of symptoms havebeen associated with long-term ingestion of mercury-contaminated fish, such as
loss of motor control, behavioral changes, blindness, deafness, and death (USEPA1981).
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Weight of Evidence: D, not a human carcinogen
Noncarcinogenic Toxicity:Oral Reference Dose: 3.0E-4 mg/kg/dayOral Uncertainty Factor: 1000Critical Effect: neurotoxicity, kidney effects
REFERENCES:
Andres, P. 1984. IgA-IgG disease in the intestine of Brown Norway ratsingesting mercuric chloride. Clin. Immunol. Immunopathol. 20:488-494.
Bernaudin, J.F., E. Druet, P. Druet and R. Masse. 1981. Inhalation or ingestionof organic or inorganic mercurials produces auto-immune disease in rats.Clin. Immunol. Immunopathol. 20:129-135.
Druet, P., E. Druet, F. Potdevin and C. Sapin. 1978. Immune typeglomerulonephritis induced by HgCl2 in the Brown Norway rat. Ann. Immunol.129C:777-792.
Lyman, W.L., I. Bodek, W.F. Reehl, and D.H. Rosenblatt. 1987. .Methods forEstimating 'Physicochemical Properties of Inorganic Chemicals ofEnvironmental Concern. U.S. Army Medical Research and Development Command,Fort Detrick, MD. Contract No. DAMD 17-83-C-3274.
Rubin, A.J., Ed. 1976. Aqueous-Environmental Chemistry of Metals. An ArborScience Publishers, Inc., Ann Arbor, Michigan.
U.S. Environmental Protection Agency (USEPA). 1980. Ambient Water QualityDocument. USEPA 440/5-80 Series.
U.S. Environmental Protection Agency (USEPA). 1984. Health Effects Assessmentfor Mercury. Office of Emergency and Remedial Response, Washington, DC,USEPA-540/1-80-042.
U.S. Environmental Protection Agency (USEPA). 1985. Ambient Aquatic Life WaterQuality Criteria for Mercury. Office of Research and Development, Duluth,Minn. PB85-22745.
U.S. Environmental Protection Agency (USEPA). 1987. Peer Review Workshop onMercury Issues. October 26-27, 1987, Summary Report. EnvironmentalCriteria and Assessment Office, Cincinnati, OH.
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U.S. Environmental Protection Agency (USEPA). 1990. Bioaccumulation of SelectedPollutants in Fish. A National Study Vol. II. Assessment and WatershedProtection Division. Office of Water Regulations and Standards, USEPA,Washington, DC. December 1990.
U.S. Environmental Protection Agency (USEPA). 1990. Health Effects AssessmentSummary Tables (HEAST). Fourth Quarter FY-1990. OSWER, USEPA.
Windholz, M., ed. 1976. The Merck Index: An Encyclopedia of Chemicals, Drugs,and Biologicals, 10th ed. Merck & Co., Rahway, New Jersey.
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TOXICITY PROFILE FOR METHYLENE CHLORIDE
GENERAL DESCRIPTION:
Chemical Properties: Methylene chloride is a colorless, volatile liquid• having a molecular weight of 84.93 g/mol (Sax 1984). Methylene chloride
is a member of the halogenated aliphatic hydrocarbon (purgeablehalocarbon) chemical class of compounds.
Molecular Formula: CH2C12
Fate: Evaporation is expected to be the predominant loss mechanism fromthe soil surface. In subsurface soil, biodegradation of a chlorinatedaliphatic hydrocarbon such as methylene chloride may be slow (Wilson etal. 1983). Therefore, in subsurface soil, the nongraded methylenechloride is expected to leach into groundwater. In the atmosphere,methylene chloride is primarily removed by photochemical reactions (NLM,1987; Cox et al. 1976; Davis et al. 1976).
CARCINOGENIC EFFECTS:
Pertinent data regarding carcinogenicity in humans associated with methylenechloride could not be located in the available literature (USEPA 1984). NPT(1985) performed a cancer bioassay and found the following: 1) inhalation ofmethylene chloride vapors was associated with an increased incidence of benignmammary gland neoplasms and primarily fibroadenomas in rats; 2) a significantincrease in hepatocellular neoplastic modules and hepatocellular carcinomas infemale rats; 3) a statistically significant increase in mesotheliomas (primarilyin the tunica vaginal is) in male rats, and 4) a significant increase in adrenalpheochromocytomas and interstititial cell tumors in male rats and combinedincidence of pituitary gland adenomas and carcinomas in male and female rats(USEPA 1985, 1984). In mice, the NTP (1985) concluded that there was someevidence supporting carcinogenicity for methylene chloride for male rats as shownby increased incidence of benign neoplasms of the mammary gland; there was clearevidence of the carcinogenicity of methylene chloride for female rats as shownby an increased incidence of benign neoplasms of the mammary gland; there was
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clear evidence for the carcinogenicity in male and female mice as shown by anincreased incidence of lung and liver tumors. Methylene chloride has been shownto be mutagenic to Salmonella tvphimurium (Simmon, et al. 1977). Thilager andKumaroo (1983) observed extensive chromosomal aberrations in cultured Chinesehamster ovarian cells exposed to methylene chloride.
Based on the above studies, USEPA (1985b, 1986c) calculated an oral slope factorof 7.5E-3 (mg/kg/day)"1 and an inhalation slope factor of 1.4E-2 (mg/kg/day)'1.Methylene chloride is considered a probable human carcinogen (Group B2).
NONCARCINOGENIC EFFECTS:
In humans, chronic inhalation of methylene chloride resulted in somnolence,lassitude, anorexia and mild lightheadedness, disturbed central nervous systemfunction and depression (MAS, 1978). In chronic inhalation exposure of animalsto methylene chloride, Burek, et al. (1980, 1984) and Dow Chemical Company (1980)found rats suffered from a disease believed to be sialodacryoadenitis (atransient viral involvement of the salivary glands), increased liver weights,histopathologic alterations of the liver, an increased incidence ofhepatocellular vacuolization indicative of fatty degeneration, multinucleatedhepatocytes (a spontaneous geriatric change in female rats), a significantincrease in the number of foci of altered hepatocytes, hepatocellular necrosisand coagulation necrosis. A chronic inhalation study (Nitschke et al. 1988)involving rats inhaling 200 ppm, 6 hours/day, 5 days/week for 2 years was usedto derive an inhalation reference dose of 8.6E-1 mg/kg/day with an uncertaintyfactor of 100 (USEPA 1990).
A 24-month drinking water study (National Coffee Association 1982) derived aNOAEL for methylene chloride of 6.47 mg/kg/day based on a female rat study. Thetarget organ was identified as the liver. An oral reference dose of 6.0E-2mg/kg/day was derived based on this study using an uncertainty factor of 100(USEPA 1990).
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SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Oral Slope Factor: 7.5E-3 (mg/kg/day)'1Inhalation Slope Factor: 1.4E-2 (mg/kg/day)"1Weight of Evidence: B2
Noncarcinogenic Toxicity:Oral Reference Dose 6.0E-2 mg/kg/dayOral Uncertainty Factor: 100Inhalation Reference Dose: 8.6E-1 mg/kg/dayInhalation Uncertainty Factor: 100
REFERENCES:
Burek, J.D., K.D. Nitschke, T.J. Bell, et al. 1980. Methylene Chloride: A Two-Year Inhalation Toxicity and Oncogenicity Study in Rats and Hamsters.Final Report. Toxicology Research Laboratory, Health and EnvironmentalSciences, Dow Chemical USA, Midland, MI 49640. Co-sponsored by DiamondShamrock Corp., Dow Chemical, Co., Imperial Chemical Industry Ltd.,Stauffer Chemical Co., and Vulcan Materials Co.
Burek, J.D., K. D. Nitschke, T.J. Bell, et al. 1984. Methylene Chloride: ATwo-Year Inhalation Toxicity and Oncogenicity Study in Rats and Hamsters.Fund Appl. Toxicol. 4(1):30.
Cox, R.A., R.C. Denwent, A.E.J. Eggleton and J.E. Lovelock. 1976. Photochemicaloxidation of halocarbons in the troposphere. Atmos. Environ. 10:305-308.
Davis, D.D., G. Machado, B. Conaway, Y. Oh and R. Watson. 1976. A temperaturedependent Kinetics study of the reaction of OH with CH0C1, CH2C12 and CH3.Br. J. Chem. Phys. 65(4):1268-1274.
Dow Chemical Co. 1980. Methylene Chloride. A Two-Year Inhalation Toxicity andOncogenicity Study in Rats and Hamsters. FYI-OTS-0281-0097. Follow-UpResponse A. USEPA, Office of Toxic Substances, Washington, DC.
NAS (National Academy of Sciences). 1978. Nonfluorinated Halomethanes in theEnvironment. Washington, DC.
National Coffee Association. 1982. 24-North Chronic Toxicity and OncogenicityStudy of Methylene Chloride in Rats. Final Report. Prepared by Hazel tonLaboratories America, Inc., Vienna, VA.
Nitschke, K.D., J.D. Bured, T.J. Bell et al. 1988. Methylene Chloride: A. 2-year inhalation toxicity and Oncogenicity study in rats. Fund. Appl.Toxicol.
NLM (National Library of Medicine). 1987. Hazardous Substance Data Bank.Report No. 66. Computer Printout.
NTP (National Toxicology Program). (1985, Feb). NTP Technical Report on thetoxicology and Carcinogenesis Studies of Dichloromethane in F344/N Ratsand B6C3F1 Mice/Inhalation Studies. NTP TR 306. Board draft.
Sax, Irving I. 1984. Dangerous Properties of Industrial Chemicals. New York:Van Nostrand Reinhold Company.
Simmon, V.F., et al. 1977. Mutagenic Activity of Chemicals Identified inDrinking Water: In: Progress in Genetic Toxicology, S. Scott, et al., Ed.
U.S. Environmental Protection Agency (USEPA). 1984. Health Effects Assessmentof Methylene Chloride. Office of Health and Environmental Assessment,Environmental Criteria and Assessment Office, Cincinnati, OH; Office ofSolid Waste and Emergency Response, Washington, DC. USEPA/540/1-867/028.NTIS PB 86-134392.
U.S. Environmental Protection Agency (USEPA). 1985. Addendum to the HealthAssessment Document for Dichloromethane (Methylene Chloride), UpdatedCarcinogenicity Assessment of Dichloromethane (Methylene Chloride).Office of Research and Development, Washington, DC. USEPA/600/8-82/004F.
U.S. Environmental Protection Agency (USEPA). 1986c. Integrated RiskInformation System (IRIS). Carcinogenicity Assessment for LifetimeExposure to Methylene Chloride. On-line. (Verification date 12/04/86.)Office of Health and Environmental Assessment, Environmental Criteria andAssessment Office, Cincinnati, OH.
U.S. Environmental Protection Agency (USEPA). 1990. Health Effects AssessmentSummary Tables (HEAST). Fourth Quarter FY-1990. OSWER, USEPA.
Wilson, J.T., J.F. McNabb, B.H. Wilson, and M.J. Noonan. 1983.Biotransformation of Selected Organic Pollutants in Groundwater. Dev.Ind. Microbiol. 24:255-233.
HR3QI33I
TOXICITY PROFILE FOR TETRACHLOROETHENE
GENERAL DESCRIPTION:
Chemical Properties: Tetrachloroethane is a member of the halogenatedaliphatic hydrocarbon (purgeable halocarbon) chemical class of compounds.Tetrachloroethane has a molecular weight of 165.83 g/mol (USEPA 1988).
Molecular Formula: C2CL4
Absorption: Tetrachloroethene is almost completely absorbed by thegastrointestinal tract. One study involving an oral dose oftetrachloroethene found that 98% of the dose was eliminated in expired airand 2% in urine of rats (Daniel 1963). A second study using a dose of 500mg/kg tetrachloroethene found that 85% of the dose was eliminated inexpired air and 12% in urine of mice (Schumann et al. 1980). For humans,tetrachloroethene is readily absorbed by the lungs (von Oettingen 1964).
Fate: Tetrachloroethene is primarily removed from the atmosphere byphotochemical reactions. Tetrachloroethene is removed from surface watersand surface soils by volatilization. Tetrachloroethene is very mobile insoil and is expected to leach into groundwater (NLM 1987).Tetrachloroethene may undergo dechlorination reactions through microbialbiodegradation to form trichloroethene.
CARCINOGENIC EFFECTS:
NCI (1977) in an oral carcinogenic bioassay administered various levels oftetrachloroethene in corn oil by gavage to Osborne-Mendol rats and mice. Thestudy ran 5 days/week for 78 weeks. In both species, decreased survival rateswere observed. Of the rats treated, no increases in tumor incidence wereobserved. However, of the mice treated, there were significant increases inhepatocellular carcinomas. Based on this study, an oral slope factor of 5.1E-2(mg/kg/day)"1 was derived (USEPA 1990). Evidence of carcinogenicity oftetrachloroethene cited by NTP (1986) showed an increased incidence of
/1R30I332
mononuclear cell leukemia in F344/N male and female mice, uncommon renal tubularcell neoplasms for F344/N male mice, and increased evidence of hepatocellularadenomas and carcinomas for either sex of B6C3F1 mice following inhalationexposure. USEPA (1990) derived an inhalation slope factor of 3.3E-3 (mg/kg/day)'1 based on results of this study.
NONCARCINOGENIC EFFECTS:
Bruben and O'Flaherty (1985) administered tetrachloroethene in corn oil to maleSwiss-Cox mice by gavage in doses of 0, 20, 100, 200, 500, 1500, and 2000 mg/kg,5 days/week for 6 weeks. Several hepatotoxic effects were observed including:increased liver weight/body weight ratio, decreased DNA content, increased livertriglycerides, and increased SGPT. An oral reference dose of IE-2 mg/kg/day was
.calculated based on the above study (USEPA 1991).
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Oral Slope Factor: 5.1 E-2 (mg/kg/day)"1Inhalation Slope Factor: 3.3 E-3 (mg/kg/day)"1Weight-of-Evidence: 82
Noncarcinogenic Toxicity:Oral Reference Dose: IE-2 mg/kg/dayOral Uncertainty Factor: 1000Critical Effect: Hepatotoxicity in mice, weight gain in rats
REFERENCES:
Buben, J.A. and E.J. O'Flaherty. 1985. Delineation of the role of metabolism inthe hepatotoxicity of trichloroethylene and perchloroethylene: A dose -effect study. Toxicol. Appl. Pharmacol. 78:105-122.
Daniel, J.W. 1963. The metabolism of Cl-labeled trichloroethylene andtetrachlorbethylene in the rat. Biochem. Pharmacol. 12:795-801.
NCI (National Cancer Institute). 1977. Bioassay of Tetrachloroethylene forPossible Carcinogenicity. NCI Carcinogenesis Tech. Rep. Ser. No. NCI-CGTR-13. [Also publ. as DHHS (NIH) 77-813].
NLM (National Library of Medicine). 187. Hazardous Substance Data Base. RecordNo. 124:on-line.
NTP (National Toxicology Program). 1986. Toxicology and carcinogenesis studiesof tetrachloroethylene (perchloroethylene) in F344/N rats and B6C31 mice(inhalation studies). NTP Tech. Report Series No. 311.
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Schumann, A.M., J.F. Quast and P.G. Watanabe. 1980. The pharmacokinetics andmacromolecular interactions of perchloroethylene in mice and rats asrelated to oncogenicity. Toxicol. Appl. Pharmacol. 55:207-219.
U.S. Environmental Protection Agency (USEPA). 1990. Health Effects AssessmentSummary Tables (HEAST). Fourth Quarter FY-1990. OSWER, USEPA.
von Oettingen, W.R. 1964. The Halogenated Hydrocarbons of Industrial andToxicological Importance. Elsevier Press, Amsterdam, p. 271-283.
BR30I33I4
TOXICITY PROFILE FOR TRICHLOROETHENE
GENERAL DESCRIPTION:
Chemical Properties: Trichloroethene is a halogenated aliphatichydrocarbon with a molecular weight of 131.4 g/mol (USEPA 1988). Thevapor pressure for trichloroethene is 57.9 mmHg and the water solubilityis 1100 mg/L both at 20°C (Callahan et al., 1979). The reported Log Kowis 2.42 from Hansch and Leo (1985). The Koc value has been determined torange from 87-150 (NLM 1987).
Absorption: Rats and mice, given doses ranging 10-2000 mgtrichloroethene/kg in corn oil by gavage, showed a 92-100% absorptionafter 24-72 hours of exposure. This percentage was determined aftermeasuring the radioactivity in the urine, feces, expired air, andcarcasses (Prout et al. 1985). In humans, rapid absorption oftrichloroethene by the lungs occurs, and complete tissue equilibrium isachieved after -8 hours of exposure (USEPA 1985).
Fate: Reaction with photochemically generated hydroxyl radicals is theprimary mechanism of removal of trichloroethene from the atmosphere.Phosgene, dichlorocetyl chloride, and formyl chloride are products of thisreaction. Trichloroethene degrades in hours in photochemical smogsituations (NLM 1987). Trichloroethene also may undergo dechlorinationreaction via microbial biodegradation to form 1,2-dichloroethene.Trichloroethene volatilizes in water and neither bioaccumulation inaquatic organisms nor adsorption to sediments are expected to be importantfate processes (NLM 1987).
Based on its Koc and a retardation factor of soil mobility of 1.6,trichloroethene is considered to be fairly mobile in soil (Wilson et al.1981). Leaching from soil into groundwater is a significant route fortrichloroethene (NLM 1987). Volatilization from soil is also expected,though this would be slower than volatilization from water (Wilson et al.1981).
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CARCINOGENIC EFFECTS:
Oral: NCI (1976) performed a bioassay in which groups of 50 or each sex of ratsand mice were given trichloroethene by gavage over a 78-week period. Asignificant increase in hepatocellular carcinomas was noted in males at low andhigh dose levels and in females at the high dose level. NTP (1982) alsoperformed a gavage study with two different dosages on similar numbers of ratsfor 103 weeks. Males given the higher dosage had a significant increase in renaladenocarcinomas. Results from a single-dose gavage bioassay on mice were alsopublished with this study (NTP, 1982). Again there was a significant increasein the incidence of hepatocellular carcinomas for males and females, which helpsto support the NCI (1976) study. Based on the geometric means for risk estimatesextrapolated to humans for both of these studies, USEPA (1988) derived an oralslope factor of 1.1E-2 (mg/kg/day)"1.
Inhalation: In a study by Fukada et al. (1983) mice which were exposed tovarying levels of trichloroethene for more than one year showed an increase inlung adenocarcinomas. Maltoni et al. (1986) performed a similar study in whichthey observed a significant dose-related increase in testicular Leydig cellcarcinomas, leukemia, and renal tumors in male rats. Increased hepatomas andlung tumors were noted in mice (Maltoni 1986). USEPA (1988) used the geometricmeans of the risk estimates form the results for mice in the two studiesdiscussed above to derive an inhalation slope factor of 1.7E-2 (mg/kg/day)"1.The data from mice were used because the results were seen in many mice strainsand in both sexes.
NONCARCINOGENIC EFFECTS:
A chronic bioassay study of trichloroethene performed on rats showed a decreasein body weights and a decrease in survival. The same experiment was performedon mice which showed no effects of chronic exposure to trichloroethene (NCI1976). Similar studies by NTP (1982, 1986) showed comparable results to the NCIstudy with dose-related responses using doses ranging from 0-1000 mg/kgtrichloroethene. A subchronic inhalation study in rats showed an elevation ofliver weight to occur following exposure to 55 ppm, 5 days/week for 14 weeks(Kimmerle and Eben 1973). USEPA (1987) derived an oral reference dose (RfD) of
7.35 x 10'3 mg/kg/day based on results of this study and using an uncertaintyfactor of 1000. This RfD is currently under review for verification by ECAO.Because trichloroethene is the primary contaminant for the Butz Landfill site,the use of this tentative RfD is important to evaluate potential noncarcinogeniceffects for the site.
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:. Oral Slope Factor: 1.1E-2 (mg/kg/day)'1
Inhalation Slope Factor: 1.7E-2 (mg/kg/day)'1Weight-of-Evidence: B2
Noncarcinogenic Toxicity:Oral Reference Dose: 7.35E-2 mg/kg/dayOral Uncertainty Factor: 1000
REFERENCES:
Callahan, M.A., M.W. Slimak, N.W. Gabel, et al. 1979. Water-RelatedEnvironmental fate of 129 Priority Pollutants, Vol. II. USEPA, Office ofWater Planning and Standards, Office of Water and Waste Management,Washington, DC. USEPA 440/4-79-029b.
Fukuda, K., K. Takemoto and H. Tsuruta. 1983. Inhalation carcinogenicity oftrichlorethylene in mice and rats. Ind. Health. 21: 243-254.
Hansch C. and A.J. Leo. 1985. MedChem Project Issue No. 26, Pomona College,Claremont, CA.
Kimmerle G. and A. Eben. 1973. Metabolism, excretion and toxicology oftrichloroethene after inhalation. 1. Experimental exposure on rat, Arch.Toxicol. 30: 115.
Maltoni, C., G. Lefemine and G. Cotti. 1986. Experimental research ontrichloroethylene carcinogenesis. Arch. Res. Industrial CarcinogenesisSeries. C. Maltoni and M.A. Mehlman, Ed. Vol. V. Princeton ScientificPubl. Co. Inc., Princeton, NY. 393pp. (Cited in USEPA, 1987)
NCI (National Cancer Institute). 1976. Bioassay of Trichlorethylene. NCICarcinogenesis Tech. Rep. Ser. No. 2.. 197 p. [Also publ. as DHEW (NIH)76-802]
NLM (National Library of Medicine). 1987. National Library of MedicineHazardous Substance Data Base. Report No. 133. On line.
NTP' (National Toxicology Program). 1982. Carcinogenesis bioassay oftrichloroethylene. NTP Tech. Rep. Ser. No. 81-84. [Also published as NIH82-1799.] (Cited in USEPA, 1985)
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NTP (National Toxicology Program). 1986. NTP Board Draft Technical Report onthe Toxicology and Carcinogenesis Studies of Trichloroethylene in FourStrains of Rats (ACI, August, Marshall, Osborne-Mendel) (Gavage Studies).NTP Tech. Rep. Ser. No. 273. [Also published as NIH 86-2529.]
U.S. Environmental Protection Agency (USEPA). 1985. Health Assessment Documentfor Trichloroethene. Office of Health and Environmental Assessment,Environmental Criteria and Assessment Office, Research Triangle Park, N.C.
U.S. Environmental Protection Agency (USEPA). 1987. Health Advisory forTrichlororethene. Office of Drinking Water, Washington, D.C. March 31,1987.
U.S. Environmental Protection Agency (USEPA). 1988. Health Effects Assessmentfor Trichloroethylene. Office of Health and Environmental Assessment,Cincinnati, OH.
U.S. Environmental Protection Agency (USEPA). 1990. Subsurface ContaminationReference Guide. Office of Emergency and Remedial Response, Washington,D.C.
Wilson, J.T., C.G. Enfield, W.J. Dunlop, R.L. Cosby, D.A. Foster and L.B.Baskin. 1981. Transport and Fate of Selected Pollutants in a StudySoil. J. Environ. Qua!. 10: 501-506.
3R301338
TOXICITY PROFILE FOR VINYL CHLORIDE
GENERAL DESCRIPTION:
Chemical Properties: Vinyl chloride is a member for the halogenatedaliphatic hydrocarbon class of compounds. This compound has a molecularweight of 62.5 g/mol and a vapor pressure of 2660 mm Hg at 25°C (Calahanet al. 1979). The water solubility of vinyl chloride ranges from 2760mg/1 at 25'C (Horvath 1982) to 1100 mg/kg at 28°C (USEPA 1980).
Absorption: Rapid absorption of vinyl chloride form the gastrointestinaltract into the blood has been documented by Withey (1976) and Watanabe etal. (1976), however, no quantitative data are available. Sufficientquantitative data are available to suggest rapid absorption andequilibration of vinyl chloride from the lungs into the blood stream.Rats exposed to 20,000 ppm for five minutes were found to have vinylchloride permeating several tissues 10 minutes later (Duprat et al. 1977).In addition, Withey and Collins (1976) found that inhalation of 1.97 ppmvinyl chloride was equivalent to gavage treatment with 4.5 mg/kg/day.
Fate: The half-life of vinyl chloride in air has been shown to be 1.2days (Singh et al. 1981). In water, the half-life has been estimated torange from several minutes to five days (Callahan et al. 1979). The half-lives for vinyl chloride in water have been derived based on thereaeration ratio (0.675) and the oxygen reaeration rate of 0.19-0.96 day-1(Mabey et al. 1981). The fate of vinyl chloride in soil is not known withcertainty. Evaporation is expected to be the predominant loss mechanism(Callahan 1979).
CARCINOGENIC EFFECTS:
USEPA (1990) derived an oral slope factor of 1.9 (mg/kg/day)"1 based on an oralbioassay performed on rats by Feron et al. (1981). A group of 60 male and 60.female rats were given polyvinyl chloride powder (not containing more than 0.3ppm) in their diets or by gavage. Polyvinyl chloride powder acted as a liquidcarrier for vinyl chloride monomer. The feeding trials lasted 135 weeks for the
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male rats and 144 weeks for the female rats. At 80 weeks of treatment, doserelated decrease in survival was reported as well as, for both sexes, anincreased incidence of hepatocellular carcinomas and lung and liverangiocarcinomas.
Infante (1981) reviewed epidemiological data concerning humans inhaling vinylchloride. Data recovered indicates an association between the inhalationexposure to vinyl chloride and the occurrence of liver cancer, brain cancer, andlung cancer. Waxweiler et al. (1976) reported a small rise in the frequency ofliver, lung, and brain cancer in workers exposed to vinyl chloride. Maltoni(1977b) performed a bioassay on Sprague-Dawley rats exposed to vinyl chloride byinhalation. Maltoni reported an increased incidence of hepatic angiosarcoma andrenal nephroblastomas. USEPA (1985), based on the above studies, calculated aninhalation slope factor of 2.95E-1 (mg/kg/day)"1.
NONCARCINOGENIC EFFECTS:
Feron et al. (1981) performed a study on rats in which they were administered avinyl chloride monomer. Rats had increased liver size, decreased adrenal size,and decreased number of leukocytes in males. There was decreased blood sugar inboth sexes. Also, with dietary levels of vinyl chloride at doses of 0, 1.7, 5.0,and 14.1 mg/kg/day as determined by measured food consumption, a dose relatedincrease in mortality was reported, with decreased survival at all dose levels.No noncarcinogenic toxicity criteria have been derived for vinyl chloride.
SUMMARY OF TOXICITY CRITERIA:
Carcinogenic Toxicity:Oral Slope Factor: 1.9 (mg/kg/day)'1Inhalation Slope Factor: 2.95E-1 (mg/kg/day)'1Weight of Evidence: A
Noncarcinogenic Toxicity: ND
REFERENCES:
Calahan, M.A., M.W. Slimak, N.W. Gabel et al., 1979. Water-relatedenvironmental fate of 129 priority pollutants. Vol. II. Office of WaterPlanning and Standards, Office of Water and Waste Management, USEPA,Washington, O.C.
Duprat, P., et al., 1977. Metabolic approach to industrial poisoning: Bloodkinetics and distribution of 14-C vinyl chloride monomer (VCM). Toxicol.Pharmacol. Suppl. 142.
Feron, V.J., C.F.M. Hendriksen, A.J. Speek, H.P. Til and B.J. Spit. 1981.Lifespan oral toxicity study of vinyl chloride in rats. Food Cosmet.Toxicol. 19: 317-333.
Horvath, A.L. 1982. Halogenated Hydrocarbons Solubility. Miscibility withwater. Marcel Dekker, Inc., NY. p. 494.
Infante, P.F. 1981. Observations of the site-specific carcinogenicity of vinylchloride to humans. Environ. Health Perspect. 41: 89.
Mabey, W.R., J.H. Smith,. R.T. Rodoll, et al., 1981. Aquatic Fate Process Datafor Organic Priority Pollutants. Monitoring and Data Support Division,Office of Water Regulation and Standards, Washington, D.C.
Maltoni, C. 1977b. Recent findings on the carcinogenicity of chlorinatedolefins. Environ. Health Perspect. 21: 1-5.
Singh, H.B., L.J. Salas, A.J. Smith and H. Shigeishi. 1981. Measurements ofsome potentially hazardous organic chemicals in urban environments.Atmos. Environ. 15: 601-612.
U.S. Environmental Protection Agency (USEPA). 1984. Health Effects Assessmentsfor Vinyl Chloride. Office Research and Development. Office of Health anEnvironmental Assessment, Cincinnati, OH.
U.S. Environmental Protection Agency (USEPA). 1984. Review of acarcinogenicity study on vinyl chloride. Prepared by the CarcinogenAssessment Group, OHEA, Washington, DC for the Office of Drinking Water.Washington, DC. Memorandum from Larry Anderson and Steven Bayard toJoseph Cotruvo. January 6.
U.S. Environmental Protection Agency (USEPA). 1985. Drinking Water CriteriaDocument for Vinyl Chloride. Office of Drinking Water, Washington, DC.Final Draft.
U.S. Environmental Protection Agency (USEPA). 1990. Health Effects AssessmentSummary Tables. September 1990.
Watanabe, P.G., G.R. McGowan and P.J. Gehring. 1976a. Fate of (UC) vinylchloride after single oral administration in rats. Toxicol Appl.Pharmacol. 36: 339-352.
Waxweiler, R.J., W. Stringer, J.K. Wagoner, J. Jones, H. Falk, and C. Carter.1976. Neoplastic risk among workers exposed to vinyl chloride. Ann. NYAcad. Sci. 271: 40-48.
Withey, J.R. 1976. Pharmacodynamics and uptake of vinyl chloride monomeradministered by various routes to rats. J. Toxicol. Environ. Health. 1:381-394.
Withey, J.R. and B.T. Collins, 1976. A statistical Assessment of thequantitative uptake of vinyl chloride monomer for aqueous solutions. J.Toxicol. Environ. Health. 2:311.
TCN 4204RI REPORT
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£830131*3
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-2
NO ACTION WITH MONITORING
DIRECTITEM______________________ CAPITAL ANNUAL O&M
Ground Water Monitoring - BiannuallyDirect Capital • -0-
Annual O&Msampling & travel (2 days@ $2,000/day for 3 people) 8,00055 gal. disposal carbon units
(direct cost plus disposal) , 10,000laboratory analysis (3 shallow
and 3 deep wells @ $4,000 ea.) 48,000QA/QC sampling (3 @ $4,000 ea.) 24,000laboratory coordination, data validation,
data evaluation, and report preparation 15,000
Total Direct Capital Costs . $ -0-
Total Annual O&M Costs $ 105,000
Remedial Action & Remedial DesignConsulting Services 30,000
Legal & Administrative 20,000Contingency 20,000 20,000
Total Capital $ 70,000
Total Annual O&M $ 125,000
Present Worth of Annual O&M(8 % % for 30 years) $ 1.321.000
TOTAL PRESENT WORTH COST $ 1,391,000
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-3
GROUND WATER - INSTITUTIONAL CONTROLS
DIRECT DIRECTITEM____________________ CAPITAL COST 1997
Institutional Controls & Deed RestrictionsDirect Capital -0- -0-
Total Direct Capital Costs -0- -0-Remedial Action & Remedial Design
Consulting Services 25,000Legal & Administrative 50,000Contingency 50,000
Total Capital Cost $ 125,000
Institutional Controls Review in 1997 $ 20,000
Present Worth of Future Cost(8 % % for 5 years) $ 13.000
TOTAL PRESENT WORTH COST $ 138,000
TCN 4204RI/FS REPORT
REV. il30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-4A
GROUND WATER CONTAINMENT, TREATMENT BY AIR STRIPPING, AND DISPOSAL
DIRECTITEM_______________________ CAPITAL ANNUAL O&M
Bedrock Aquifer Extraction Well SystemDirect Capital
clearing & grubbing (0.5 acre foraccess & pipes) 4,000
tree removal (0.25 acre) 2,000piping to treatment plant (800 LF @ $20/LF) 16,0006" <p well installation, * 150 feet deep
(5 wells <a $15,000 ea.) 75,000decontamination; disposal of cuttings &
water (5 @ $6,000 ea.) 30,000electrical power (5 @ $2,000 ea.) 10,000electrical equipment, controls, 15 gpm
pumps, pit-less adaptor, low watershut-off, etc. (5 (<> $7,000 ea.) 35,000
$ 172,000Annual O&M
power (5 @ $2,000 ea.) 10,000equipment replacement 5,000
$ 15,000
Site Work/Road to Treatment PlantDirect Capital
1,500 LF & $50/LF $ 75,000
Chemical Precipitation System - 75 gpmDirect Capital $ 500,000
Annual O&Mequipment replacement
and sludge disposal $ 20,000
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-4A
GROUND WATER CONTAINMENT, TREATMENT BY AIR STRIPPING, AND DISPOSAL
DIRECTITEM___________________ CAPITAL ANNUAL O&M
Air Stripping Towers and Vapor Phase Carbon - 75 gpraDirect Capital - based on 25 mg/2 VOC Influent
System: two towers ea. 2' $ 26 ft. talltowers, two vapor phase carbon units,dual heaters, two blower, two pumps,2,000 gallon flow equalization tank,control panel, and installation 250,000
clearing & grubbing (0.25 acre) 3,000tree removal (0.25 acre) 2,000building 60,000electrical power supply from North Road 40,000
$ 355,000Annual O&M
equipment replacement, power,and carbon regeneration or disposal $ 140,000
Stream DischargeDirect Capital
clearing & grubbing (0.25 acre foraccess & pipes) 3,000
tree removal (0.25 acre) 2,000pipe (500 LF (<> S70/LF) 35,000
$ 40,000
Annual O&Mstream monitoring ($4,000/month) $ 48,000laboratory coordination, data validation,
data evaluation, and report preparation 36,000
Sub Total $ 1,162,000
Direct Capital Contingency (10%) 116,000
$ 84,000
Start Up $ 20,000
Total Direct Capital Costs $ 1,278,000
Total Annual O&M Costs $ 259,000
flR30l3i*7
TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-4A
GROUND WATER CONTAINMENT, TREATMENT BY AIR STRIPPING, AND DISPOSAL
DIRECTITEM______________________ CAPITAL ANNUAL O&M
SUMMARY
Total Direct Capital Costs $ 1,278,000
Total Annual O&M Costs $ 259,000
Remedial Action & Remedial DesignConsulting Services (40%) 511,000
Legal & Administrative (25%) 320,000Contingency (25%) 320,000 65,000
Total Capital $ 2,429,000
Total Annual O&M $ 324,000
Present Worth of Annual O&M(8 % % for 30 years) S 3.425.000
TOTAL PRESENT WORTH COST $ 5,854,000
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-4B
GROUND WATER CONTAINMENT, TREATMENT BY CARBON ADSORPTION, AND DISPOSAL
DIRECTITEM___________________________ CAPITAL ANNUAL O&M
Bedrock Aquifer Extraction Well SystemDirect Capital
clearing & grubbing (0.5 acre foraccess & pipes) 4,000
tree removal (0.25 acre) 2,000piping to treatment plant (800 LF @ $20/LF) 16,0006" 0 well installation, ~ 150 feet deep
(5 wells & $15,000 ea.) 75,000decontamination; disposal of cuttings &
water (5 @ $6,000 ea.) 30,000electrical power (5 @ $2,000 ea.) 10,000electrical equipment, controls, 15 gpm
pumps, pit-less adaptor, low watershut-off, etc. (5 @ $7,000 ea.) 35,000
$ 172,000Annual O&M
power (5 @ $2,000 ea.) 10,000equipment replacement 5,000
$ 15,000
Site Work/Road to Treatment PlantDirect Capital
1,500 LF 9 $50/LF $ 75,000
Chemical Precipitation System - 75 gpmDirect Capital $ 500,000Annual O&M
equipment replacementand sludge disposal $ 20,000
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-4B
GROUND WATER CONTAINMENT, TREATMENT BY CARBON ADSORPTION, AND DISPOSAL
DIRECTITEM_______________________ CAPITAL ANNUAL O&M
Granular Activated Carbon (GAC) - 75 gpmDirect Capital - based on 25 mg/2 influent
System: two skids, equalization tank,control panel, transfer pump, twoGAC units in series, installation 300,000
clearing & grubbing (0.25 acre) 3,000tree removal (0.25 acre) 2,000building 70,000electrical power supply from North Road 40,000
$ 415,000Annual O&M
equipment replacement, power,and carbon regeneration/replacement $ 200,000
Stream DischargeDirect Capital
clearing & grubbing (0.25 acre foraccess & pipes) 3,000
tree removal (0.25 acre) 2,000pipe (500 LF 9 $70/LF) $ 35,000
$ 40,000
Annual O&Mstream monitoring ($4,000/month) • $ 48,000laboratory coordination, data validation,
data evaluation, and report preparation 36,000
Sub Total $ 1,222,000
Direct Capital Contingency (1-0%) 122,000
$ 84,000
Start Up $ 20,000
Total Direct Capital Costs $ 1,344,000
Total Annual O&M Costs $ 319,000
AR30I350
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-4B
GROUND WATER CONTAINMENT, TREATMENT BY CARBON ADSORPTION, AND DISPOSAL
DIRECTITEM_______________________ CAPITAL ANNUAL O&M
SUMMARY
Total Direct Capital Costs $ 1,344,000
Total Annual O&M Costs $ 319,000
Remedial Action & Remedial DesignConsulting Services (40%) 538,000
Legal & Administrative (25%) 336,000Contingency (25%) 336,000 80,000
Total Capital $ 2,554,000
Total Annual O&M $ 399,000
Present Worth of Annual O&M(8 % % for 30 years) $ 4.217.000
TOTAL PRESENT WORTH COST $ 6,771,000
8
3R30I35I
TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-5A
GROUND WATER PLUME COLLECTION, TREATMENT BY AIR STRIPPING, AND DISPOSAL
DIRECTITEM_________________________ CAPITAL ANNUAL O&M
Bedrock Aquifer Extraction Well SystemDirect Capital
clearing & grubbing (3.0 acre foraccess & pipes) 20,000
tree removal (1.5 acre) 10,000piping to treatment plant (6,400 LF @ $20/LF) 128,0006" 0 well installation, = 150 feet deep
(15 wells 0 $15,000 ea.) 225,000decontamination; disposal of cuttings &
water (15 0 $6,000 ea.) 90,000electrical power (15 @ $3,000 ea.) 45,000electrical equipment, controls, 15 gpm
pumps, pit-less adaptor, low watershut-off, etc. (15 9 $7,000 ea.) 105,000
$ 623,000Annual O&M
power (15 @ $2,000 ea.) 30,000equipment replacement 15,000
$ 45,000
Site Work/Road to Treatment PlantDirect Capital
1,500 LF 0 $50/LF $ 75,000
Chemical Precipitation System - 225 gpmDirect Capital $ 1,000,000
Annual O&Mequipment replacement
and sludge disposal $ 60,000
AR30I352
TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-5A
GROUND WATER PLUME COLLECTION, TREATMENT BY AIR STRIPPING, AND DISPOSAL
DIRECTITEM__________________________ CAPITAL ANNUAL O&M
Air Stripping Towers and Vapor Phase Carbon - 225 gpmDirect Capital - based on 25 mg/£ VOC influent
System: two towers ea. 4' 0 26 ft. talltowers, two vapor phase carbon units,dual heaters, two blower, two pumps,5,000 gallon flow equalization tank,control panel, and installation 450,000
clearing & grubbing (0.5 acre) 5,000tree removal (0.5 acre) 3,000building 150,000electrical power supply from North Road 40,000
$ 648,000Annual O&M
equipment replacement,power, and carbon regenerationor disposal $ 260,000
Stream DischargeDirect Capital
clearing & grubbing (0.25 acre foraccess & pipes) 3,000
tree removal (0.25 acre) 2,000pipe (500 LF @ $80/LF) $ 40,000
Sub Total $ 2,431,000
Direct Capital Contingency (10%) 243,000
$ 45,000
Annual O&Mstream monitoring ($4,000/month) $ 48,000laboratory coordination, data validation,
data evaluation, and report preparation 36,000
$ 84,000Start Up $ 40,000
Total Direct Capital Costs $ 2,674,000
Total Annual O&M Costs $ 449,000
10
SR30J353
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-5A
GROUND WATER PLUME COLLECTION, TREATMENT BY AIR STRIPPING, AND DISPOSAL
DIRECTITEM________________________ CAPITAL ANNUAL O&M
SUMMARY
Total Direct Capital Costs $ 2,674,000
Total Annual O&M Costs $ 449,000
Remedial Action & Remedial Design •Consulting Services (40%) 1,070,000
Legal & Administrative (25%) 669,000Contingency (25%) 669,000 112,000
Total Capital $ 5,082,000
Total Annual O&M $ 561,000
Present Worth of Annual O&M(8 \ % for 30 years) $ 5.930.000
TOTAL PRESENT WORTH COST $ 11,012,000
11
TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-5B
GROUND WATER PLUME COLLECTION, TREATMENT BY CARBON ADSORPTION, AND DISPOSAL
DIRECTITEM__________________________ CAPITAL ANNUAL O&M
Bedrock Aquifer Extraction Well SystemDirect Capital
clearing & grubbing (3.0 acre foraccess & pipes) 20,000
tree removal (1.5 acre) 10,000piping to treatment plant (6,400 LF @ $20/LF) 128,0006" 0 well installation, = 150 feet deep
(15 wells @ $15,000 ea.) 225,000decontamination; disposal of cuttings &
water (15 9 $6,000 ea.) 90,000electrical power (15 @ $3,000 ea.) 45,000electrical equipment, controls, 15 gpm
pumps, pit-less adaptor, low watershut-off, etc. (15 @ $7,000 ea.) 105,000
$ 623,000Annual O&M
power (15 (a $2,000 ea.) 30,000equipment replacement 15,000
$ 45,000
Site Work/Road to Treatment PlantDirect Capital
1,500 LF @ $50/LF $ 75,000
Chemical Precipitation System - 225 gpmDirect Capital $ 1,000,000
Annual O&Mequipment replacement
and sludge disposal $ 60,000
12
AR30I355
TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-5B
GROUND WATER PLUME COLLECTION, TREATMENT BY CARBON ADSORPTION, AND DISPOSAL
DIRECTITEM_________________________ CAPITAL ANNUAL O&M
Granular Activated Carbon (GAC) - 225 gpraDirect Capital - based on 25 mg/JH influent
System: four skids, equalization tank,control panel, transfer pump, twoGAC units in series and two inparallel, installation 600,000
clearing & grubbing (0.5 acre) 5,000tree removal (0.5 acre) 3,000building 150,000electrical power supply from North Road 40,000
$ 798,000Annual O&M
power, equipment replacement,and carbon regeneration/replacement $ 500,000
Stream DischargeDirect Capital
clearing & grubbing (0.25 acre foraccess & pipes) 3,000
tree removal (0.25 acre) 2,000pipe (500 LF 9 $80/LF) $ 40,000
$ 45,000Annual O&M
stream monitoring ($4,000/month) $ 48,000laboratory coordination,,data validation,
data evaluation, and report preparation 36,000$ 84,000
Start Up $ 40,000
Sub Total $ 2,581,000
Direct Capital Contingency (10%) 258,000
Total Direct Capital Costs $ 2,839,000Total Annual O&M Costs $ 689,000
13
1356
TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE GW-5B
GROUND WATER PLUME COLLECTION, TREATMENT BY CARBON ADSORPTION, AND DISPOSAL
DIRECTITEM___________________________ CAPITAL ANNUAL O&H
SUMMARY
Total Direct Capital Costs $ 2,839,000
Total Annual O&M Costs $ 689,000
Remedial Action & Remedial DesignConsulting Services (40%) 1,136,000
Legal & Administrative (25%) 710,000Contingency (25%) 710,000 172,000
Total Capital $ 5,395,000
Total Annual O&M $ 861,000
Present Worth of Annual O&M(8 % % for 30 years) $ 9.100.000
TOTAL PRESENT WORTH COST $ 14,495,000
14
SR30I357
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE LF-2
LANDFILL - INSTITUTIONAL CONTROLS
DIRECT DIRECTITEM______________________ CAPITAL COST 1997
Institutional Controls & Deed RestrictionsDirect Capital -0- -0-
Total Direct Capital Costs -0- -0-
Remedial Action & Remedial DesignConsulting Services 20,000
Legal & Administrative 40,000Contingency 50,000
Total Capital Cost $ 110,000
Institutional Controls Review in 1997 $ 10,000
Present Worth of Future Cost(8 % % for 5 years) $ 7.000
TOTAL PRESENT WORTH COST $ 117,000
15
4R30I358
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE LF-3
SOIL CAP RESTORATION AND MAINTENANCE
DIRECTITEM___________________________ CAPITAL ANNUAL O&M
Landfill Repair & MaintenanceDirect Capital
soil borings (100 @ $50 ea.) 5,000soil (4,000 cy @ $50/cy) 200,000seed, mulch, fertilizer
(5 acres @ $15,000/acre) 75,000
Annual O&Msite review and repair 10,000mowing grass (10 times/year @ $1,500 ea.) 15,000
Sub Total $ 280,000
Direct Capital Contingency (10%) 28,000
Total Direct Capital Costs $ 308,000
Total Annual O&M Costs $ 25,000
Remedial Action & Remedial DesignConsulting Services (30%) 92,000
Legal & Administrative (25%) 77,000Contingency (25%) 77,000 6,000
Total Capital $ 554,000
Total Annual O&M $ 31,000
Present Worth of Annual O&M(8 % % for 30 years) $ 328.000
TOTAL PRESENT WORTH COST $ 882,000
16
AR30I359
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE LF-4
PENNSYLVANIA MUNICIPAL LANDFILL CAP
DIRECTITEM___________________________ CAPITAL ANNUAL O&M
Municipal Landfill CapDirect Capital
Mobilization/demobilization/decon pad 100,000site clearing (8 acres @ $6,000/acre) 48,000tree removal (3 acres @ $3,000/acre) 9,000trash relocation (5,000 cy @ $10/cy) 50,000on-site borrow for trash replacement
(5,000 cy <a $20/cy) 100,000sediment and erosion control 100,000passive gas vent system with carbon
cannister (50 ea. @$5,000 ea.) 250,000site regrading (15,000 cy @ $10/cy) 150,00012-inch clay layer (14,000 cy @ $30/cy) 420,00012-inch drainage layer (14,000 cy @ $25/cy) 350,000geotextile fabric (40,000 sy G> $7/sy) 280,00018-inch soil cover layer
(21,000 cy (a $20/cy) 420,0006-inch top soil layer (7,000 cy @ $30/cy) 210,000seed, mulch, fertilizer (40,000 sy @ $3/sy) 120,000surface erosion protection gravel
(500 cy <a $30/cy) 15,0008-feet security fence (3,000 LF & S25/LF) 75,000land acquisition for 50 feet buffer
(3 acres @ $5,000/acre) 15,000
Sub Total $ 2,712,000
Direct Capital Contingency (10%) 271,000
Annual O&Msite review and cap repair 20,000mowing grass (10 times/year @ $2,000 ea.) 20,000gas vent system monitoring and repair • 5,000fence repair 5,000
Total Direct Capital Costs $ 2,983,000
Total Annual O&M Costs $ 50,000
17
AR30J360
, . TCN 4204RI/FS REPORT
REV. II30/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE LF-4
PENNSYLVANIA MUNICIPAL LANDFILL CAP
DIRECTITEM___________________________ CAPITAL ANNUAL O&M
Total Direct Capital Costs $ 2,983,000
Total Annual O&M Costs $ 50,000
Remedial Action & Remedial DesignConsulting Services (30%) 895,000
Legal & Administrative (25%) 746,000Contingency (25%) 746,000 13,000
Total Capital $ 5,370,000
Total Annual O&M $ 63,000
Present Worth of Annual O&M(8 % % for 30 years) $ 666.000
TOTAL PRESENT WORTH COST $ 6,036,000
18
flR30J36i
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE LF-5
RCRA HAZARDOUS WASTE LANDFILL CAP
DIRECTITEM_______________________ CAPITAL ANNUAL O&M
RCRA Landfill CapDirect Capital
Mobilization/demobilization/decon pad 100,000site clearing (8 acres 9 $6,000/acre) 48,000tree removal (3 acres @ $3,000/acre) 9,000trash relocation (5,000 cy 9 $10/cy) 50,000on-site borrow for trash replacement
(5,000 cy 9 $20/cy) 100,000sediment and erosion control 100,000passive gas vent system with carbon
cannister (50 ea. @$5,000 ea.) 250,000site regrading (15,000 cy @ $10/cy) 150,00024-inch clay layer (28,000 cy @ $30/cy) 840,00012-inch drainage layer (14,000 cy 9 $25/cy) 350,000Two geotextile fabric layers
(80,000 sy 9 $7/sy) 560,000Geomembrane cap (40,000 sy 9 $10/sy) 400,00018-inch soil cover layer
(21,000 cy 9 $20/cy) 420,0006-inch top soil layer (7,000 cy 9 $30/cy) 210,000seed, mulch, fertilizer (40,000 sy 9 $3/sy) 120,000surface erosion protection gravel
(500 cy 9 $30/cy) 15,0008-feet security fence (3,000 LF 9 $25/LF) 75,000land acquisition for 50 feet buffer
(3 acres 9 $5,000/acre) 15,000
Sub Total $ 3,812,000
Direct Capital Contingency (10%) 381,000
Annual O&Msite review and cap repair 20,000mowing grass (10 times/year 9 $2,000 ea.) 20,000gas vent system monitoring and repair 5,000fence repair 5,000
Total 'Direct Capital Costs $ 4,193,000
Total Annual O&M Costs $ 50,000
19
38301362
TCN 4204RI/FS REPORT
REV. #130/SEPT/91
BUTZ LANDFILL SITEALTERNATIVE LF-5
RCRA HAZARDOUS WASTE LANDFILL CAP
DIRECTITEM___________________________ CAPITAL ANNUAL O&M
Total Direct Capital Costs $ 4,193,000
Total Annual O&M Costs $ 50,000
Remedial Action & Remedial DesignConsulting Services (30%) 1,258,000
Legal & Administrative (25%) 1,048,000Contingency (25%) 1,048,000 13,000
Total Capital $ 7,547,000
Total Annual O&M $ 63,000
Present Worth of Annual O&M(8 % % for 30 years) $ 666.000
TOTAL PRESENT WORTH COST $ 8,213,000
20
3R30J363
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