Ontario Air Standards for Propylene - ontla.on.ca · Ontario Air Standards for Propylene ii propylene emissions also increased in 2002 and 2003, likely accounting for the increase

Ontario Air Standards

For

Propylene

June 2007

Standards Development Branch Ontario Ministry of the Environment

Ontario

Ontario Air Standards for Propylene

Executive Summary

The Ontario Ministry of the Environment (MOE) has identified the need to develop and/or update air quality standards for priority contaminants. The Ministry’s Standards Plan, which was released in October, 1996 and revised in November, 1999, identified candidate substances for which current air quality standards will be reviewed or new standards developed. Propylene was identified as a priority compound for review due to lack of an existing standard and its pattern of use in Ontario. Once a decision is made on the air standards, they will be incorporated into Ontario Regulation 419: Air Pollution – Local Air Quality (O. Reg. 419/05). The Ambient Air Quality Criterion (AAQC) will be incorporated into Schedule 3 of the regulation and the half hour standards will be incorporated into Schedule 2. An ‘Information Document’ containing a review of scientific and technical information relevant to setting an air quality standard for propylene was previously posted on the Environmental Bill of Rights Registry for public comments. This was followed more recently by the posting of a document providing the rationale (‘Rationale Document’) for recommending an Ambient Air Quality Criterion (AAQC) and a half hour standard for propylene. This document, referred to as the ‘Decision Document’, summarizes the comments received from stakeholders on the proposed standards and the Ministry responses to these comments. This document also provides the rationale for the decision on the air quality standards for propylene.

Propylene (CAS No. 115-07-1) is a colourless, flammable gas which has a mild odour. The detection odour threshold has been reported as 23 ppm (40 mg/m3) and it is classified as a simple asphyxiant by ACGIH. Release of propylene into the environment is most likely a function of its use in the manufacture of plastics as well as its production during gasoline refining. Propylene is produced as a result of catalytic or thermal cracking of hydrocarbons, during the process of gasoline refining from petroleum oils. In addition, propylene can be a product of the catalytic dehydrogenation of propane, and is a chemical intermediate in the manufacture of acetone, isopropylbenzene, isopropanol, isopropyl halides, propylene oxide, acrylonitrile, cumene, and vinyl resins. Other releases of propylene can occur from automobile exhaust, cigarette smoke, the combustion of coal, wood and refuse, and such industries as paper mills, petroleum refining and crude petroleum and natural gas extraction. Natural releases of propylene can occur from germinating beans, corn, cotton, and pea seeds, as well as from such trees as ash, elm, cypress, and hackberry.

Data from the National Pollutant Release Inventory (NPRI) indicated that there was a decreasing national trend in the release of propylene from 1995 to 2000, which was followed by an increase in emissions in 2001. In the year 2002, propylene emission across Canada again fell whereas emission in Ontario rose. In 2003 propylene emissions climbed in both Ontario and Canada. The number of facilities reporting

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propylene emissions also increased in 2002 and 2003, likely accounting for the increase in propylene emissions. For the year 2003, Ontario reported releases of 593 tonnes of propylene, which accounted for approximately 50% of the total releases in Canada. During the period of 1995 to 2001, Ontario contributed an average of approximately 46% of the total propylene releases in Canada. The high Ontario emission rates in 2002 were the result of an increase in releases from chemical manufacturing facilities and petroleum refineries. The steel product manufacturing sector also contributed to propylene releases in Ontario.

Propylene is not readily absorbed from the lungs with inhalation exposure and is therefore not well distributed in the body. A recent report has stated that, at low concentrations, 93% of propylene inhaled is exhaled unchanged in humans. Studies have shown that propylene metabolites appear to be fairly evenly distributed throughout the body. However, higher concentrations will likely be found in fatty tissue based on its observed tissue: air partition coefficient. The propylene which is absorbed into the blood and distributed is rapidly metabolized by the cytochrome P-450 system to propylene oxide. Limited data is available concerning its elimination following metabolism. Based on the low absorption of propylene and its rapid elimination, it has been suggested that the concentration of bioavailable propylene may not reach high enough levels in classical long-term inhalation studies to show positive or serious chronic effects.

There is limited toxicological data available for propylene, possibly due to its low toxicity. It has been reported to act as a simple asphyxiant, with relatively low acute toxicity and mild anaesthetic properties. Symptoms of acute human exposures to extremely high concentrations of propylene (110 g/m3) have been reported to include mild intoxication, paresthesia and inability to concentrate. Even higher concentrations (> 400 g/m3) have been reported to result in loss of consciousness, nausea, vertigo and coughing. Animal studies suggest that acute exposure to extremely high concentrations of propylene may result in cardiac effects (e.g., atypical ventricular ectopic beat). Chronic effects with exposure to propylene have not been characterized; however several studies have identified toxicity in animals. Chronic exposure of rats to propylene concentrations of ~8600 mg/m3 have been reported to result in respiratory system effects including squamous metaplasia, epithelial hyperplasia and inflammation of the nasal cavity.

The limited genotoxicity and mutagenicity data for propylene are negative for bacterial systems, and inconclusive for mammalian systems even at extremely high concentrations of propylene (> 344,000 mg/m3). The NTP (1985) has concluded that there is no evidence of carcinogenicity, as no propylene related increases in malignant or benign neoplasms were observed following a 2-year inhalation study on rats and mice. Both IARC and the ACGIH have concluded that the experimental evidence is inadequate for humans and experimental animals.


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In revising the air quality standards for Ontario, the Ministry of the Environment is considering risk assessments and standards and guidelines used by environmental agencies world-wide for propylene. This report reviews the scientific basis for air quality guidelines and standards developed by the States of California, Michigan, New Jersey, New York and Texas.

From 1989 to 2005 the ACGIH had not established a TLV for propylene and classified the compound as a simple asphyxiant. The ACGIH has reviewed recent toxicological information available and in 2006 adopted a TLV-TWA of 500 ppm (860 mg/m3) for propylene. The TLV is based on changes in nasal mucosa, as identified in various chronic animal studies. This is the same endpoint found in Quest et al. (1984).

The states of Michigan and California were the only jurisdictions reviewed that have derived air quality criteria for propylene based on toxicological studies. Due to the lack of available data, both jurisdictions have chosen the same study, Quest et al. (1984), from which to derive their guideline values. However, different approaches were taken to address the uncertainties associated with the study results. Michigan didn’t use pharmacokinetic data in converting the animal dose to a human equivalent concentration (HEC), resulting in the use of a default uncertainty factor of 10 for interspecies variability. California chose to reduce their uncertainty factor for interspecies variability to only 3, through the use of pharmacokinetic data in deriving a HEC. Michigan applied an uncertainty factor of 10 to account for the conversion of a LOAEL to a NOAEL; California applied a “LOAEL uncertainty factor” of 3.

With the lack of new toxicological information available, the MOE has also chosen the Quest et al. (1984) study as the most appropriate to derive Ambient Air Quality Criteria.

Based on an evaluation of the scientific rationale of air guidelines from leading agencies, an examination of current toxicological research, and comments from stakeholders, the following Air Quality Standards are set for propylene (115-07-1):

• A 24-hour average AAQC of 4,000 μg/m3 (micrograms per cubic metre of air) for propylene based on the respiratory effects of this compound; and

• A half-hour standard of 12,000 μg/m3 (micrograms per cubic metre of air) for propylene based on the respiratory effects of this compound.

These effects-based standards (which include the AAQCs and the corresponding effects-based half hour standards) will be incorporated into Ontario Regulation 419/05: Air Pollution – Local Air Quality (O. Reg. 419/05). The AAQCs will be incorporated into Schedule 3 of O. Reg. 419/05; the half-hour standard will be incorporated into Schedule 2.


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MOE generally proposes a phase-in for new standards or standards that will be more stringent than the current standard or guideline. The phase-in for propylene is set out in O. Reg. 419/05.

Among other things, O. Reg. 419/05 sets out the applicability of standards, appropriate averaging times, phase-in periods, types of air dispersion model and when various sectors are to use these models. There are 3 guidelines that support O. Reg. 419/05. These guidelines are:

• “Guideline for the Implementation of Air Standards in Ontario” (GIASO);

• “Air Dispersion Modelling Guideline for Ontario” (ADMGO); and

• “Procedure for Preparing an Emission Summary and Dispersion Modelling Report” (ESDM Procedure).

GIASO outlines a risk-based decision making process to set site specific alternative air standards to deal with implementation barriers (time, technology and economics) associated with the introduction of new/updated air standards and new models. The alternative standard setting process is set out in section 32 of O. Reg. 419/05.

For further information on these guidelines and O. Reg. 419/05, please see the Ministry’s website http://www.ontario.ca/environment and follow the links to local air quality.

http://www.ontario.ca/environment


Table of Contents

Executive Summary........................................................................................................ i Table of Contents .......................................................................................................... v

1.0 Introduction ......................................................................................................... 1

2.0 General Information............................................................................................ 3 2.1 Physical and Chemical Properties..................................................................... 3 2.2 Production and Uses of Propylene .................................................................... 4 2.3 Sources and Levels........................................................................................... 4 2.4 Environmental Fate ........................................................................................... 6

3.0 Toxicology of Propylene .................................................................................... 6 3.1 Acute Toxicity .................................................................................................... 7 3.2 Subchronic and Chronic Toxicity ....................................................................... 8 3.3 Developmental and Reproductive Toxicity ........................................................ 9 3.4 Genotoxicity and Mutagenicity........................................................................... 9 3.5 Carcinogenicity................................................................................................ 10 3.6 Environmental Effects ..................................................................................... 11

4.0 Review of Existing Air Quality Criteria............................................................ 12 4.1 Overview ......................................................................................................... 12 4.2 Evaluation of Existing Criteria.......................................................................... 14

5.0 Responses of Stakeholders to the Information Draft .................................... 15

6.0 Responses of Stakeholders to the Rationale Document............................... 16

7.0 Considerations in the Development of an Ambient Air Quality Criterion for Propylene ..................................................................................................................... 19

8.0 Decision............................................................................................................. 22

9.0 References......................................................................................................... 24

10.0 Appendix: Agency-Specific Reviews of Air Quality Guidelines.................. 33 10.1 Agency-Specific Summary: Federal Government of Canada ......................... 33 10.2 Agency-Specific Summary: Federal Government of the United States .......... 35 10.3 Agency-Specific Summary: California ............................................................. 37 10.4 Agency-Specific Summary: Commonwealth of Massachusetts....................... 40 10.5 Agency-Specific Summary: State of Michigan................................................. 42 10.6 Agency-Specific Summary: North Carolina .................................................... 45 10.7 Agency-Specific Summary: World Health Organization (WHO) ..................... 47

11.0 Acronyms, Abbreviation, and Definitions....................................................... 49

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1.0 Introduction

Ontario regulates air emissions in order to achieve and maintain air quality which is protective of human health and the environment. The Environmental Protection Act (Section 9) requires stationary sources that emit, or have the potential to emit, a contaminant to obtain a Certificate of Approval which outlines the conditions under which the facility can operate.

The Ministry of the Environment uses a combination of regulated point of impingement (POI) standards and guidelines (MOE, 2005) in reviewing Emission Summary and Dispersion Modelling Reports submitted to support a Certificate of Approval application or a Ministry request for a compliance assessment. Ambient Air Quality Criteria form the basis for an air standard or guideline and represent human health or environmental effects-based values, normally set at a level not expected to cause adverse effects based on continuous exposure. As such, factors such as technical feasibility and costs are not considered when establishing AAQCs or the equivalent half hour standards which are derived from the AAQCs using a mathematical scaling factor. The risk based process for alternative standards, as set out in section 32 of O. Reg. 419/05, is the mechanism created to deal with the time, technical and economic issues. The Guideline for the Implementation of Air Standards in Ontario (GIASO) is the supporting document for stakeholders who are interested in more information on alternative standards. For further information on O. Reg. 419/05 and GIASO, please see the Ministry’s website http://www.ene.gov.on.ca/envision/air/regulations/localquality.htm.

Air standards referenced in O. Reg. 419/05 are used for compliance and enforcement. Dispersion modelling, as referenced in the regulation, is used to relate emission rates from a source to resulting concentrations of a particular contaminant. Air standards specified under O. Reg. 419/05 apply to stationary sources only.

In addition to air standards established under O. Reg. 419/05, the Ministry also has a large number of guidelines (including AAQCs). Similar to standards, guidelines are used by the Ministry to assess general air quality and the potential for causing adverse effect (MOE, 2005). Like the air standards specified in O. Reg. 419/05, guidelines (and now AAQCs) are used in reviewing Emission Summary and Dispersion Modelling reports submitted in support of applications for Certificates of Approval, to approve new and modified emission sources or other requirements. Once incorporated into a legal instrument such as a Certificate of Approval, guidelines can become legally binding.

The Ontario Ministry of the Environment continues to develop and/or update air standards for priority toxic contaminants. The Ministry’s Standards Plan, which was released in October 1996 and revised in November 1999 (MOEE, 1996 & MOE, 1999),

http://www.ene.gov.on.ca/envision/air/regulations/localquality.htm


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identified candidate substances for which current air standards will be reviewed. The MOE 1999 Standards Plan outlines a multi-step process for developing air quality standards (MOE, 1999). Each standard has undergone a two step consultation process involving postings on the Environmental Registry, under the Environmental Bill of Rights (EBR):

• Information Drafts (Risk assessment/science review only)

• Rationale Documents (Proposed numerical limits)

Propylene was identified as a priority for review based on its pattern of use in Ontario, and recent toxicological information. The initial step, an Information Draft (MOE 2005), provided risk assessment information relevant to establishing a standard for a particular substance. This provided stakeholders with the opportunity to critically review the information and provide any additional information they felt should be considered by the Ministry in setting an air quality standard for a particular compound. The Ministry considered comments received on the Information Draft and recommended proposed standards: Ambient Air Quality Criterion (AAQC) and a half hour point of impingement (POI) standard, in a Rationale Document (MOE 2006) and again solicited comments from stakeholders by posting on the Environmental Registry. After assessing comments on the Rationale Document the Ministry has finalized its work by making a decision on the air quality standards for propylene. This decision, which also highlights key comments from stakeholders on the proposed standards and the responses provided by the MOE, is documented by posting a Decision Notice (and supporting ‘Decision Document’, which provides the rationale for the decision on the air quality standards) onto the Environmental Registry.

In the 1999 Standards Plan, MOE made a commitment to consider time, technical, and economic issues for air standards and develop a risk management framework to address implementation issues. The risk-based framework has been developed and is part of O. Reg. 419/05. The alternative standards setting process is a risk-based process that considers time, technical and economic issues on a site specific basis. For further information on Regulation 419/05 and the process for requesting an alternative site specific air standard, please see the Ministry’s website and follow the links to local air quality.

http://www.ene.gov.on.ca/envision/air/regulations/localquality.htm


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2.0 General Information

2.1 Physical and Chemical Properties

Propylene is a colourless, flammable gas that has a yellow, sooty flame when burning (ARB, 1997a; ACGIH, 2002a; Beije, 1995; Budavari et al., 1996). This substance has a mild odour (Beije, 1995) and is soluble in both alcohol and ether, while being only slightly soluble in water (ARB, 1997a). This chemical is classified as a simple asphyxiant by the ACGIH (2002a) with a reported odour threshold range of 17-170 mg/m3 (geometric mean of 40 mg/m3) (AIHA, 1989; Amoore and Hautala, 1983). The following list provides some specific information on propylene and its properties (ACGIH, 2002a; Beije, 1995; Budavari et al., 1996; Chemfinder, 2003; HSDB, 2003; Sax and Lewis, 1987; Sax and Lewis, 1989):

Chemical Name Propylene

CAS # 115-07-1

RTECS # UC6740000

UN # 1077

Molecular Formula C3H6

Molecular Weight 42.08 g/mol

Melting Point -185 EC

Boiling Point -48 EC

Henry’s Law Constant 0.196 atm-m3/mole at 25 EC

Flash Point -108 EC

Water Solubility Slightly soluble

Log KOW 1.77

Log KOC 2.34 to 2.37

Specific Gravity (water=1) 0.51 at 20 EC


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Vapour Density (air=1) 1.49

Vapour Pressure 1043 kPa at 21.1 EC

Conversion Factors 1 ppm = 1.72 mg/m3

@ 25EC 1 mg/m3 = 0.58 ppm

Common Synonyms 1-propene, propene, methylethene, methylethylene

Production and Uses of Propylene

Propylene is produced during the process of gasoline refining from petroleum oils. This substance is always produced as a result of catalytic or thermal cracking of hydrocarbons, and propylene can be a product of the catalytic dehydrogenation of propane (Budavari et al., 1996). For 1991, Canada produced approximately 700 kilo tonnes of propylene (Anderson, 1992). The production of this chemical was the 9th highest by volume in 1995 in the United States (Lewis, 1997). In Europe, an estimate of the total propylene production in 1993 was 12 million tonnes (Beije, 1995).

Propylene is used for octane improvement as an alkylation or polymer-gasoline feedstock (ACGIH, 2002a). In its polymerized form of polypropylene, this chemical is used in plastics and carpet fibres (ACGIH, 2002a; ARB, 1997a; Budavari et al., 1996). Propylene is also a chemical intermediate in the manufacture of: acetone; isopropylbenzene; isopropanol; isopropyl halides; propylene oxide; acrylonitrile; cumene; and vinyl resins (ACGIH, 2002a; ARB, 1997a; Budavari et al., 1996).

Sources and Levels

Some sources of propylene are biological in origin, as it is a component of garlic essential oils, such trees as ash, elm, cypress, hackberry, European fir, and Scots pine and natural gases. It is also released by germinating beans, corn, cotton, and pea seeds (Khalil et al., 1990; Khalil and Rasmusen, 1992; Vancura and Stotzky, 1976). Propylene's release to the environment is wide spread since it is a common product of incomplete combustion. Propylene is released to the atmosphere in emissions from the combustion of gasoline, coal, wood and refuse (HSDB, 2003). This substance has also been detected in the gases that were desorbed from coal samples (Kim and Douglas, 1973).

Propylene is found in urban air (Beije, 1995), possibly due to its presence in motor vehicle exhaust (ARB, 1995), from the burning of gasoline, diesel, and from turbine engines (Graedel et al., 1986). It is also released from industries in which it is produced


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and used as a chemical intermediate (HSDB, 2003). In addition, this substance is found in cigarette smoke (Beije, 1995).

Data from the National Pollutant Release Inventory (NPRI) indicated that there was a decreasing national trend in the release of propylene from 1995 to 2000, which was followed by an increase in emissions in 2001. In the year 2002, propylene emission across Canada again fell whereas emission in Ontario rose. In 2003 propylene emissions climbed in both Ontario and Canada. The number of facilities reporting propylene emissions also increased in 2002 and 2003, likely accounting for the increase in propylene emissions. (NPRI, 1995, 1996, 1997, 1998, 1999, 2000,2001,2002, 2003). Ontario propylene release amounts for 1995, 1996, 1997, 1998, 1999, 2000, 2001, 2002 and 2003 were 620, 497, 505, 413, 459, 407, 489, 575, and 593 tonnes, respectively. Ontario reported releases of 593 tonnes of propylene, which accounted for approximately 50% of the total releases in Canada. The high Ontario emission rates in 2002 were the result of an increase in releases of propylene from petroleum refinery facilities and chemical manufacturing facilities. Increased emissions from the metal product manufacturing sector also contributed to propylene releases in Ontario. In 2002, over half (331 tonnes) of the net Ontario releases of propylene were from the chemical manufacturing industry. Increases in emissions from the petroleum sector, however, were greater than for any other sector.

Propylene levels in rural areas have been reported to range between 0.02 and 8.3 µg/m3, while those of urban areas range between 0.6 and 448 µg/m3 (Beije, 1995). Samples taken from two suburban areas in Sweden during the winter months had concentrations of propylene from 1.8 to 70 µg/m3 (Ehrenberg and Törnqvist, 1993). In Gothenburg, Sweden, air samples in a road tunnel during rush hour had propylene levels of 100 µg/m3, inside a car had levels of 9 and 15 µg/m3, and in a café with cigarette smoke had levels of 37 and 73 µg/m3 on two separate days (Giannovario et al., 1976). Ambient propylene levels in a suburban and industrial community of Philadelphia ranged from 12 to 448 µg/m3 (Giannovario et al., 1976), in Los Angeles ranged from 12 to 55 µg/m3 (Grosjean and Fung, 1984), and in Chicago ranged from 0.6 to 4.7 µg/m3 (Aronian et al., 1989). A median propylene level of 7.7 ppb (13.24 µg/m3) for 39 cities in the United States has been reported (Seinfeld, 1989). The concentrations of propylene in ambient air samples appear to vary diurnally and with wind direction (U.S. EPA, 1986).

Under the National Air Pollution Surveillance program (NAPS) propylene was measured in ambient air by Environment Canada in a number of 24-hour samples collected across Canada between the years of 1993 and 2000 (Dann, 2002). More than forty different suburban, rural and urban locations in eight provinces were used. In examining the data set collected, the values ranged from non-detectable up to 175.2 μg/m3 (Dann, 2002). The mean concentration of propylene for the years of 1993-2000 was calculated to be approximately 0.74 μg/m3.


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2.4 Environmental Fate

In the air, propylene will exist solely as a vapour (Eisenreich et al., 1981). Vapour-phase propylene may be degraded by ozone (half-life of 24 hr; Atkinson, 1984; Sabljic and Guesten, 1990), nitrate radicals (half-life of 4 days; Atkinson, 1984; Sabljic and Guesten, 1990), or photochemically produced hydroxyl radicals (estimated half-life of 14.6 hr; Atkinson, 1989). The calculated atmospheric half-life (incorporating all atmospheric degradation processes) of propylene was 7.7 hours (Graedel et al., 1976).

Wet deposition during rainfall is likely to be the primary mechanism of transfer from air to soil since a vapour is not subject to dry deposition. Upon entering the soil, propylene is expected to have a medium mobility (Swann et al., 1983) although, due to its high vapour pressure, the gas may permeate through the soil. Volatilization from soil is expected to be the primary fate process due to its high vapour pressure (HSDB, 2003). Propylene present in soil has been reported to be oxidized to its corresponding 1,2-epoxide (Hou et al., 1983; Hou et al., 1979). Pure culture studies suggest that propylene may be susceptible to microbial degradation; however, it is unknown whether propylene biodegrades in the environment. Hydrolysis, adsorption, and biodegradation are not expected to be important fate processes in soil ecosystems (SRC, 2003).

A small amount of propylene may dissolve into water (U.S. EPA, 1986). Upon entering water, propylene is likely to be subjected to rapid volatilization (Lyman et al., 1990). The half-life in a model river was estimated to be 1.9 hours (Lyman et al., 1990), whereas the half-life in a model pond was 23 hours (U.S. EPA, 1987). Propylene is not expected to adsorb to suspended solids and sediment as the gas phase of propylene can permeate through the organic matter (HSDB, 2003). Pure culture studies suggest that propylene may biodegrade; however, it is unknown whether biodegradation will occur in the aquatic environment (HSDB, 2003). As was found in soil, propylene may oxidize to its corresponding 1,2-epoxide (Hou et al., 1983; Hou et al., 1979). Hydrolysis, adsorption, and biodegradation are not expected to be important fate processes for propylene in aquatic ecosystems.

3.0 Toxicology of Propylene

For consideration of airborne propylene, the following toxicological review is focussed primarily on the inhalation of propylene, as this is the predominant route of human exposure to this chemical in air. Data on other exposure routes are included in this review where relevant or where inhalation exposure data are lacking.

Recently the toxicokinetics of inhaled propylene were reported for mice, rats and humans (Filser et al., 2000). Data from this study suggests that, at low exposure


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concentrations, uptake of propylene from the lungs does not occur readily (based on the blood/air partition coefficient of 0.44) and can be limited by amount of blood flow through the lungs (Filser et al., 2000). Experimental data in other animal studies has also reported low absorption into the blood stream in rats, and thus low systemic bioavailability, as a large proportion is exhaled immediately following inhalation (Filser et al., 2000; Golka et al., 1989). Golka et al. (1989) reported that following exposure of rats to 86 mg/m3, 42% of inhaled propylene was exhaled unchanged, while Filser et al. (2000) reported that 93% was exhaled unchanged in humans. Based on 2-hydroxypropyl adducts in haemoglobin and DNA in different organs in mice, propylene metabolites would appear to be fairly evenly distributed throughout the body (Svensson et al., 1991). However data from the Filser et al. (2000) study suggests that propylene will likely be found in higher concentrations in fatty tissue based on its observed tissue: air partition coefficient of 5.15.

Svensson et al., (1991) investigated alkylation of DNA at the N7 position of guanine in male CBA mice exposed to labelled propylene by inhalation. The study found that the adduct levels were related to the concentration of propylene oxide and concluded that propylene oxide is the primary metabolite of propylene in CBA mice. Specifically, in animal experiments, propylene is metabolised using a cytochrome P450-mediated process, resulting in propylene oxide, the 1,2-epoxide of propylene (Groves et al., 21986; Wistuba et al., 1989).

IARC (1994) reported 3 possible metabolic/elimination pathways for propylene oxide in humans. It is predominantly conjugation with glutathione, and eliminated rapidly. It may also be hydrolysed by epoxide hydrolase to 1,2-propanediol, which is subsequently metabolized to lactic and pyruvic acids. In addition, propylene oxide forms adducts with proteins, including haemoglobin, in man, dog, rat and mouse (IARC, 1994).

Acute Toxicity

Propylene has been reported to act as a simple asphyxiant, with relatively low toxicity and mild anaesthetic properties (ACGIH, 2002a). Asphyxiation, associated with unconsciousness or death, results from the tendency of propylene to displace oxygen in the atmosphere at high concentrations (Sittig, 1991; Beije, 1995). Symptoms of human exposures to propylene have included mild intoxication, paresthesia and inability to concentrate at levels of 110 g/m3 (2.25 minute exposures reported) (von Oettingen, 1940). Loss of consciousness has been observed to occur within 3 minutes at concentrations of 410 g/m3 (Davidson, 1926; von Oettingen, 1940), while in another early study by Riggs and Goulden (1925), unconsciousness was not observed in humans exposed to 396 g/m3 for 3 to 4 minutes. Exposures to higher concentrations (713 g/m3) for several minutes were associated with reports of nausea, vertigo, eyelid reddening, face flushing, secretion of tears, coughing, and occasionally leg flexing


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(Halsey et al., 1926; Kahn and Riggs, 1932). Inhalation of large amounts of this substance may induce a reduction in blood pressure and heart arrhythmias (ILO, 1983). The acute effects of propylene have been found to be reversible, as Brown (1924) reported complete recovery following propylene-induced anaesthesia.

Experimental studies with laboratory animals found that similar to humans, propylene exposure results in anaesthesia at concentrations of 344 g/m3 and higher (Brown, 1924, Riggs, 1924). The anaesthetic effects noted were not reported to be accompanied by significant toxic effects at concentrations below 690 to 860 g/m3 (Brown, 1924). Such effects included an atypical ventricular ectopic beat in cats (Brown, 1924), and cardiac sensitization in dogs (Krnatz et al., 1948).

Although propylene has been reported to cause a temporary decrease in hepatic and nasal microsomal P450 levels at 10.3 mg/m3 (Maples and Dahl, 1991), there is no evidence that propylene induces hepatotoxicity following short term exposures to concentrations up to 112 g/m3 (Osimitz and Conolly, 1981, 1985). However, propylene was hepatotoxic (as indicated by weight, haemorrhage, and enzyme changes) in rats pre-exposed to polycholorinated biphenyls (PCB: Aroclor 1254). When the PCB-pre-exposed rats received SKF-525A, an inhibitor of cytochrome P450-dependent metabolism, no hepatotoxicity was observed. This was interpreted as indicating that cytochrome P450-mediated metabolism was responsible for activating propylene into a liver toxicant, although some induction of the P450 system was required for sufficient metabolism to cause damage; alternately, PCBs may have simply predisposed the liver to damage by otherwise harmless amounts of the propylene metabolites (Osimitz and Conolly, 1985).

Subchronic and Chronic Toxicity

No data were available regarding subchronic or chronic effects of propylene in humans.

No apparent adverse effects were noted in a 14-day repeated exposure study of male and female F344/N rats and B6C3F1 mice, for concentrations of propylene up to 17,200 mg/m3 (6 hours/day, 5 days/week) (NTP, 1985), as only slight increases (not statistically significant) in body weight were observed. CNS depression and slight to moderate fatty degeneration of the liver was observed in a chronic study in which mice were exposed to 600,000 mg/m3 for 60 to 90 minutes on up to 20 different occasions (Reynolds, 1926). There was no concurrent control group within the study, the propylene used was impure, and the only organ that was analysed was the liver.

The long term effects of propylene in rats and mice was studied by Ciliberti et al. (1988) as the rats were exposed to propylene at concentrations of 344, 1720, 8600 mg/m3 for 7 hours/day, 5 days/week for 104 weeks, while the mice were only exposed for 78


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weeks. The only effect reported from the study was a slightly increased rate of mortality at the two highest doses (1720 and 8600 mg/m3) in rats and in the 1720 mg/m3 dose group in mice; however this was not a statistically significant finding.

A two-year investigation of the chronic effects of propylene was conducted by Quest et al. (1984) (results of this study were also reported in NTP, 1985), in which F344/N rats and B6C3F1 mice were exposed to propylene via inhalation. Nominal exposure levels were 8600 or 17,200 mg/m3 for six hours per day, five days per week for 103 weeks. In both rats and mice, exposure to either concentration of propylene did not result in substantial changes in weight gain, survival, or clinical signs. Non-neoplastic effects were seen at both exposure levels in rats. Squamous metaplasia was observed in female rats; this effect was observed only at the low dose in male rats. Epithelial hyperplasia was also reported in the high exposure group of female rats, and inflammatory changes, characterized by an influx of lymphocytes, macrophages, and granulocytes into the submucosa and granulocytes into the lumen, were seen in males of both dose groups and high concentration females. Mild focal inflammation was noted in the kidneys of the treated mice at both concentrations. This effect appears to be related to propylene exposure although the mechanistic relationship is unknown. A LOAEL of 8600 mg/m3, based on squamous metaplasia, epithelial hyperplasia and nasal inflammation was established from this study, while a NOAEL was not observed (Quest et al., 1984; NTP, 1985).

Developmental and Reproductive Toxicity

No data were available on the developmental and reproductive toxicity of propylene (ACGIH, 2002a; Cavender, 1994; IARC, 1994; OEHHA, 2000).

Genotoxicity and Mutagenicity

The limited genotoxicity and mutagenicity data for propylene are negative for bacterial systems, and inconclusive for mammalian systems. Negative results have been reported in studies of the mutagenicity of propylene in Salmonella typhimurium TA100 (with and without metabolic activation) (Victorin and Ståhlberg, 1988). Inconclusive results were reported for studies of cytotoxicity and mutagenicity in cultures of L5178Y mouse lymphoma cells when cultures were exposed to 344,000 to 860,000 mg/m3 of propylene for a 4-hour period with metabolic activation (McGregor et al., 1991). Alkylation of DNA was observed in the spleen, liver and kidney of male CBA mice following 7 hours of exposure to 800,000 mg/m3 of propylene in a closed chamber (Svensson et al., 1991). The authors noted that the incidence of 2-hydroxypropyl-DNA adducts was related to the formation of propylene oxide as the major propylene metabolite (Svensson et al., 1991). Walker et al. (2004) exposed 6-week-old male F344


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3.5

rats to 1, 200, 2000 or 10,000 ppm of propylene by inhalation for 4 weeks. Following exposure, mutant frequencies were determined in the Hprt gene of splenic T-lymphocyces. It was observed that Hprt mutation frequency did not significantly increase over background. The study concluded that these finding support the hypothesis that inhalation exposure of rats to propylene does not cause mutation or cancer.

Carcinogenicity

A cohort study was conducted by Acquavella et al. (1988) to investigate a possible cluster of colorectal cancers observed at a polypropylene manufacturing plant. An excess incidence of colorectal cancer was observed in men who had worked at the plant for six months or more during the years of 1960 to 1985, with a ten-year induction period from the first exposure. The investigators then performed a case-control study in the same workforce, screening for large bowel adenomatous polyps and carcinomas. Occupational exposure comparisons were made between a control group of 72 individuals (without polyps) and a case group of 24 people (Acquavella et al., 1991). The study does not address the potential for concomitant exposures to other chemicals, and presents uncertainties in actual exposure to the chemical of concern. It has been concluded that the collective weight of the toxicologic and epidemiologic evidence do not support a linkage between the production of polypropylene and colorectal cancer (ECETOC, 1994). In these studies propylene was handled by the workforce at the plant, along with various other chemicals, however specific propylene exposure was not identified.

Animal studies have indicated generally negative evidence for the carcinogenicity of propylene. Neither Maltoni et al. (1982), ILO (1983), nor Ciliberti et al. (1988) observed an increase in tumour incidence in rats and mice exposed to propylene via inhalation at concentrations of up to 8,600 mg/m3 (7 hours per day, 5 days per week for 104 weeks for rats or 78 weeks for mice). The National Toxicology Program (NTP, 1985) performed a 2 year inhalation study in F344/N rats and B6C3F1 mice to test the carcinogenesis of propylene. Rats and mice (50 for each species and sex) were exposed to concentrations either of 0, 5000 or 10,000 ppm, 6 hours/day, 5 days/week for 103 weeks. The NTP concluded at the end of this study that there was no evidence of carcinogenicity in male and female F344/N rats or in male and female B6C3F1 mice. The study did observe squamous metaplasia of the respiratory epithelium in male and female rats and epithelial hyperplasia in female rats in the nasal cavity (as reported in the Quest et al. 1984 study).

Propylene oxide is produced during the first step of propylene metabolism (Groves et al., 1986; Wistuba et al., 1989). Propylene oxide is a known carcinogen in experimental animals. The metabolism of propylene in rats and mice has been reported to be


11

3.6

saturable (Golka et al., 1989; Svensson and Osterman-Golkar, 1984). Golka et al. (1989) observed that the rate of propylene metabolism showed saturation kinetics at concentration above 50 ppm (86 mg/m3). A mechanism has been postulated by Maples and Dahl (1991) that a rapid deactivation of a propylene-specific cytochrome P450 isozyme may occur during propylene exposure, resulting in a reduction in propylene oxide formation. A transient decrease in P450 levels was observed in rats at 10.3 mg/m3 following 20 minutes of exposure (Maples and Dahl, 1991), and in rats at 688 mg/m3 following 30 minutes of exposure (Kunze et al., 1983).

Both the International Agency for Research on Cancer (IARC) and the American Conference of Governmental Industrial Hygienists (ACGIH) have concluded that the evidence for the carcinogenicity of propylene is inadequate for humans and experimental animals, and that propylene is not classifiable as to its carcinogenicity to humans (Group 3 - IARC, A4 - ACGIH) (IARC, 1994; ACGIH, 2006).

Environmental Effects

The environmental impacts associated with propylene in ambient air are uncertain. Most anthropogenic emissions of propylene are expected to dissipate quickly through degradation in the atmosphere. However, this degradation process, since propylene has a double bond, could also lead to formation of ozone under the proper conditions, Ozone is associated with effects on agricultural crops and vegetation. Minimization of such indirect effects of a substance, due to formation of ozone, is best addressed through broad-based emission reduction strategies of volatile organic compounds (VOCs), such as propylene, on a regional airshed basis

There are no available data for measured toxicological effects of propylene on aquatic plants and animals. Verschueren (2001) reports declination in pea seedlings at 1746 mg/m3 in air and epinasty in tomato petioles at 87.3 mg/m3 after 3- and 2-day exposures, respectively.

Propylene is expected to have medium mobility in soil and sediment, and rapid volatilization from environmental waters. Due to the rapid loss of propylene from soil and water it is unlikely that it will be accumulated to any significant degree in terrestrial or aquatic organisms. Based on the limited available data, it is assumed that propylene has low toxicity to aquatic plants and animals. It is therefore unlikely to have a significant impact on the ecological receptors at a level that is protective of human health.


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4.0 Review of Existing Air Quality Criteria

4.1 Overview

There are currently no air quality criteria for propylene in Ontario.

In establishing the air quality standards for Ontario, the Ministry of the Environment is considering risk assessments and the scientific rationale of guidelines and criteria used by other environmental protection agencies. This report reviewed the scientific basis for air quality guidelines and criteria developed by the States of California, Michigan New Jersey, New York and Texas. Agency-specific summaries of guidelines are presented in Section 7. A brief summary of available criteria is presented in Table 1.

Table 1: Summary of Existing Air Quality Guidelines1 for Propylene

Agency Guideline Value Basis of Guideline Date2 Comments

Canada

(CEPA, CCME)

No guideline listed Not listed on PSL 1 or PSL 2

Ontario

(MOE)

No guideline listed

U.S. EPA

(IRIS)

No guideline listed

California

(OEHHA)

3,000 µg/m3

(Chronic REL)

Based on the observed squamous metaplasia, epithelial hyperplasia and inflammation of the nasal cavity in rats. (Quest et al., 1984; NTP, 1985)

2000 Chronic Reference Exposure Level

Louisiana

(DEQ)

No guideline listed

Massachusetts

(MADEP)

No guideline listed


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Agency Guideline Value Basis of Guideline Date2 Comments

Michigan

(DEQ)

1,500 µg/m3

(24-hr ITSL)

Based on the observed squamous metaplasia, epithelial hyperplasia and inflammation of the nasal cavity in rats. (Quest et al., 1984; NTP, 1985)

1994 Initial Threshold Screening Level

New Jersey

(DEP)

3,000 µg/m3

(RfC)

Based on the CalEPA’s chronic REL value

2001 Reference Concentration

New York

(DEC)

3,000 µg/m3

(AGC)

Based on the CalEPA’s chronic REL value

2000 Annual Guideline Concentration

North Carolina

(DENR)

No guideline listed

Texas

(CEQ)

117,000 µg/m3

(1-hour ESL)

Vegetation effects 1997 Effects Screening Level

The Netherlands No guideline listed

Sweden No guideline listed

United Kingdom No guideline listed

WHO (PHE and Europe)

No guideline listed

1. Guidelines in this table can refer to: guidelines, risk-specific concentrations based on cancer potencies, and non-cancer-based reference concentrations.

2. Date here refers to when the health-based guideline background report or original legislative initiative was issued. The sources were the respective agency documents. For the U.S. EPA, date refers to when the latest review of the RfC was conducted, if applicable.

In reviewing the air quality guidelines and exposure limits presented in Table 1, it should be noted that the Ministry of the Environment typically uses a factor of 15 to convert from guidelines based on annual average concentrations to half-hour point-of-impingement limits and a factor of 3 to convert from guidelines based on 24-hour average concentrations. These factors are derived from empirical measurements and are selected to ensure that if the short-term limit is met, air quality guidelines based on longer-term exposures will not be exceeded (MOE, 1998). However, depending on the health end-point being considered, other conversion factors may also be employed.


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4.2

The states of California and Michigan were the only jurisdictions that have derived air quality criteria based on toxicological studies. The state of California recently (2000) derived their chronic Reference Exposure Level (REL) of 3000 µg/m3 for propylene based on the respiratory system effects observed in rats reported in the chronic toxicity study of Quest et al. (1984). A LOAEL for the observed effects was identified as 8600 mg/m3. Michigan also chose this study as the basis of their guideline value (1500 µg/m3) citing the NTP report of 1985.

Considering the limited amount of toxicological data available for propylene, the states of New Jersey and New York chose to adopt the chronic REL value derived by California as their long-term guideline values (Reference Concentration [RfC] for New Jersey and Annual Guideline Concentration [AGC] for New York).

The state of Texas was the only jurisdiction to derive an air quality criterion for propylene based on potential effects to vegetation. However, the toxicological basis for their guideline value of 117 mg/m3 was not available for review and therefore, will not be considered further for the development of air quality criteria for Ontario.

From 1989 to 2005 the ACGIH had not established a TLV for propylene and classified the compound as a simple asphyxiant. Simple asphyxiants are defined as “inert” gases or vapours which, when present in high concentrations in air, act primarily as simple asphyxiants without any significant physiological effects. Instead of a guideline specifically for propylene, the ACGIH (2002a,b) recommended that a minimal oxygen content of at least 18 % by volume must be maintained under normal atmospheric pressure. The ACGIH has reviewed recent toxicological information available and in 2006 adopted a TLV-TWA of 500 ppm (860 mg/m3) for propylene. The TLV is based on changes in nasal mucosa, as identified in various chronic animal studies. This is the same endpoint found in Quest et al. (1984). In a review of the industrial use and toxicity of propylene, Cavender (1994) suggested a generic TLV of 1720 mg/m3 for propylene and other simple asphyxiants.

Evaluation of Existing Criteria

There are very few chronic studies for propylene, no studies of developmental or reproductive toxicity, and no lifetime toxicity studies in non-rodent species available. In addition, the epidemiological studies available have not adequately defined exposure levels. However, jurisdictions have derived limits based on their interpretation of the available information and other criteria.

California has developed a chronic reference exposure level (REL) for propylene of 3000 µg/m3, based on the LOAEL of 8600 mg/m3 from the chronic study by Quest et al. (1984) (as also reported in NTP (1985)). The REL was calculated with adjustments for


15

continuous exposure, application of a regional gas dose ratio scaling factor for humans, and with application of a 100-fold uncertainty factor. This uncertainty factor was comprised of the following: 3-fold to extrapolate from a LOAEL to a NOAEL; 3-fold for interspecies extrapolation; and 10-fold for intraspecies differences in sensitivity. The 3-fold uncertainty factor used to extrapolate from a LOAEL to a NOAEL includes a California policy decision on incorporating consideration of the effect severity. In the case of propylene, the effects were deemed “low severity” and an uncertainty factor of 3 was applied. The use of an uncertainty factor of 3 instead of 10 for interspecies variability was not explained by California. However, the use of pharmacokinetic data in deriving a Human Equivalent Concentration (HEC) may be the justification for the use of the smaller uncertainty factor.

Michigan took a different approach in deriving their guideline value and included a cumulative uncertainty factor of 1000. In their evaluation of propylene, no adjustments were made to the experimental LOAEL of Quest et al. (1984) to assess the HEC; however, Michigan applied an uncertainty factor of 10 to account for interspecies variability. Michigan also applied a greater uncertainty factor to account for conversion of the LOAEL to a NOAEL. Therefore, it is apparent that different approaches were taken to address the uncertainties associated with the limitations of the Quest et al. (1984) study and the lack of a toxicological database for propylene.

5.0 Responses of Stakeholders to the Information Draft

In August 2005, the Ministry posted Information Draft documents for twelve chemicals, including propylene, for air standards development under the Standards Plan (MOEE, 1996; MOE, 1999) to the Environmental Registry. The Ministry requested input regarding: the completeness of relevant inhalation toxicological information examined by the Ministry; the rationales of the agencies that the Ministry has considered appropriate for the development of air quality standards; and specifically the appropriate uncertainty factor for interspecies variability to use for deriving an air standard.

During the consultation period the Ministry received no submissions from various stakeholders regarding the draft document for propylene.


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6.0 Responses of Stakeholders to the Rationale Document

In June, 2006, the Ministry posted to the Environmental Registry a document titled “Rationale for the Development of Ontario Air Standards for Propylene” and requested public comments over a period of 91 days. The Ministry received comments from five stakeholders. Highlights from these comments are summarized below.

Comments Specific to Propylene:

Comment: It was suggested that the lack of data for reproductive and developmental toxicity for propylene warrants the use of an additional uncertainty factor.

Response: The U.S. EPA (1994) has stated that if toxicokinetic data indicates insignificant distribution to sites remote from the respiratory tract at exposure concentrations under considerations for deriving an RfC, the requirements for reproductive and developmental data can be mitigated, except when these endpoints are suggested as potential target by other inhalation data.

Filser et al. (2000) studied the toxicokinetics of inhaled propylene in mice, rats and humans. In humans exposed to high concentration of propylene, metabolism of propylene becomes saturated, and the major elimination route observed was exhalation. At low concentration exposures, the metabolism of propylene followed first order kinetics in humans, and 93% of inhaled propylene was exhaled unchanged. This means that a significant share of propylene inhaled is exhaled immediately without reaching the blood.

Metabolically, the rate of clearance for propylene is fast, as is evident by the maximum rate of metabolism (Vmax). In humans the Vmax was 7.7 µmol/h/kg, obtained by allometric scaling from rats. Also, the concentration ratio under steady state conditions for propylene (whole body/air) is 0.7, which indicates propylene accumulates very little in the body. Finally, the reproductive system is considered a richly perfused tissue. The partition coefficient for propylene in humans for richly perfused tissues is 1.2, which indicates that the reproductive organs are likely not a target organ.

Considering the toxicokinetics information available, the Ministry does not feel any additional uncertainty factor is warranted to account for possible developmental and reproductive effects.

Comment: It was suggested that the conflicting information on carcinogenicity for propylene warrants the use of an additional uncertainty factor.


17

Response: The only human study available is a cohort study conducted by Acquavella et al. (1988). They investigated the possible relationship between colorectal cancers and the manufacturing of polypropylene. The study concluded that the collective weight of the toxicological and epidemiological evidence did not support a linkage between the production of polypropylene and colorectal cancer.

Several chronic animal studies have indicated generally negative evidence for the carcinogenicity of propylene (Maltoni et al., 1982; ILO, 1983; Quest et al., 1984; Ciliberti et al., 1988). These have been tested in both mice and rat species via inhalation at concentrations of up to 8,600 mg/m3 (7 hours per day, 5 days per week for 104 weeks for rats or 78 weeks for mice).

Propylene oxide is produced during the first step of propylene metabolism. Propylene oxide is a known carcinogen in experimental animals. The metabolism of propylene in rats and mice has been reported to be saturable, which is used in the literature as an explanation as to why chronic inhalation studies on propylene do not indicate any carcinogenic endpoints.

Both the International Agency for Research on Cancer (IARC) and the American Conference of Governmental Industrial Hygienists (ACGIH) have concluded that the evidence for the carcinogenicity of propylene is inadequate for humans and experimental animals, and that propylene is not classifiable as to its carcinogenicity to humans (Group 3 - IARC, A4 - ACGIH).

The Ministry is satisfied by the information available that propylene is not a carcinogen, and as such does not feel any additional uncertainty factor is warranted.

Other Notes: An explanation was requested for how the MOE calculated the Regional Gas Dose Ratio (RGDR) used in the Human Equivalent Calculation. This explanation is available in Section 7.0 of this document.

Comment: Based on recent toxicological research, the validity of applying uncertainty factors after Human Equivalent Concentration (HEC) calculations was questioned. It was reported that this approach does not always result in a margin of safety reflective of the level of uncertainty in the assessment.

Response: The authors of the toxicological research cited state that the application of the uncertainty factors to the internal dose obtained by using PBPK modeling and internal dosimetry rather than the HEC can produce exposure limits that have a margin of safety equivalent to the assumed uncertainty in the assessment. The MOE acknowledges that the U.S. EPA standard approach of applying the uncertainty factors to the HEC do not always result in an equivalent decrease in the target tissue dose, especially when the exposure:tissue dose relationship is non linear. However, due to the limited amount of studies on the outcome of applying uncertainty factors to the internal


18

doses vs HECs, the MOE considers that this question still requires additional evaluation. The Ministry regards the PBPK models as a useful tool for extrapolation from animal experimental exposures to human equivalent estimates and will continue to follow investigations on how incorporation of PBPK modeling and internal dosimetry data will affect the use of uncertainty factors. Developments on the effect of uncertainty factor placement on the reference concentration value will also be followed. Nonetheless, in the case of lack of toxicokinetic data and/or the absence of reliable PBPK models, the MOE will continue to use the standard approach of applying uncertainty factors after HEC calculations as recommended by the U.S. EPA in its guidance document “Methods for Derivation of Inhalation Reference Concentrations and Application of Inhalation Dosimetry” to develop its air standards. It can be further noted that HEC calculations involve only the toxicokinetic considerations, even when PBPK models are used. The toxicodynamic variability between species also needs to be addressed. Hence a need to apply uncertainty factors arises in spite of the use of sophisticated toxicokinetic tools and approaches.

General Comments:

In addition to technical comments on this specific substance, MOE received ‘general’ comments related to the standard setting process, implementation of standards and odour issues. Some of these comments formed part of the response to the Rationale Documents, which were posted from June 26, 2006 to September 25, 2006. Other comments were in response to the "Proposal to amend Ontario Regulation 419/05: Air Pollution-Local Air Quality" posted from June 15 to September 25, 2006, with a subsequent posting April 7, 2007 to May 7, 2007 of the proposed draft amendments to O. Reg. 419/05. With the June to September, 2006 posting the MOE also introduced a “Proposed Approach for the Implementation of Odour-Based Standards and Guidelines” to which it also received comments.

A detailed summary of these general comments and MOE’s responses to them can be found in the following two related postings:

1) EBR #: 010-0000 – Proposal to Amend Ontario Regulation 419/05:Air Pollution-

Local Air Quality under the Environmental Protection Act; and 2) EBR #: RA06E0006 – Proposed Approach for the Implementation of Odour-

Based Standards and Guidelines.

http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=MTAwMDAw&statusId=MTQ5Mzgx&language=en

http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=MTAwMDAw&statusId=MTQ5Mzgx&language=en

http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=Mjc4ODc=&statusId=Mjc4ODc=&language=en

http://www.ebr.gov.on.ca/ERS-WEB-External/displaynoticecontent.do?noticeId=Mjc4ODc=&statusId=Mjc4ODc=&language=en


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7.0 Considerations in the Development of an Ambient Air Quality Criterion for Propylene

There are currently no air quality criteria for propylene in Ontario.

There is limited toxicological data available for propylene. However, it has been reported to act as a simple asphyxiant with relatively low acute toxicity and mild anaesthetic properties. Symptoms of acute human exposures to extremely high concentrations of propylene (110 g/m3) have been reported to include mild intoxication, paresthesia and inability to concentrate. Even higher concentrations (> 400 g/m3) have been reported to result in loss of consciousness, nausea, vertigo and coughing. Animal studies suggest that acute exposure to extremely high concentrations of propylene may result in cardiac effects (e.g., atypical ventricular ectopic beat). Effects resulting from chronic exposure to propylene have not been characterized. Several studies, however, have identified toxicity in animals; chronic exposure of rats to propylene concentrations of ~8600 mg/m3 have been reported to result in respiratory system effects including squamous metaplasia, epithelial hyperplasia and inflammation of the nasal cavity.

Propylene is not readily absorbed from the lungs with inhalation exposure and is therefore, not well distributed in the body. A recent report has stated that, at low concentrations, 93% of propylene inhaled is exhaled unchanged in humans. Studies have shown that propylene metabolites appear to be fairly evenly distributed throughout the body. However, higher concentrations will likely be found in fatty tissue based on its observed tissue: air partition coefficient. The propylene which is absorbed into the blood and distributed is rapidly metabolized by the cytochrome P-450 system to propylene oxide. Limited data is available concerning its elimination following metabolism. Based on the low absorption of propylene and its rapid elimination, it has been suggested that the concentration of bioavailable propylene may not reach high enough levels in classical long-term inhalation studies to show positive or serious chronic effects (Golka, 1989).

The limited genotoxicity and mutagenicity data for propylene are negative for bacterial systems, and inconclusive for mammalian systems even at extremely high concentrations of propylene (> 344,000 mg/m3). The NTP (1985) has concluded that there is no evidence of carcinogenicity, as no propylene related increases in malignant or benign neoplasms were observed following a 2-year inhalation study on rats and mice. Both IARC and the ACGIH have concluded that the experimental evidence is inadequate for humans and experimental animals.

The low toxicity of propylene is likely responsible for the lack of toxicological data. The ACGIH, in acknowledging this low potential for toxicity, has not derived a guideline value for occupational exposures and has classified propylene as a simple asphyxiant.


20

However, the ACGIH (2006) is in the process of revising their classification, and has proposed a trial TLV of 500 ppm (860 mg/m3) listed under “Notice of Intended Changes” (NIC). NICs trial values typically remain in this category for one year, during which interested parties are invited to comment on the proposed TLV. The TLV proposed for propylene is based on changes in nasal mucosa, as identified in various chronic animal studies. This trial TLV is based on the same endpoint found in Quest et al. (1984).

The states of Michigan and California were the only jurisdictions that have derived air quality criteria for propylene based on toxicological studies. Not surprisingly, with the lack of available data, both jurisdictions have chosen the same study data from which to derive their guideline values. However, different approaches were taken to address the uncertainties associated with the study (Quest et al., 1984; NTP, 1985) results. Michigan’s lack of use of pharmacokinetic data in converting the animal dose to a HEC resulted in the use of a default uncertainty factor of 10 for interspecies variability. California chose to reduce their uncertainty factor for interspecies variability to only 3 through the use of pharmacokinetic data in deriving a HEC. California’s application of a 3-fold uncertainty factor to extrapolate from a LOAEL to a NOAEL includes a California policy decision on incorporating consideration of the effect severity. In the case of propylene, the effects were deemed “low severity” and this uncertainty factor of 3 was applied. Michigan did not consider the severity of toxic effects resulting from exposure. Therefore, both of the jurisdictions have made decisions in deriving their air quality criteria for propylene which are open to interpretation.

With the lack of new toxicological information available, the MOE has also chosen the study by Quest et al. (1984) as the most appropriate basis to derive Ambient Air Quality Criteria. Quest et al. (1984) observed squamous metaplasia, epithelial hyperplasia and inflammation of the nasal cavity in rats. An AAQC can be derived using the following method:

A LOAEL of 5000 ppm (8605 mg/m3) was identified in this study.

To convert the LOAEL to continuous exposure (LOAELadj):

LOAELadj = 8605 mg/m3 x 6 hours/24 hours x 5 days/7 days = 1536 mg/m3

To convert to a human equivalent LOAEL (LOAELHEC):

LOAELHEC= LOAELadj x RGDR = 1536 mg/m3 x 0.27 = 410 mg/m3

Assumptions for this RGDR:


21

The Quest et al. 1984 study established that at 5000 ppm (8605 mg/m3) inflammatory changes in the nasal cavity was observed in male F344/N rats, and squamous metaplasia was observed in male and female F344/N rats. As inflammatory changes and squamous metaplasia was observed in only the male rats, the sensitive species was considered to be male F344/N rats.

RGDR = (MVA/MVH)/(SAA/SAH) where;

MVH = default minute volume in humans = 13.8 L/min, assuming 70 kg body weight

MVA = minute volume in F344/N male rats in Quest et al. (1984) = 0.28 L/min, assuming 0.447 kg body weight

SAH = default surface area for extrathoracic region in humans = 200 cm2

SAA = default surface area for extrathoracic region in rats = 15 cm2

According to the U.S. EPA (1994), the MVA calculated above uses the following assumptions.

lnMVA = b0 +b1 ln(BW), where:

b0 = default rat intercept used to calculate minute volume based on body weight = -0.578

b1 = default rat coefficient used to calculate minute volume based on body weight = 0.821

BW = body weight of F344/N male rats exposed to 5000 ppm in Quest et al. (1984) = 0.447

Using the above values, the MVA = 0.28 L/min, resulting in a RGDR of 0.27. All default values in this calculation are available in U.S. EPA (1994) document.

A cumulative uncertainty factor of 100 is applied to the LOAELHEC to derive the 24-hour AAQC value of 4000 μg/m3. The uncertainty factor of 100 incorporates a factor of 3 to extrapolate from a LOAEL to a NOAEL, a factor of 3 to account for interspecies extrapolation, and finally a factor of 10 to address intraspecies variability.

As a human equivalent concentration was calculated, an uncertainty factor of 3 (10½) for interspecies extrapolation was considered sufficient. This factor will account for


22

uncertainty between species in regards to pharmacodynamics (U.S. EPA, 2002). A factor of 3 (10½) for extrapolating from a LOAEL to a NOAEL was considered sufficient, as the observed changes in the nasal cavity of rats was not considered severe. Finally, an uncertainty factor of 10 for intraspecies was considered appropriate to account for variations in susceptibility within the human population and to protect sensitive individuals within the population.

8.0 Decision

The Ministry has reviewed and considered air quality guidelines and standards used by leading agencies worldwide. After reviewing additional toxicological information, the Ministry considers the rationale supporting the Reference Exposure level (REL) by the California EPA, based on the respiratory effects of this compound, to be the most appropriate basis for the derivation of health-based air standards for propylene.

The Ministry of the Environment uses a factor of 3 to convert from criteria based on 24-hour average concentrations to half-hour average concentration. This factor is derived from empirical measurements and is selected to ensure that if the short-term half hour average concentration is met, the air quality standards based on longer-term exposures will not be exceeded (MOE, 1987; MOEE, 1994).

After an evaluation of the scientific rationale of air guidelines from leading agencies and an examination of current toxicological research for the review of air quality standards for propylene (115-07-1) for Ontario, the standards for propylene are as follows:

• A 24-hour average AAQC of 4,000 μg/m3 (micrograms per cubic metre of air) based on the adverse respiratory effects of this compound; and

• A half-hour standard of 12,000 μg/m3 (micrograms per cubic metre of air) based on the adverse respiratory effects of this compound.

These effects-based AAQCs and the corresponding effects-based half hour standards will be incorporated as standards into Ontario Regulation 419/05: Air Pollution – Local Air Quality (O. Reg. 419/05). The AAQCs will be incorporated into Schedule 3 of O. Reg. 419/05; the half-hour standard will be incorporated into Schedule 2.

MOE generally proposes a phase-in period for new standards or standards that will be more stringent than the current standard or guideline. The phase-in for this compound is as set out in O. Reg. 419/05.

Among other things, O. Reg. 419/05 sets out the applicability of standards and appropriate averaging times, phase-in periods, types of air dispersion models and when


23

various sectors are to use these models. There are 3 guidelines that support O. Reg. 419/05. These guidelines are:

• “Guideline for the Implementation of Air Standards in Ontario” (GIASO);

• “Air Dispersion Modelling Guideline for Ontario” (ADMGO); and

• “Procedure for Preparing an Emission Summary and Dispersion Modelling Report” (ESDM Procedure).

GIASO outlines a risk-based decision making process to set site specific alternative air standards to deal with implementation barriers (time, technology and economics) associated with the introduction of new/updated air standards and new models. The alternative standard setting process is set out in section 32 of O. Reg. 419/05.

For further information on these guidelines and O. Reg. 419/05, please see the Ministry’s website http://www.ontario.ca/environment and follow the links to local air quality.

http://www.ontario.ca/environment


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9.0 References

ACGIH. 2002a. Documentation of the threshold limit values and biological exposure to indices. American Conference of Governmental Industrial Hygienists (ACGIH) Inc., Cincinnati, OH.

ACGIH. 2002b. Guide to occupational exposure values – 2002. Compiled by the American Conference of Governmental Industrial Hygienists (ACGIH) Inc., Cincinnati, OH.

ACGIH. 2006. Guide to occupational exposure values – 2005. Compiled by the American Conference of Governmental Industrial Hygienist (ACGIH) Inc., Cincinnati, OH.

Acquavella, J.F., Douglass, T.S. and Phillips, S.C. 1988. Evaluation of excess colorectal cancer incidence among workers involved in the manufacture of polypropylene. J Occup Med 30:438-442. Cited In: IARC, 1994.

Acquavella, J.F., Owen, C.V., Bird, M.G., Yarborough, C.M. and Lynch, J. 1991). An adenomatous polyp case-control study to assess occupational risk factors following a workplace colorectal cancer cluster. Am J Epidemiol 133:357-367. Cited In: IARC, 1994.

AIHA. 1989. Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, Akron, OH.

Altshuller, A. 1983. Review: natural volatile organic substances and their effect on air quality in the United States. Atmos Environ 17:2131-2165. Cited In: Beije, 1995.

Amoore, J.E. and Hautala, E. 1983. Odor as an aid to chemical safety: Odor thresholds compared with threshold limit values and volatilities for 214 industrial chemicals in air and water dilution. J Appl Toxicol 3:272-290.

Anderson, E. 1992. Canada’s Chemical Industry Struggles to Recover from Recession. Chem & Eng News June 29, 1992 p. 11.

ARB (Air Resources Board). 1995. Personal communication from Jim Shikiya, Monitoring and Laboratory Division to Kitty Martin, Stationary Source Division. Data from the ARB Surveillance Vehicle Program. Air Resources Board. Sacremento, CA. Cited In: ARB, 1997a.


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ARB. 1997a. Toxic Air Contaminant Identification List (Summaries) California Environmental Protection Agency, Air Resources Board (ARB), Sacramento, CA.

ARB. 1997b. Data retrieved from ATEDS (Air Toxics Emission Data System). Run date: July 11, 1997. Technical Support Division, Special Pollutants Emission Inventory Section. Sacremento, CA. Cited In: ARB, 1997a.

Aronian, P., Scheff, P. and Wadden, R. 1989. Wintertime source-reconciliation of ambiant organics. Atmos Environ 23:911-920. Cited In: Beije, 1995.

Atkinson, R and Carter, W.P.L. 1984. Kinetics and mechanisms of the gas-phase reactions of ozone with organic compounds under atmospheric conditions. Chem Rev 84: 437-70.

Atkinson, R. 1989. Kinetics and mechanisms of the gas-phase reactions of the hydroxyl radical with organic compounds. J Chem Phys Ref Data Monograph 1 p. 103.

Beije, B. 1995. 117: Propene. The Nordic Expert Group for Criteria Documentation of Health Risks from Chemicals. Arbete och Hälsa 7:1-41.

Brown, W.E. 1924. J Pharmacol Exp Therap 23:485. Cited In: Cavender, 1994.

Budavari, S., O’Neill, M.J., Smith, A., Heckelman, P.A. and Kinneary, J.F. eds. 1996. The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals. 12th Ed. Merck & Co., Inc. Whitehouse Station, N.J.

CalEPA (California Environmental Protection Agency). 1997. Toxic air contaminant identification list compound summaries. Final Report. State of California, California Environmental Protection Agency, Air Resources Board, Stationary Sources Division.

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29

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http://www.pwc.bc.doe.ca/ep/npri/index.html



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10.0 Appendix: Agency-Specific Reviews of Air Quality Guidelines

10.1 Agency-Specific Summary: Federal Government of Canada

1. Name of Chemical: Propylene (CAS no. 115-07-1)

2. Agency: Canadian Environmental Protection Act (CEPA) under the auspices of Health Canada and Environment Canada

3. Guideline Value(s):

No guideline is listed.

4. Application:

Under the Canadian Environmental Protection Act (CEPA), the Ministers of the Environment and Health are advised to investigate various substances with the potential to cause adverse effects on the environment and human health. In 1994, 44 chemicals were on the first Priority Substances List (PSL 1). Further to this, in 1995, the second PSL list was established and it identified other substances which were scheduled to be evaluated over the upcoming years.

Some of the substances listed in Health Canada (1996) have Tolerable Concentrations (TC) in mg/m3 for non-carcinogenic effects. These values are airborne concentrations which can be exposed to a person, continuously over a lifetime without adverse health effects.

Canadian Council of Ministers of the Environment (CCME) is in the process of developing new Canada-Wide Standards (CWSs) which include qualitative or quantitative standards, guidelines, objectives, and criteria for protecting the environment and reducing the risk to human health. The focus of the Standards Sub-Agreement is on ambient standards which will include air as a media. The CWSs will not be legally enforceable and governments will be responsible for implementing them.

5. Documentation Available:

No information.

Key Reference(s):


34

Not applicable.

6. Peer Review Process and Public Consultation:

No information.

7. Status of Guideline:

Not applicable.

8. Key Risk Assessment Considerations:

Not applicable.

9. Key Risk Management Considerations:

No information.

10. Multimedia Considerations of Guidelines:

No information.

11. Other Relevant Factors:

No information.


35

10.2 Agency-Specific Summary: Federal Government of the United States


2. Agency: United States Environmental Protection Agency (U.S. EPA)



4. Application:

The U.S. EPA, through the Integrated Risk Information System (IRIS), posts cancer and non-cancer exposure limits for the inhalation and oral routes of exposure which can be used towards the derivation of ambient air guidelines or standards by other jurisdictions. The IRIS database is designed to provide consistent information on chemical substances used in risk assessments, decision-making and regulatory activities. The main intention of IRIS is to provide information which can be used towards the protection of public health through risk assessment and risk management. The values presented in IRIS do not represent guidelines on their own. IRIS also contains a summary of current American government regulatory actions under various mandates.


No information.


Not applicable.


Not applicable.


Not applicable.


No information.


36


No information.


No information.


37

10.3 Agency-Specific Summary: California


2. Agency: California Environmental Protection Agency (CalEPA)


A chronic Reference Exposure Level (REL) of 3,000 µg/m3 has been derived by the Office of Environmental Health Hazard Assessment (OEHHA).

4. Application:

“The intent of the Committee in developing the guideline was to provide risk assessment procedures for use in the Air Toxics ‘Hot Spots’ program.” (CAPCOA, 1993). This program is based on a California State Law, the Air Toxics ‘Hot Spots’ Information and Assessment Act of 1987 (Health and Safety Code Section 44360 et Seq.). The act specifies how local Air Pollution Control Districts determine which facilities in the area will prepare a health risk assessment, how such health risk assessments should be prepared, and how the results are to be prioritized. These Guidelines were prepared to provide consistent risk assessment methods and report presentation to: 1) compare one facility against another, 2) expedite the review of risk assessments by reviewing agencies, and 3) minimize revisions and re-submission of risk assessments. The various health-based exposure levels developed for and employed in this program should not be used outside the framework of the program.


CalEPA. 1997. Toxic air contaminant identification list compound summaries. Final Report. State of California, California Environmental Protection Agency (CalEPA), Air Resources Board, Stationary Sources Division.

CAPCOA. 1993. Air toxics “hot spots” program: revised 1992 risk assessment guidelines. Prepared by CAPCOA (California Air Pollution Control Officers Association), the Office of Environmental Health Hazard Assessment and the California Air Resources Board.

OEHHA. 2000. Air toxics hot spots program risk assessment guidelines. Part III. Technical support document for the determination of noncancer chronic reference exposure levels. December 2000. Office of Environmental Health Hazard Assessment (OEHHA), California Environmental Protection Agency (CalEPA), CA.


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Key Reference(s):

Quest, J.A., Tomaszewski, J.E., Haseman, J.K., Boorman, G.A., Douglas, J.F. and Clarke, W.J. 1984. Two-year inhalation toxicity study of propylene in F344/N rats and B6C3F1 mice. Toxicol Appl Pharmacol 76:288-295.

NTP. 1985. National Toxicology Program. Toxicology and carcinogenesis studies of propylene in F344/N rats and B6C3F1 mice. Technical Report Series NTP-TR-272, NIH publication no. 86-2528.


Cancer potency slope factors and acute and chronic reference levels were prepared by the California Office of Environmental Health Hazard Assessment (OEHHA) using peer-reviewed scientific data. Both the exposure and health assessments have undergone public review and comment prior to finalization. Under the CAPCOA risk assessment process, each assessment is site-specific and public notice to all exposed individuals is required when the assessment concludes that a significant health risk is associated with emissions from a facility. Public input is obtained in identifying and ranking areas and facilities for risk assessment screening. Further additional input is expected as the process moves forward.


Current.


The chronic REL is based on a chronic inhalation study (Quest et al.,1984). This study was a comprehensive two-year study in F344/N rats and B6C3F1 mice. Groups of 50 mice and 50 rats of each sex were exposed to levels of propylene of 0, 8600, and 17,200 mg/m3, with mean daily concentrations of 8575 and 17,013 mg/m3, respectively, for the rat study, and 8599 and 17,126 mg/m3, respectively, for the mouse study. The animals were exposed for six hours per day, five days per week for 103 weeks. Treatment-related chronic effects were noted in the nasal cavity of exposed rats. Squamous metaplasia was observed in both dosage groups of female rats, while epithelial hyperplasia occurred in the 17,200 mg/m3 exposure group of female rats. In male rats, squamous metaplasia was observed only in the low dosage group, however both dosage groups had inflammatory changes characterized by an influx of lymphocytes, macrophages, and granulocytes into the submucosa and granulocytes into the lumen. In mice, the inflammatory lesions were more severe at the 17,200 mg/m3 exposure level. Mild focal inflammation was noted in the kidneys of the treated mice, although there was no clear relationship to propylene exposure. Neither nasal lesions nor other treatment-related effects


39

including clinical signs, mortality, mean organ and body weights and histopathology were observed in the mice. The LOAEL identified from this study is 8575 mg/m3, while a NOAEL was not observed.

The chronic REL of 3,000 μg/m3 is derived from the LOAEL of 8575 mg/m3. The LOAEL is based on critical effects in the respiratory system which include: squamous metaplasia (males and females), epithelial hyperplasia (females only) and inflammation (males only) of the nasal cavity. The LOAEL was then adjusted to account for continuous exposure by multiplying by 6/24 (fraction of hours exposed per day) and 5/7 (fraction of days exposed per week) for a result of 1531 mg/m3. This average experimental exposure is multiplied by the Regional Gas Dose Ratio (RGDR) of 0.21 (based on a BW = 305 g, MV = 0.21 L/min, SA(ET) = 15 cm2) to obtain the human equivalent concentration of 327 mg/m3. A cumulative uncertainty factor of 100 was applied (a LOAEL to NOAEL uncertainty factor of 3 (only 3 because the OEHHA deemed the effect of low severity), an interspecies uncertainty factor of 3 and an intraspecies uncertainty factor of 10. When rounded, this results in a chronic REL of 3 mg/m3 or 3,000 µg/m3.


The exposure guidelines were prepared for non-cancer-based endpoints. The non-cancer guidelines are based on the most sensitive adverse health effect report in the scientific literature and are designed to protect the most sensitive individuals in the population.

The State of California allows local options to address the possible economic impacts of emission control. It appears that the options are under local control and are based on local risk, socioeconomic analyses, and feedback from public workshops and hearings. The enforcement mechanism is via operating permits. Thus, the process is primarily directed towards site-specific evaluations and development of further regulatory tools rather than towards enforceable levels in themselves.


In the exposure modelling process, non-inhalation pathways should be considered for a number of substances (specified in Table III-5 in CAPCOA, 1993). Propylene is not one of the substances requiring non-inhalation modelling.


No information.


40

10.4 Agency-Specific Summary: Commonwealth of Massachusetts


2. Agency: Massachusetts Department of Environmental Protection


No guideline value is listed for propylene.

4. Application:

“...The Division of Air Quality Control, which is responsible for implementing the Department’s air programs, plans to employ the AALs in the permitting, compliance, and enforcement components of the commonwealth’s air program in general, and the air toxics program in particular.” (MADEP, 1990, Volume 1, p. ix). The Massachusetts Department of Environmental Protection (MADEP) is responsible for developing, among other environmental programs, the air toxics program, the primary objective of which is to protect human health. The limits generated by the program are “health-based only and were developed without regard to production volume, exposure level, or regulatory implication. Similarly, economic and control technology issues are neither discussed nor considered here.” (MADEP, 1990, Volume 1, p. 4). Thus, the ambient air levels developed in this process are not to be considered as legally-enforceable air standards; rather, they should be employed as guidelines in the development of subsequent regulatory action.


MDEP (Massachusetts Department of Environmental Protection). 1995. Massachusetts Threshold Effects Exposure Limits (TELs) and Allowable Ambient Limits (AALs) for Ambient Air. Commonwealth of Massachusetts, Department of Environmental Protection, Boston, MA.

Key Reference(s):

No information.


The Office of Research and Standards (ORS) reviews the scientific literature and revises the guidelines taking into account new toxicological data. The revisions typically undergo external scientific peer review.


41


Not applicable


Not applicable.


Not applicable.


Not applicable.


None.


42

10.5 Agency-Specific Summary: State of Michigan


2. Agency: Michigan Department of Environmental Quality (MDEQ)


The MDEQ has derived a value of 1,500 µg/m3 for its 24-hour Initial Threshold Screening Level (ITSL).

4. Application:

The screening levels are health-based screening levels for non-carcinogenic effects under Michigan’s air toxic rules. These values are only used as a tool for the evaluation of ambient air impacts from new or modified air emission sources when a permit is requested. These values are not considered as general ambient air quality levels nor are they considered standards. The air toxics rules require that each source must apply the best available control technology for toxics (T-BACT) and the maximum ambient concentration of each toxic air contaminant cannot exceed its screening level. Some exceptions to the T-BACT requirement include processes emitting low potency carcinogens or non-carcinogens that have relatively low toxicity.


MDEQ (Michigan Department of Environmental Quality). 1998. Addendum: 97-033EQ. Air pollution control rules. Part 2. Air use approval. R 336.1224 to R 336.1232 and R 336.1299. Effective date: November 10, 1998. Michigan Department of Environmental Quality, Air Quality Division, Lansing, MI.

MDEQ. 1999. List of screening levels (ITSL, IRSL and SRSL). Verification date: July 6, 1999. Michigan Department of Environmental Quality (MDEQ), Air Quality Division, Lansing, MI.

MDNR. 1994. Screening level determination. Interoffice Communication To: “File for Propylene (CAS # 115-07-1)”. December 5, 1994.

Key Reference(s):

NTP. 1985. Toxicology and carcinogenesis studies of propylene (CAS no. 115-07-1) in F344/N rats and B6C3F1 mice (inhalation studies). National Toxicology Program. US Department of Health and Human Services. Public Health Service. National


43

Institutes of Health. NTP TR 272. NIH Publication No. 86-2528. Cited In: MDNR, 1994.


This value is based on a review of information from a variety of scientific agencies. For final derivation of the IRSL, data from the National Toxicology Program (NTP) 2-year inhalation study was used in the scientific assessment by a staff toxicologist from the Air Quality Division. No other specific information on peer-review, external review or public consultation is mentioned.


Current. An updated list of screening levels that have been revised or newly established is produced every two months, while a complete list of all screening levels is published at the beginning of each year.


The ITSL of 1,500 µg/m3 is based on an identified LOAEL of 8600 mg/m3 (NTP, 1985). This study was a comprehensive two-year study in F344/N rats and B6C3F1 mice. Groups of 50 mice and 50 rats of each sex were exposed to levels of propylene of 0, 8600, and 17200 mg/m3, with mean daily concentrations of 8575 and 17013 mg/m3, respectively, for the rat study, and 8599 and 17126 mg/m3, respectively, for the mouse study. The animals were exposed for six hours per day, five days per week for 103 weeks. Treatment-related chronic effects were noted in the nasal cavity of exposed rats. Squamous metaplasia was observed in both dosage groups of female rats, while epithelial hyperplasia occurred in the 17200 mg/m3 exposure group of female rats. In male rats, squamous metaplasia was observed only in the low dosage group; however both dosage groups had inflammatory changes characterized by an influx of lymphocytes, macrophages, and granulocytes into the submucosa and granulocytes into the lumen. In mice, the inflammatory lesions were more severe at the 17210 mg/m3 exposure level. Mild focal inflammation was noted in the kidneys of the treated mice, although there was no clear relationship to propylene exposure. Neither nasal lesions nor other treatment-related effects including clinical signs, mortality, mean organ and body weights and histopathology were observed in the mice. The LOAEL identified from this study is 8575 mg/m3 (rounded to 8600 mg/m3), while a NOAEL was not observed.

The LOAEL value was adjusted to account for continuous exposure by multiplying by 6/24 (fraction of hours exposed per day) and 5/7 (fraction of days exposed per week). A 1000-fold safety factor was applied: 10 for animal to human extrapolation;


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10 for individual variation; 10 for LOAEL to NOAEL conversion. The resulting ITSL is 1,500 µg/m3.


These considerations are performed separately by the permitting section. No other specific information is available for this chemical assessment.


No information.


No information.


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10.6 Agency-Specific Summary: North Carolina


2. Agency: North Carolina Department of Environment and Natural Resources (DENR)



4. Application:

The acceptable ambient air level is a product of initial recommendations by the Scientific Advisory Board (SAB) from which averaging times are assigned by the staff of the Toxics Protection Branch. These toxic air pollutant values are considered guidelines only and apply to all facilities that emit a toxic air pollutant that are required to have a permit under 15A NCAC 2Q.0700 of North Carolina Air Quality Rules. A facility shall not emit any toxic air pollutant under North Carolina Air Quality Rules in such quantities that may cause or contribute beyond the premises (adjacent property boundary) to any significant ambient air concentration that may adversely affect human health.


No information.

Key Reference(s):

Not applicable.


Not applicable


Not applicable.


Not applicable.



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No information.


No information.


No information.


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10.7 Agency-Specific Summary: World Health Organization (WHO)


2. Agency: World Health Organization - Protection of the Human Environment (WHO-PHE) and World Health Organization - Europe (WHO-Europe)



4. Application:

The WHO Air Quality Guidelines are designed to reduce air pollution and to protect human health. ... “The Guidelines are intended to provide background information and guidance to national or international authorities in making risk assessment and risk management decisions. In providing pollutant levels below which exposure, for lifetime or for a given period of time, does not constitute a significant public health risk, the guidelines form a basis for setting (inter)national standards or limit values for air pollutants.”


WHO. 1999. Air quality guidelines. World Health Organization (WHO), Protection of the Human Environment.

WHO. 2000. Air quality guidelines for Europe. World Health Organization (WHO), Regional Office for Europe, Copenhagen. WHO regional publications.

Key Reference(s):

Not applicable.


Not applicable.


Not applicable.



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Not applicable.


Not applicable.


Not applicable.


Not applicable.


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11.0 Acronyms, Abbreviation, and Definitions

AAL Allowable Ambient Level (Massachusetts) or Acceptable Ambient Level (North Carolina)

AAQC Ambient Air Quality Criteria - used by the Ontario Ministry of the Environment to define the potential for causing an adverse effect

AAS Ambient Air Standard (Louisiana)

ACGIH American Conference of Governmental Industrial Hygienists - a non-governmental organization which establishes occupational safety exposure limits for workers

AGC Annual Guideline Concentration (New York State)

ATSDR Agency for Toxic Substances and Disease Registry - an agency of the U.S. Department of Health and Human Services

BMC05 Benchmark Concentration - a statistical lower confidence limit (5%) on the dose producing a predetermined, altered response for an effect

bw body weight

CAPCOA California Air Pollution Control Officers Association

CAS Chemical Abstracts Service - ascribes a unique, identification (registry) number to each chemical to help clarify multiple listings for the same chemical structure

CCME Canadian Council of Ministers of the Environment

CEIL Ceiling Value - used by ACGIH for the concentration that shall not be exceeded during any part of the working exposure

CEPA Canadian Environmental Protection Act

DEC Department of Environmental Conservation - Department in state agency of New York

DEL Department of Environment and Labour - Department in provincial agency of Newfoundland


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DENR Department of Environment and Natural Resources - Department in state agency of North Carolina

DEP Department of Environmental Protection - Department in state agencies of Massachusetts, New Jersey, and Florida

DEQ Department of Environmental Quality - Department in state agencies of Michigan and Louisiana

ESL Effects Screening Level (Texas)

GLC Ground Level Concentration - the concentration of contaminant predicted by dispersion modelling

HEAST Health Effects Assessment Summary Tables - prepared by U.S. EPA’s Office of Health and Environmental Assessment. HEAST contains risk assessment information on chemicals that have undergone reviews, although generally not as extensive as the reviews conduced under IRIS

HEC Human Equivalent Concentration

IARC International Agency for Research on Cancer

IRIS Integrated Risk Information System - a database published by the U.S. EPA containing risk assessment information on a wide range of chemicals

IRSL Initial Risk Screening Level - a limit corresponding to a one in a million lifetime risk of cancer used by Michigan for screening new sources of emissions

ITSL Initial Threshold Screening Level – an air quality limit derived by Michigan for non-carcinogenic compounds

LC50 Median Lethal Concentration - the concentration of a substance in the medium (e.g., air, water, soil) to which a test species is exposed, that will kill 50% of the population of that given species

LD50 Median Lethal Dose - the dose of a substance given to a test species, that will kill 50% of the population of that given species

LOAEL Lowest-Observed-Adverse-Effect Level

LOEC Lowest-Observed-Effect Concentration

LOEL Lowest-Observed-Effect Level


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MAC Maximum Acceptable Concentration

MACT Maximum Achievable Control Technology

ME Manitoba Environment

MIC Maximum Immission Concentration (Netherlands)

MOEE Ontario Ministry of the Environment and Energy - as known between 1993 and 1997, which is now known as OMOE or Ontario Ministry of the Environment

MRL Minimal Risk Level - a term used by ATSDR, which defines a daily exposure (either from an inhalation or oral route) not likely to induce adverse non-carcinogenic effects within a given time period, i.e., acute, intermediate, or chronic

MTLC Maximum Tolerable Level Concentration

NIEHS National Institute of Environmental Health Sciences (USA)

NIOSH National Institute for Occupational Safety and Health (an agency of the U.S. Department of Health and Human Services)

NOAEL No-Observed-Adverse-Effect Level

NOEC No-Observed-Effect Concentration

NOEL No-Observed-Effect Level

NPRI National Pollutant Release Inventory

NTP National Toxicology Program (USA)

OEHHA Office of Environmental Health Hazard Assessment (California EPA)

OEL Occupational Exposure Limit

OSHA Occupational Safety and Health Association - a branch of the U.S. Department of Labour

PEL Permissible Exposure Limit (OSHA air standard)

PM Particulate Matter


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POI Point of Impingement - used in conjunction with dispersion modelling to define the area in which the maximum ground level concentration (GLC) of a contaminant is predicted to occur

PSL1 First Priority Substances List (CCME)

PSL2 Second Priority Substances List (CCME)

RD50 Median Respiration Rate Decrease - the dose at which respiration rate is decreased 50%

REL Either Reference Exposure Limit as used by the California EPA which defines the concentration at or below which no adverse health effects are expected in the general population or Recommended Exposure Limit used by both NIOSH and ATSDR

RfC Reference Concentration - an estimate of a daily inhalation exposure not likely to induce adverse health effects during a lifetime

RfD Reference Dose - an estimate of a daily exposure to the human population that is likely to be without appreciable risk of deleterious non-cancer effects during a lifetime

RTECS Registry of Toxic Effects of Chemical Substances - database maintained by NIOSH

SGC Short-term Guideline Concentration (New York State)

SRSL Secondary Risk Screening Level - a limit corresponding to one in one-hundred-thousand lifetime risk of cancer used by Michigan for screening new sources of emissions

STEL Short-term Exposure Limit

TC Tolerable Concentration - used by Health Canada to define the airborne concentration to which a person can be exposed for a lifetime without deleterious effects (for non-carcinogens)

TC01 Tumorigenic Concentration - the concentration of a contaminant in air generally associated with a 1% increase in incidence or mortality due to tumours


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TC05 Tumorigenic Concentration - the concentration of a contaminant in air generally associated with a 5% increase in incidence or mortality due to tumours

TCEQ Texas Commission on Environmental - agency in the state of Texas after September 2003, which was previously named the TNRCC or the Texas Natural Resource Conservation Commission

TD05 Tumorigenic Dose - the total intake of a contaminant generally associated with a 5% increase in incidence or mortality due to tumours

TEL Threshold Effects Exposure Level (Massachusetts)

TLV Threshold Limit Value - an exposure concentration that should not induce an adverse effect in a work environment

TWA Time-Weighted-Average - allowable exposure averaged over an 8-hour workday or 40-hour work week

U.S. EPA United States Environmental Protection Agency

WHO World Health Organization

ppm parts per million

ppb parts per billion

mg a milligram, one thousandth of a gram

µg a microgram, one millionth of a gram

ng a nanogram, one billionth of a gram