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ASSESSMENT REPORT ON
AACCRROOLLEEIINN
FOR DEVELOPING
AMBIENT AIR QUALITY
OBJECTIVES
ASSESSMENT REPORT ON ACROLEIN
FOR DEVELOPING AN AMBIENT AIR QUALITY OBJECTIVES
Prepared by Meridian Environmental Inc.
for Alberta Environment
February 2011
ISBN: 978-1-4601-0583-2 (Print) ISBN: 978-1-4601-0584-9 (Online) Web Site: http://www.environment.alberta.ca/ Although prepared with funding from Alberta Environment (AENV), the contents of this report/document do not necessarily reflect the views or policies of AENV, nor does mention of trade names or commercial products constitute endorsement or recommendation for use. Any comments, questions, or suggestions regarding the content of this document may be directed to: Air Policy Alberta Environment 9th floor, Oxbridge Place 9820 – 106th Street Edmonton, Alberta T5K 2J6 Additional copies of this document may be obtained by contacting: Information Centre Alberta Environment and Sustainable Resource Development Phone: (780) 427-2700 Email: [email protected] Website: www.environment.alberta.ca
FOREWORD Alberta Environment maintains Ambient Air Quality Objectives to support air quality management in Alberta. Alberta Environment currently has ambient objectives for more than thirty substances and guidelines for five related parameters. These objectives are periodically updated and new objectives are developed as required. With the assistance of the Clean Air Strategic Alliance, a multi-stakeholder workshop was held in November 2009 to set Alberta’s priorities for the next work plan. Based on those recommendations to Alberta Environment, a work plan was developed to review the nominated substances. This report summarizes technical information that will be considered in the development of an Ambient Air Quality Objective for Acrolein.
Laura Blair Project Manager Air Policy
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives i
ACKNOWLEDGEMENTS The authors of this report would like to thank Ms. Laura Blair of Alberta Environment for inviting them to submit this report. The authors are grateful for the help and guidance provided by Ms. Blair and her colleagues at Alberta Environment. The report was authored by Ian Mitchell, Dan Stein and David Williams, all of Meridian Environmental Inc.
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives ii
TABLE OF CONTENTS FOREWORD.................................................................................................................... i ACKNOWLEDGEMENTS............................................................................................... ii LIST OF TABLES ........................................................................................................... v LIST OF FIGURES.......................................................................................................... v ACRONYMS AND ABBREVIATIONS........................................................................... vi SUMMARY.................................................................................................................... vii 1.0 INTRODUCTION.................................................................................................. 1 2.0 GENERAL SUBSTANCE INFORMATION .......................................................... 2
2.1 Physical, Chemical and Biological Properties .........................................................2 2.2 Emission Sources and Ambient Levels....................................................................3
2.2.1 Natural Sources ...........................................................................................3 2.2.2 Anthropogenic Sources ................................................................................4 2.2.3 Ambient Levels .............................................................................................4
3.0 ATMOSPHERIC CHEMISTRY AND FATE.......................................................... 7 4.0 EFFECTS ON HUMANS AND ANIMALS ............................................................ 8
4.1 Overview of Chemical Disposition..........................................................................8
4.1.1 Absorption, Distribution, Metabolism and Excretion..................................8 4.1.2 Effects on Enzyme Systems...........................................................................9
4.2 Genotoxicity and Carcinogenicity .........................................................................10 4.3 Acute and Sub-Acute Effects.................................................................................10
4.3.1 Acute Human Effects..................................................................................11 4.3.2 Acute and Sub-Acute Animal Effects..........................................................12
4.3.2.1 Respiratory ............................................................................................ 13 4.3.2.2 Immunological Effects.......................................................................... 14 4.3.2.3 Cardiovascular Effects ......................................................................... 14 4.3.2.4 Mortality ................................................................................................. 14 4.3.2.5 Other Effects ......................................................................................... 14
4.4 Sub-Chronic and Chronic Effects ..........................................................................15 4.4.1 Sub-Chronic and Chronic Human Effects .................................................15 4.4.2 Sub-Chronic and Chronic Animal Effects..................................................15
4.4.2.1 Respiratory System .............................................................................. 15 4.4.2.2 Mortality ................................................................................................. 16 4.4.2.3 Immunological Effects.......................................................................... 16
4.5 Summary of Adverse Health Effects of Acrolein Inhalation.................................16
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives iii
5.0 EFFECTS ON VEGETATION............................................................................. 18 6.0 AIR SAMPLING AND ANALYTICAL METHODS.............................................. 19
6.1 Reference Methods ................................................................................................19
6.1.1 US EPA Method TO-11a............................................................................19 6.1.2 US EPA Method TO-15..............................................................................20 6.1.3 NIOSH Method 2501/OSHA Method 52 ....................................................21 6.1.4 CARB Method 430 .....................................................................................21
6.2 Alternative Methods...............................................................................................21 6.2.1 Chromatography ........................................................................................21 6.2.2 Mass Spectrometry.....................................................................................22 6.2.3 Colorimetric Methods ................................................................................22 6.2.4 Mist Chambers ...........................................................................................22
7.0 AMBIENT OBJECTIVES IN OTHER JURISDICTIONS..................................... 23
7.1 Air Quality Guidelines and Objectives for Acrolein .............................................23
7.1.1 Canada.......................................................................................................23 7.1.2 United States ..............................................................................................23 7.1.3 International agencies ...............................................................................24
8.0 REFERENCES................................................................................................... 26 APPENDIX A ................................................................................................................ 32
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives iv
LIST OF TABLES Table 1 Identification of Acrolein........................................................................................... 2 Table 2 Physical and Chemical Properties of Acrolein .......................................................... 3 Table 3 NPRI Reported Emissions of Acrolein to Air in 2008 and 2009............................... 5 Table 4 Effects Associated with Acute Acrolein Inhalation (Experimental Animals) ......... 12 Table 5 Effects Associated with Sub-Chronic and Chronic Acrolein Inhalation
(Experimental Animals)........................................................................................... 17 Table 6 Summary of Air Quality Objectives and Guidelines for Acrolein .......................... 25
LIST OF FIGURES
Figure 1 Metabolism of acrolein .............................................................................................. 9
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives v
ACRONYMS AND ABBREVIATIONS ACGIH American Conference of Governmental Industrial Hygienists
AEGL Acute Exposure Guidance Level
AENV Alberta Environment
ATSDR Agency for Toxic Substances and Disease registry
DNPH dinitrophenylhydrazine
EC Environment Canada
GC-MS Gas Chromatography-Mass Spectrometry
HC Health Canada
HEI Health Effects Institute
HPLC High Pressure Liquid Chromatography
HSDB Hazardous Substance Databank
IARC International Agency for Research on Cancer
IRIS Integrated Risk Information System
LD50 Lethal Dose 50%
LOAEL Lowest observable adverse effect level
MOE Ministry of Environment
NIOSH National Institute for Occupational Health and Safety
NOAEL No observed adverse effect level
NPRI National Pollutant Release Inventory
OEHHA Office of Environmental Health Hazard Assessment
OEL Occupational Exposure level
OSHA Occupational Safety and Health Administration
PEL Permissible exposure level
PMRA Pest Management Regulatory Authority
RfC Reference Concentration
REL Relative exposure level
TRV Toxicological Reference Value
US EPA United Stated Environmental Protection Agency
VOC Volatile Organic Compound
WHO World Health Organization
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives vi
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives vii
SUMMARY Acrolein is a reactive unsaturated aldehyde that exists as a highly volatile clear or yellow liquid. The largest commercial use of acrolein is as a biocide for aquatic environments, specifically for eradicating floating aquatic weeds or bacteria in produced water. There are currently three registered acrolein-based biocide products permitted for use in Canada; however, these are currently under re-evaluation by the Pest Management Regulatory Agency. In Alberta, acrolein has also been used to scavenge hydrogen sulphide from produced fluid in petroleum operations. Acrolein is manufactured by the air oxidation of propylene and is used as an intermediate chemical during the production of acrylic acid and several other chemicals. Naturally occurring acrolein is generated from the combustion of organic materials. Combustion of artificial materials such as tobacco products, plastics, refined vehicle fuels, and cooking oils can also generate acrolein. In the atmosphere, acrolein is unstable and reacts with photochemically produced hydroxyl radicals in the troposphere that can form carbon monoxide, formaldehyde, and glycoaldehyde. Long-range transport of acrolein emissions is considered unlikely, and it is not likely to partition to soil or sediment or dissolve in surface water. The largest natural source of acrolein is incomplete combustion of organic material during forest fires, although a small amount of acrolein may also be generated from fermentation and ripening processes. The largest source of anthropogenic acrolein in the atmosphere is combustion of organic matter, predominantly from fuel sources such as vehicles, incinerators, furnaces, fireplaces, power plants and agricultural burning. Due to its highly reactive nature, when humans or animals are exposed the adverse effects generally involve cytotoxicity at the site of entry into the body rather than systemic toxicity. As a result, effects in both humans and animals primarily involve sensory irritation and respiratory system effects. Common sampling methods for ambient air monitoring involve either a solid sorbent matrix followed by HPLC analysis, or canister sampling followed by GC-MS analysis; the United States Environmental Protection Agency (US EPA) and National Institute for Occupational Safety and Health (NIOSH) have established reference methods. Several regulatory agencies have developed acute and long-term ambient air quality objectives for acrolein, primarily based on its properties as an irritant and its effects on the respiratory system.
1.0 INTRODUCTION Ambient air quality objectives are established by Alberta Environment as part of the Alberta air quality management system, Section 14 of the Environmental Protection and Enhancement Act (AENV, 2000). The purpose of this assessment report is to provide a review of scientific and technical information to assist in evaluating the basis and background for an ambient air quality objective for acrolein. The following aspects were examined as part of the review: Physical and chemical properties; Existing and potential anthropogenic emissions sources in Alberta; Effects on humans, animals, and vegetation; Monitoring techniques, and; Ambient air guidelines and objectives in other Canadian jurisdictions, the United States, and
international jurisdictions, and the basis for development and use. The physical and chemical properties identified for acrolein include chemical structure, molecular weight, melting and boiling points, water solubility, density, organic carbon partition coefficient, octanol water partition coefficient, vapour pressure, Henry's Law constant, bio-concentration factor (fish), and odour threshold. A discussion of the behaviour of acrolein in the environment is also presented. Existing and potential natural and anthropogenic sources of acrolein emissions in Alberta were examined. Anthropogenic emissions are provided in Environment Canada’s National Pollutant Release Inventory (NPRI). Scientific information about the effects of acrolein on humans, animals, and vegetation were identified. Data on effects in animals and humans was available from toxicity and epidemiology studies cited in peer reviewed evaluations by the US EPA, Health Canada, Environment Canada, and the World Health Organization. Information on the effects of acrolein on vegetation was limited. Air sampling and analytical methods for acrolein used by regulatory agencies were included in this assessment. Currently utilized reference air monitoring methods from the US EPA, National Institute for Occupational Health and Safety (NIOSH), and the Occupational Safety and Health Administration (OSHA) have been included as well as some more specialized methods used in academic studies. Several ambient air quality guidelines were identified for acrolein following a review of jurisdictions in North America, Europe and elsewhere. As acrolein is considered a hazardous air pollutant (HAP) in the United States, guideline values were available from several US jurisdictions. The basis for the guidelines in use by different jurisdictions was also summarized in this report.
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 1
2.0 GENERAL SUBSTANCE INFORMATION Acrolein is a reactive unsaturated aldehyde that exists as a highly volatile clear or yellow liquid (ATSDR, 2007). The largest commercial use of acrolein is as a biocide for aquatic environments, specifically for eradicating floating aquatic weeds or bacteria in produced water during oil exploration (Environment Canada/Health Canada, 2000). There are currently three registered acrolein-based biocide products permitted for use in Canada; however, these are currently under re-evaluation by the Pest Management Regulatory Agency (PMRA) (Health Canada, 2010). In Alberta, acrolein has also been used to scavenge hydrogen sulphide from produced fluid in petroleum operations (WHO, 2002). Acrolein is manufactured by the air oxidation of propylene and is used as an intermediate chemical during the production of acrylic acid and several other chemicals (NRC, 2010). Naturally occurring acrolein is generated from the combustion of organic materials. Combustion of artificial materials such as tobacco products, plastics, refined vehicle fuels, and cooking oils can also generate acrolein (ATSDR, 2007). The chemical formula, structure, registry number, trade names and synonyms for acrolein are provided in Table 1. Table 1 Identification of Acrolein
Property Value
Formula C3H4O
Structure
CAS Registry Number 107-02-8
Trade Names Aqualin, Biocide, Crolean, Magnacide B, Magnacide H, Slimicide
Synonyms acraldehyde, acrylic aldehyde, allyl aldehyde, ethylene aldehyde, propenal, prop-2-enal, propylene aldehyde
ATSDR, 2007
2.1 Physical, Chemical and Biological Properties
The physical and chemical properties of acrolein are summarized in Table 2.
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 2
Table 2 Physical and Chemical Properties of Acrolein Property Value Reference
Molecular Weight 56.063 g/mol Mackay, 2006
Melting Point -87.7°C Lide, 2003a
Boiling Point 52.6°C Lide, 2003a
Physical State colorless or yellow liquid Lewis, 1997b
Density 0.8389 gcm-3 Riddick et al., 1986a
Vapour Pressure 35.3 kPa at 25°C Riddick et al., 1986a
Solubility miscible with organics Tomlin, 2003b
Solubility in Water 208 g/L at 25°C Riddick et al., 1986a
Henry’s Law Constant 12.36 Pa•m3mol-1 at 25°C Gaffney et al., 1987a
Octanol Water Partition Coefficient 0.977 Hansch et al., 1995a
Organic Carbon Partition Coefficient 24 (estimated) Howard et al., 1989a
Odour Threshold 250 μg m-3 (110 ppb) in water 370 μg m-3 (160 ppb) in air
Amoore and Hautala, 1983b
Flash Point -18°C (open cup) NLM, 2007b
Explosive Limits 2.8-31 %vol. NLM, 2007b
Auto-ignition Temperature 220°C NLM, 2007b
Bioconcentration Factor in Fish 346.7 Barrows et al., 1980a Veith et al., 1980a
Conversion Factors for Vapour 1 ppb = 2.328 μg m-3 at 25°C Verschueren, 2001b
a – cited in Mackay, 2006 b – cited in ATSDR, 2007
2.2 Emission Sources and Ambient Levels
Acrolein is emitted to the atmosphere from both natural and anthropogenic sources. These emission sources, as well as ambient acrolein concentrations, are described in the following sections.
2.2.1 Natural Sources The largest natural source of acrolein is incomplete combustion of organic material during forest fires, although small amounts of acrolein may also be generated from fermentation and ripening processes (Environment Canada/Health Canada, 2000). There are no quantitative estimates of natural acrolein production in Alberta.
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 3
2.2.2 Anthropogenic Sources Acrolein can be emitted directly from sources such as industrial processes using acrolein, combustion of organic material, or emissions from treated water. An evaluation of direct acrolein emissions in the United States in 2005 found that forest, prescribed, and wild fires contributed to 69% of acrolein emissions, mobile sources made up 15% of acrolein emissions, and the remaining emissions were from structural fires, residential wood combustion, agricultural field burning, internal combustion engines, and other sources (Shelow et al., 2009). Acrolein can also be produced as a secondary pollutant that is generated from chemical reactions of other emissions in the atmosphere. Secondary sources of acrolein include the reaction of 1,3-butadiene (a component of diesel and gasoline exhaust) or other aldehydes with hydroxide radicals in the presence of NOx (Berndt and Boge, 2007; Cahill et al., 2010), or photooxidation of organic pollutants such as 1,3-butadiene, allyl chloride (Maldotti et al., 1980), or propylene (Faroon et al., 2008). The amount of acrolein produced as a secondary pollutant from the photooxidation of vehicle emissions is difficult to quantify (Environment Canada/Health Canada, 2010). A study of vehicular exhaust emissions found that acrolein emissions averaged 8 mg/mi (5.0 mg/km) for personal vehicles and were as high as 13.2 mg/mi (8.1 mg/km), with emissions greatly reduced by the presence of an oxidation catalyst (Zhu et al., 2004). Emissions of acrolein from engines and backup generators ranged from 0 to 12.73 mg/kw-hr (Zhu et al., 2004). US emissions of acrolein comprise 2% of total organic gases emitted from commercial aircraft, with total acrolein emissions from this source estimated as 938 tons/year (851 tonnes/year) (US FAA, 2003). The largest source of anthropogenic acrolein in the atmosphere is combustion of organic matter, predominantly from fuel sources such as: vehicles, incinerators, furnaces, fireplaces, power plants, and agricultural burning (Environment Canada/Health Canada, 2000). Emissions from use of acrolein as a chemical intermediate is thought to be insignificant compared to non-industrial diffuse sources (European Union, 1999). Other smaller sources include wine (Bauer et al., 2010) and alcohol (Serjak et al., 1953) production or heated cooking fats (Umano and Shibamoto, 1987). Emissions of acrolein from major industrial sources in Canada, based on the results of the 2008 and 2009 National Pollutant Release Inventory (NPRI) are presented in Table 3. Acrolein has also been used as a biocide for aquatic algae, weed and mollusc control (Ghilarducci and Tjeerdema, 1995; ATSDR, 2007).
2.2.3 Ambient Levels Acrolein was detected in 57% of Canadian samples by the National Air Pollution Surveillance (NAPS) program in rural, suburban and urban locations between 1989 and 1996 with evidence for trends in increasing concentration in urban and suburban sites (Environment Canada and Dann, cited in Environment Canada/Health Canada, 2000). Mean acrolein concentrations in
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 4
Table 3 NPRI Reported Emissions of Acrolein to Air in 2008 and 2009
NPRI ID
Company
City/Location
Province/ Territory
2008 (tonnes)
2009a (tonnes)
4880 Ainsworth Lumber Co. Ltd. - Grande Prairie OSB Mill
Grande Prairie AB 32 36
6505 Millar Western Forest Products Ltd. - Solid Wood Division
Whitecourt AB 0.237 0.186
6506 Millar Western Forest Products Ltd. -Wood Products Division
Boyle AB 0.101 0.054
5285 Apache Canada- Zama Gas Processing Complex
Zama AB - 0.600
Total Alberta sources 32.3 36.8
4559 Grant Forest Products- Oriented Strand Board Plant
Englehart ON 24 21
20104 Canfor-LP OSB - Peace Valley Fort St John BC 22 16
1195 Domtar Inc. Windsor QC 12 -
7170 Ainsworth Engineered Barwick ON 11 11
6688 NW Energy Corp. - Williams Lake Power Plant
Williams Lake BC 10 -
8684 PTT polycanada Montreal QC 6.9 -
8070 Enligna Canada Inc. -Upper Musquodoboit Mill Site
Middle Musquodoboit
NS 1.1 1.4
2363 Longlac Wood Industries Inc. Longlac ON 0.919 0
18241 Diavik Diamond Mines Inc Lac de Gras NT 0.004 -
656 Durez Canada Company Ltd. –Durez Canada
Fort Erie ON 0.001 0
Total Canadian sources 120 86
a – 2009 NPRI data is preliminary Canadian urban areas are generally less than 0.2 μg m-3 (0.086 ppb) (Environment Canada/Health Canada, 2000). The highest mean acrolein concentration in ambient air measured by NAPS between 1989 and 1996 was 1.58 μg m-3 (0.68 ppb) from an urban area in Montréal, Québec (Environment Canada, cited in Environment Canada/Health Canada, 2002).
In a study of air quality near various industrial activities (including municipal waste incinerators, steel refining, and coke operations), 24 of 29 samples of ambient air collected from Windsor, Ontario in 1992 contained acrolein at concentrations up to 0.5 μg m-3 (0.2 ppb), with a mean concentration of 0.16 μg m-3 (0.069 ppb) (Ontario Ministry of Environment and Energy, 1994). A study of ambient acrolein concentrations in Ontario in 1996 found concentrations ranging from 0.14 to 0.25 μg m-3 (0.06-0.1 ppb) (Ontario Ministry of the Environment, 2005).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 5
The US EPA Air Quality System measured average acrolein concentrations ranging from 1.1 to 7.4 μg m-3 (0.5-3.2 ppb) (US EPA cited in Faroon et al., 2008) and median ambient air concentrations in US urban areas predicted by the US EPA are frequently greater than 0.06 μg m-3 (0.03 ppb) (Rosenbaum et al., 1999). Woodruff et al. (1998) found that the median acrolein concentration measured in urban ambient air in the US exceeded the US EPA reference concentration (RfC) of 0.02 μg m-3 (0.0086 ppb) and the maximum measured concentration was approximately 1,000 times greater than the RfC. In urban areas, acrolein concentrations may be influenced by automobile exhaust emissions (Grosjean et al., 2002), but this is not always the dominant source of atmospheric acrolein in urban areas, as smoke from burning biomass may provide a larger contribution, especially during winter months (Spada et al., 2008). Concentrations of acrolein measured near a major roadway in California were estimated to range from 0.031 to 0.047 μg m-3 (0.013-0.020 ppb) (Destaillats et al., 2002). Indoor air concentrations of acrolein are up to 20 times higher than outdoor concentrations (Environment Canada/Health Canada, 2000), as acrolein can be generated from indoor sources such as tobacco smoke and heated cooking oils at concentrations exceeding regulatory limits (Seaman et al., 2009); these two sources are considered to be the most common sources of exposure of children to acrolein (Office of Environmental Health Hazard Assessment (OEHHA), 2008). Indoor air concentrations of acrolein in homes measured in winter 2002 in Prince Edward Island ranged from 0.1 to 4.9 μg m-3 (0.04-2.1 ppb).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 6
3.0 ATMOSPHERIC CHEMISTRY AND FATE Acrolein has a high vapour pressure and preferentially volatilizes from solid and liquid environmental media and is not likely to partition to soil or sediment or dissolve in surface water (Environment Canada/Health Canada, 2000). Acrolein does not bioaccumulate (Environment Canada/Health Canada, 2000) and is removed from soil and surface water primarily through volatilization (Faroon et al., 2008). While acrolein can react reversibly with water to form 3-hydroxupropanol and 3,3’-oxydipropoionaldehyde this is not expected to occur to a significant extent (European Union, 1999). Once in the atmosphere acrolein is quickly removed (half-life of approximately 12 hours) from ambient air through a reaction with photochemically produced hydroxyl radicals in the troposphere that can form carbon monoxide, formaldehyde, and glycolaldehyde (Ghilarducci and Tjeerdema, 1995; Faroon et al., 2008). Similar reactions removing acrolein from the atmosphere involving nitrate, ozone, or direct photolysis may also occur to a lesser extent (Gardner et al., 1987). Degradation rates for acrolein increase in the presence of water vapour (Gold et al., 1978). Acrolein is not expected to partition from the vapour phase to particulates in the atmosphere (Faroon et al., 2008). The estimated environmental half-life of atmospheric acrolein ranges from 3 hours to 20 hours (Zhu et al., 2004; Mackay et al., 2006; Faroon et al., 2008) and is typically estimated as being less than 10 hours. Due to the unstable nature and high reactivity of atmospheric acrolein, long-range transport of acrolein emissions is considered unlikely (Environment Canada/Health Canada, 2000).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 7
4.0 EFFECTS ON HUMANS AND ANIMALS
4.1 Overview of Chemical Disposition
4.1.1 Absorption, Distribution, Metabolism and Excretion Data are limited on acrolein absorption; due to its highly reactive nature, acrolein generally interacts directly with nucleophilic binding sites at the point of exposure (ATSDR, 2007). Studies conducted using dogs found that 80-85% of inhaled acrolein, at concentrations ranging from 4.10 x 105 to 6.17 x 105 μg m-3 (176,000 to 265,000 ppb) was retained in the upper respiratory tract (nose, throat, and trachea), and only about 20% was estimated to reach the lower respiratory tract (Egle, 1972). Similarly, Morris et al. (2003) found that acrolein was almost entirely absorbed in the upper respiratory tract after exposing rats to 2,100 to 21,000 μg m-3 (900 to 9,100 ppb) acrolein; the absorption was lower at high breathing rates. Acrolein is believed to be retained primarily in tissues directly exposed to acrolein, and not widely distributed throughout the body (US EPA, 2003a). A rat inhalation study by McNulty et al. (1984) suggested that inhaled acrolein does not reach the liver to great extents, based on the absence of a reduction in liver glutathione following inhalation. Acrolein is also produced within the body. It is a metabolite of allyl alcohol, allylamine, spermine, and spermidine, and is formed during lipid peroxidation, and can be formed when the skin lipid triolein is exposed to UV radiation (Ghilarduci and Tejeerdema, 1995; Esterbauer et al., 1991; Uchida et al., 1998a,b; Auerback et al., 2008). Acrolein has been detected in plaque deposits associated with atherosclerosis and Alzheimer’s disease (Uchida, 1999). Most inhaled acrolein rapidly becomes irreversibly bound to protein and non-protein sulfhydryl groups, and particularly glutathione (GSH) (WHO, 2002). Based on animal studies, it is believed that the primary metabolic pathway involves conjugation with glutathione and conversion to N-acetylcysteine compounds (mercapturic acids) (WHO, 2002; Parent et al., 1998). Alternate pathways involve epoxidation of the double bond, with the epoxide subsequently attacked by glutathione, leading to the formation of mercapturic acid, or Michael addition (a type of chemical conjugation) of water as a hydroxide group, followed by oxidation to form malonic and then oxalic acids (Parent et al., 1998). Compounds formed from the combination of acrolein and glutathione can be oxidized in the liver by the hepatic enzymes ALDH and ADH (Mitchell and Peterson, 1989). No data were located regarding excretion after inhalation exposure. After oral exposure by gavage to 2.5 mg/kg radio-labelled acrolein, Parent et al. (1996) found 27-31% to be exhaled as CO2, 52-63% to be excreted in urine, and 12-15% to be excreted in feces. At a higher dose of 15 mg/kg, a larger portion of the metabolites were found in feces and less in urine.
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 8
The proposed metabolic pathways for acrolein after inhalation are summarized in Figure 1 below.
Figure 1 Metabolism of acrolein (from WHO, 2002)
4.1.2 Effects on Enzyme Systems Acrolein inhalation has been shown to result in glutathione (GSH) depletion in several in vivo and in vitro tests, potentially affecting the resistance of cells to reactive metabolites (US EPA, 2003a; Esterbauer et al., 1991). Arumugam et al. (1999) found that the activity of several components of the antioxidant defense system, including ascorbic acid, α-tocopherol, GSH peroxidase and catalase, was decreased in rat lungs after inhalation of acrolein. It can react with sulfhydryl groups, including proteins and enzymes involved in thiol redox equilibrium, which are critical for cell survival. Myers and Myers (2009) found that acrolein applied to bronchial epithelial cells oxidized cystolic and mitochondrial thioredoxins and reduced the activity of thioredoxin reductase; these effects persisted after exposure ended. Acrolein can also inhibit enzymes with thiol groups, including DNA-polymerase α and DNA repair enzymes, once GSH is depleted (Esterbauer et al., 1991).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 9
4.2 Genotoxicity and Carcinogenicity
Acrolein has shown evidence of genotoxicity in vitro, in both bacteria and mammalian cells, producing DNA-protein cross-links and DNA strand breaks, although results have been mixed and limited to high concentrations (Environment Canada/Health Canada, 2002; IARC, 1995; US EPA, 2003a). Due to its high reactivity, acrolein has the potential to bind directly to DNA. However, in the only relevant in vivo study, there was no increase in DNA-protein cross-links in the nasal mucosa of rats after inhaling acrolein (Lam et al., 1985) and the few in vivo studies of acrolein genotoxicity at systemic sites have been negative (Environment Canada/Health Canada, 2000). Only a single human study of acrolein carcinogenicity has been identified; Ott et al. (cited in IARC 1995 and WHO 2002) conducted a case-control study of employees of chemical manufacturing companies and found slightly higher than expected incidences of non-Hodgkin’s lymphoma with an odds ratio (the ratio of the probability of being affected in the exposed group to the probability of being affected in the control group) of 2.6, multiple myeloma (odds ratio 1.7) and non-lymphocytic leukaemia (odds ratio 2.6) in workers exposed to acrolein; however, the results were not statistically significant, acrolein exposures were not well characterized, and there were confounding exposures to other chemicals. A single animal inhalation study of carcinogenicity involved the exposure of Syrian golden hamsters to acrolein vapours at 0 to 9,000 μg m-3 (0-4,000 ppb) for 52 weeks (Feron and Kruysse, 1977). A single respiratory tract papilloma was identified in one exposed female hamster; inflammation and epithelial metaplasia of the respiratory tract occurred in approximately 20% of exposed hamsters 6 months after exposure ended. A limited number of oral and dermal carcinogenicity studies have also been conducted on animals, with generally negative results (IARC, 1995). Acrolein is metabolized by liver and lung microsomes to glyceraldehyde in vitro, which has been found to be carcinogenic in animal subcutaneous injection studies. Health Canada considered the available data inadequate to assess whether acrolein can induce tumours or interact directly with DNA following inhalation (Environment Canada/Health Canada, 2002). Similarly, IARC (1995) determined that acrolein is not classifiable as to its carcinogenicity (Group 3) due to inadequate evidence in humans and animals, and US EPA (2003a) concluded that the potential carcinogenicity of acrolein cannot be determined due to inadequate data.
4.3 Acute and Sub-Acute Effects
Acute effects occur rapidly as a result of short-term exposures (less than 24 hours), while sub-acute effects occur as a result of exposures lasting from a few days to one month (Eaton and Klaassen, 1996).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 10
4.3.1 Acute Human Effects Accidental exposure to acrolein has resulted in effects such as weakness, nausea, vomiting, diarrhoea, severe respiratory and ocular irritation, shortness of breath, bronchitis, pulmonary oedema, unconsciousness and death (Environment Canada/Health Canada, 2000). Exposure to 350,000 μg m-3 (150,000 ppb) has been fatal after 10 minutes (Henderson and Haggard cited in NRC, 2010) Weber-Tschopp et al. (cited in US EPA, 2003) conducted three experiments on human volunteers. The first involved gradually increasing the acrolein concentration to 1,400 μg m-3 (600 ppb) over 35 minutes, and then keeping the concentration constant for a further 5 minutes; a control group was unexposed. Effects including eye irritation, nasal irritation and throat irritation were observed at concentrations as low as 210 μg m-3 (90 ppb). The second experiment involved 1.5 minute exposures to successively increasing acrolein concentrations; eye irritation was observed at a concentration of 700 μg m-3 (300 ppb) and nasal irritation was observed at 1,400 μg m-3 (600 ppb). The third experiment involved a 60 minute exposure to a constant concentration of 700 μg m-3 (300 ppb); eye blink and breathing frequency and subjective irritation symptoms were increased compared to the controls, with a plateau in the severity of effects occurring after 20 to 30 minutes. Overall the studies showed adverse effects (eye irritation) at concentrations as low as 210 μg m-3 (90 ppb) for exposure durations as short as 5 minutes. Darley et al. (1960) exposed 31 volunteers to acrolein concentrations ranging from 140 to 5,400 μg m-3 (60 to 2,300 ppb); at least some volunteers reported eye irritation in all exposure groups. Other human exposure studies have also found eye and nose irritation from exposure to high concentrations of acrolein (Esterbaur et al., 1991; Sim and Pattle, cited in US EPA, 2003a; Prentiss cited in OEHHA, 2008). In vitro studies have shown evidence that the irritancy may be increased by prior sensitization, and that acrolein may potentially exacerbate asthma (e.g. Roux et al., 1999; Borchers et al., 1999a, b). It has also been suggested that individuals wearing contact lenses may be more sensitive to eye irritation from acrolein due to the lenses trapping and concentrating volatile compounds such as acrolein as well as extending the exposure time (OEHHA, 2008). The only reported human lethality due to inhalation of acrolein was two young boys who died from lung damage after being exposed for 2 hours to smoke from an overheated fryer; however, other components of the smoke may also have contributed to this outcome (Gosselin et al., cited in ATSDR, 2007). The threshold for perception of acrolein can be as low as 70 μg m-3 (30 ppb) (Sinkuvene, cited in Environment Canada/Health Canada, 2000) while the odour threshold may be as low as 480 μg m-3 (220 ppb) (Leonardos et al., 1969); acrolein can cause lacrimation (tears) at approximately 1,100 µg m-3 (500 ppb) (Esterbauer et al., 1991).
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4.3.2 Acute and Sub-Acute Animal Effects Table 4 lists the effects reported in animals following acute inhalation exposures to acrolein. Table 4 Effects Associated with Acute Acrolein Inhalation (Experimental Animals)
Effect Reported
Exposure Period
Air Concentration μg m-3 (ppb)
Species
Reference
Respiratory Effects and Irritation
Proliferation of nasal and tracheal epithelium LOAEL 500 (200)
6 h 0-1,400 (0-600) Rat Roemer et al., 1993
Bronchial hyper-responsiveness and airway resistance
2 h 710-2,900 (310-1,260) Guinea Pig Leikauf et al., 1989
Decrease in respiratory rate 10 min 700-9,100 (300-3,900) Mice Morris et al., 2003
Sulfhydryl depletion in respiratory mucosa LOAEL 1100 (500)
3 h 0-5,800 (0-2,500) Rat Lam et al., 1985
Lesions of respiratory epithelium LOAEL- 580 (250)
6h/d for 3 d 580-1,560 (250-670) Rat Cassee et al., 1996b
Tracheal damage 27d 113,000-454,000 (48,500-195,000)
Chicken Denine et al., 1971, cited in Environment Canada/Health Canada, 2000
Decreased respiratory rate Various; effects generally within 10 min
RD50 ranging from 2,400 (1,030) to 21,700 (9,200)
Rats and mice
Several studies summarized by US EPA, 2003a
Respiratory flow resistance and decreased respiratory rate
1 h 40,000 (17,000)
Guinea pig Davis et al., 1967, cited in US EPA, 2003a
Respiratory and olfactory epithelium lesions
6 h/d, 5 d 4,000 (1,700) Mice Buckley et al., 1984
Olfactory degeneration, ulceration of respiratory epithelium
7 h/d, 3 d 4,000 (1,700) Rat Teredesai and Stinn, 1989, cited in US EPA, 2003a
Nasal exfoliation, respiratory epithelium effects LOAEL – 7,000 (3,000)
6 h/d, 5 d/wk, 3 wks
0 (0), 230 (100), 2,300 (1,000) and 7,000 (3,000)
Rat Leach et al., 1987, cited in US EPA, 2003a
Exfoliation of ciliated cells in the bronchi
4 h 14,000 (6,000) Hamsters Kilburn and McKenzie, 1978, cited in US EPA, 2003a
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Effect Reported
Exposure Period
Air Concentration μg m-3 (ppb)
Species
Reference
Severe respiratory tract irritation
4 h 27,500 (12,000) Rat Murphy et al., cited in ATSDR, 2007
Nasal epithelium effects 6 h/d, 3 d 573, 1,540, 3,210 (250, 670, 1,400)
Rats Cassee et al., 1996
Emphysema, hyperemia, lung damage
4 h 2,300 and 4,600 (1,000 and 2,000)
Rats Arumugam et al., 1999
Nasal lesions (RD50) 6 h/d, 5 d 3,900 (1,700) Mouse Buckley et al. cited in ATSDR, 2007
Immunological
Decreased antibacterial defences LOAEL 6,800 (3,000)
8 h 1,100 – 20,600 (500 – 9,000)
Mice Astry and Jakab, 1983
Decreased antibacterial defences
3 h/d, 5 d 230 (100) Mice Aranyi et al., 1986
Cardiovascular Effects
Increased blood pressure and heart rate LOAEL – 50,000 (21,000)
1 min 9,200-5,000,000 (4,000-2,181,000)
Rat Egle and Hudgins, 1974
Mortality
Mortality <1 h 229,300 (100,000) and higher
Mice Several studies summarized by ATSDR, 2007
Mortality 10 min 749,800 (337,000) Rat Catalina et al. cited in ATSDR, 2007
Mortality, lung hemorrhage 30 min 298,000 (130,000) Rat Skog cited in ATSDR, 2007
Other Effects
Decreased body weight and relative liver weight
4 h/d, 5 d 9,170 (4,000) Rat Murphy et al. cited in ATSDR, 2007
Increased liver weight NOAEL 2,290 (1,000) LOAEL 4815 (2,100)
20-81 h 2,290 and 4, 815 (1,000 and 2,100)
Rat Murphy et al. cited in ATSDR, 2007
4.3.2.1 Respiratory
Effects of acrolein exposure occur primarily at the site of entry into the body, which for inhalation exposures is the respiratory tract (Environment Canada/Health Canada, 2000). Inhalation of acrolein by lab animals results in histopathologic effects (microscopic tissue abnormalities) in the bronchi and trachea after brief exposures (WHO, 2002). As shown in Table 4, respiratory effects of acrolein exposure include damage to the nasal and tracheal epithelium and effects on respiration. Short-term rodent inhalation studies have shown effects at concentrations as low at 500 μg m-3 (200 ppb) for 6 hours (Roemer et al., 1993). Concentrations at this range primarily affect the
nasal and respiratory epithelium (e.g. Roemer et al. 1993; Cassee et al., 1996). At higher concentrations, these effects become more pronounced, and additional respiratory effects such as decreased respiratory rate and respiratory flow resistance are observed (Table 4).
4.3.2.2 Immunological Effects
Short-term rodent inhalation experiments have shown evidence that acrolein can affect the immune system, and specifically antibacterial defences. Astry and Jakab (1983) exposed mice to acrolein for 8 hours after previously exposing them to the bacteria Staphylococcus aureus. Mice exposed to acrolein concentrations of 6,800 μg m-3 (3,000 ppb) and higher had a higher percentage of viable bacteria in their lungs at the end of the experiment, indicating decreased antibacterial defences. In another experiment, Aranyi et al. (1986) exposed mice to 230 μg m-3 (100 ppb) acrolein for 3 h/d for either 1 or 5 days; the mice exposed for 5 days (but not 1 day) were more susceptible to Klebsiella pneumonia infection than controls.
4.3.2.3 Cardiovascular Effects
A single study examined potential cardiovascular effects of acrolein. Egle and Hudgins (1974) exposed male rats to acrolein concentrations of 9,200 to 5,000,000 μg m-3 (4,000-2,181,000 ppb) for 1 minute. At concentrations greater than 50,000 μg m-3 (21,000 ppb), increased heart rate and blood pressure were observed; heart rate was decreased at concentrations greater than 2,500,000 μg m-3 (1,100,000 ppb).
4.3.2.4 Mortality
Lethality has been observed at very high concentrations in animal studies. Ballantyne et al. (cited in US EPA, 2003) established a 1-hour LC50 of 60,500 μg m-3 (26,000 ppb) and 4-hour LC50 of 19,000 μg m-3 (8,300 ppb) for rats; mortality resulted from lung damage in this study. Another rat study involved exposure to concentrations ranging from 1.4 x 106 to 9.7x 107 μg m-3 (580,000-41,550,000 ppb); rats were incapacitated after 2.8 to 36.5 minutes and died shortly afterwards (Crane, cited in US EPA, 2003a). Mice, guinea pigs and rabbits died after 13, 25 and 27 minutes of exposure (respectively) to 5.3 x 106 μg m-3 (2,279,000 ppb) acrolein vapour (Salem and Cullumbine, cited in US EPA, 2003a). In a rabbit study, 15 minutes of exposure resulted in mortality to 5 of 18 animals at 873,000 μg m-3 (375,000 ppb) and 8 of 18 animals at 1,140,000 μg m-3 (489,000 ppb). Acrolein is highly cytotoxic to mammalian cells; which may be due to rapid depletion of thiols (Esterbauer et al., 1991).
4.3.2.5 Other Effects
Increased relative liver weight was observed in rats exposed to 4,815 μg m-3 (2,100 ppb) but not 2,290 μg m-3 (1,000 ppb) for up to 81 hours. Conversely, exposure of rats to 9,170 μg m-3 (4,000 ppb) for 5 days resulted in a decrease in relative liver weight (Murphy et al., cited in ATSDR, 2007).
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4.4 Sub-Chronic and Chronic Effects
Subchronic effects generally occur following one to three months of exposure, while chronic effects occur as a result of repeated exposures for a period greater than 3 months (Eaton and Klaassen, 1996).
4.4.1 Sub-Chronic and Chronic Human Effects Data on sub-chronic and chronic human exposures to acrolein are limited, although it is believed that acrolein, from tobacco smoke, is a major contributor to pulmonary irritancy (OEHHA, 2008). Finkelstein et al. (2001) found that acrolein levels similar to those found at the airway surface during smoking or exposure to environmental tobacco smoke can increase neutrophil recruitment and reduce neutrophil apoptosis (programmed cell death), leading to inflammation.
4.4.2 Sub-Chronic and Chronic Animal Effects
4.4.2.1 Respiratory System
The critical effects for sub-chronic and chronic exposure to acrolein involve the respiratory system. Several studies have evaluated the effects to the respiratory system from sub-chronic and chronic exposures (Table 5). The most comprehensive studies are those of Feron et al. (1978), which historically have been the basis of most regulatory toxicity evaluations for acrolein, and Dorman et al. (2008) which builds on the earlier study and examines lower exposure concentrations. The results of other sub-chronic and chronic animal inhalation studies (e.g. Kutzman et al., 1985; Feron and Kruysse cited in OEHHA, 2008; Lyon et al., cited in Environment Canada/Health Canada, 2000; Leach et al. and Costa et al., cited in ATSDR, 2007) showed similar effects, as well as effects such as peribronchiolar haemorrhage and bronchial lumen obstruction at very high concentrations (Catlina et al., cited in ATSDR, 2007). The Feron et al. (1978) study involved the exposure of hamsters, rats and rabbits to acrolein concentrations of 0, 900, 3,200, and 11,000 μg m-3 (0, 400, 1,400, and 4,900 ppb) for 6 h/d, 5 d/wk over a 13 week period. Rats were found to be the most sensitive of the animals studied (SPF Wistar rats, Syrian golden hamsters, and Dutch rabbits), showing histopathological effects on the nasal cavity even at the lowest dose studied (900 μg m-3 (400 ppb)). At higher concentrations, histopathological effects were also observed in the larynx, trachea, bronchi and lungs in all species tested; the highest concentration also resulted in increased mortality in rats. Dorman et al. (2008) used an identical exposure period (6 h/d, 5 d/wk, 13 wk) for rats, with concentrations of 0, 50, 140, 500, 1,400, and 4,200 μg m-3 (0, 20, 60, 200, 600 and 1,800 ppb).
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The study also involved a more extensive examination of the nasal cavity. Effects observed included inflammation, hyperplasia, and squamous metaplasia of the respiratory epithelium, as well as olfactory neuronal loss at the highest concentration. NOAELs of 500 μg m-3 (200 ppb) for the respiratory epithelium and 1,400 μg m-3 (600 ppb) for the olfactory epithelium were established; computational fluid dynamic modelling showed that this was partly due to increased uptake along the respiratory epithelium in rats, and that the olfactory epithelial lesions were actually associated with a lower delivered tissue dose.
4.4.2.2 Mortality
Mortality has been observed in subchronic inhalation studies, including a 62 day rat inhalation study at 9,300 μg m-3 (4,000 ppb) (Kutzman et al., 1985) and a 6 week monkey inhalation study at 8,480 μg m-3 (3,700 ppb) (Lyon et al., cited in ATSDR, 2007). Mortality was associated with respiratory effects, including bronchopneumonia and respiratory congestion.
4.4.2.3 Immunological Effects
Bouley et al. (1976) exposed rats to 1,300 μg m-3 (550 ppb) acrolein, and had them inhale airborne Salmonella enteritidis after 18 and 63 days of exposure at a bacterial concentration equal to the LD50 (the dose associated with 50% mortality). After 18 days of exposure, the death rate after bacterial exposure was significantly higher in the acrolein-exposed rats than in controls; however, this difference was not observed at 63 days, which the study authors attributed to adaptation. In another study, no significant differences in mortality were observed when rats were exposed to acrolein at 6,880 μg m-3 (3,000 ppb) for 3 weeks, followed by intravenous exposure to Listeria monocytogenes (Leach et al., cited in ATSDR, 2007). ATSDR (2007) suggested the apparent immunological effects may be a result of acrolein affecting alveolar macrophages in the respiratory epithelium.
4.5 Summary of Adverse Health Effects of Acrolein Inhalation
Acrolein is highly reactive, and adverse effects generally involve cytotoxicity at the site of entry into the body rather than systemic toxicity (US EPA, 2003a). As a result, effects in both humans and animals primarily involve sensory irritation and respiratory system effects.
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Table 5 Effects Associated with Sub-Chronic and Chronic Acrolein Inhalation (Experimental Animals)
Effect Reported
Exposure Period
Air Concentration μg m-3 (ppb)
Species
Reference
Respiratory Inflammation, hyperplasia, squamous metaplasia in respiratory tract NOAEL – 470 (200) LOAEL – 1,400 (600)
13 wk, 6 h/d, 5 d/wk
0-4,200 (0-1,800)
Rat Dorman et al., 2008
Nasal cavity abnormalities LOAEL – 900 (400)
13 wk, 6h/d, 5d/wk
0-11,000 (0-4,900)
Syrian golden hamster
Feron et al., 1978
Histological changes to respiratory tract
52 wk, 7h/d, 5d/wk
9,000 (4,000) Hamster Feron and Kruysse cited in OEHHA 2008
Histopathological lesions in lungs LOAEL – 900 (400)
62d, 6h/d, 5d/2 930-9,300 (400-4,000)
Female rats Kutzman et al., 1984
Histopathological changes to respiratory tract NOEL – 900 (400) LOAEL – 3,300 (1,400)
62d, 6h/d, 5d/wk
930-9,300 (400-4,000)
Rats Kutzman et al., 1985
Histopathological change to lung, trachea, liver, kidney, NOEL 1 ppm
90 d 510- 4,200 (220-1,800)
Monkey Lyon et al., cited in Environment Canada/Health Canada, 2000
Respiratory epithelial dysplasia, decreased weight gain LOAEL 6,880 (3,000)
6 h/d, 5 d/wk, 3 wk
230-6,880 (100 – 3,000)
Rat Leach et al., cited in ATSDR, 2007
Lung hyperplasia at 3,200; lung oedema, decreased lung function, decreased weight gain at 9,200
6 h/d, 5 d/wk, 62 d
920 – 9200 (400 – 4,000)
Rat Costa et al., cited in ATSDR, 2007
Peribronchiolar haemorrhage, bronchial lumen obstruction
10 m/d, 8 wk 600,000 (262,000) Rat Catilina et al., cited in ATSDR, 2007
Mortality Mortality from acute bronchopneumonia (4000 ppb), parenchymal restriction (400 ppb)
62 d, 6h/d, 5d/wk
930, 3,300, 9,300 (400, 1,400, 4,000)
Rat Kutzman et al., 1985
Mortality 6 wk, 8 h/d, 5 d/wk
8,480 (3,700) Monkey Lyon et al. cited in ATSDR, 2007
Immunological Weight loss, nasal irritation, increased susceptibility to airborne infection after 18 but not 63 days
63 d 1,300 (550) Rat Bouley et al., 1976, cited in OEHHA 2008
Other Effects Decreased body weight gain NOAEL: 138 (60) LOAEL: 734 (320)
24 h/d, 61 d 138 – 734 (60 – 320)
Rat Skinkuvene, cited in ATSDR, 2007
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5.0 EFFECTS ON VEGETATION Acrolein has been used as a biocide for aquatic vegetation: however, few studies have been conducted to determine the effects, on vegetation, of acrolein in the air. Haagen-Smit et al. (cited in European Union, 1999) exposed spinach, endive, alfalfa, oats and beets to acrolein. At 200 μg m-3 (90 ppb) for 9 hours, effects resembling smog damage were seen on alfalfa but not the other plants; concentrations of 1,300 μg m-3 (560 ppb) for 3 hours or 2,600 μg m-3 (1,100 ppb) for 4.5 hours resulted in sunken pits on the surfaces of spinach, endives and beets. The European Union risk assessment suggested a predicted no effect concentration of 2 μg m-3 (0.9 ppb) based on an lowest observable effects concentration of 200 μg m-3 (90 ppb) for alfalfa from this study, but noted that there was some uncertainty in the results due to analytical limitations at the time of the study. Darley et al. (1960) exposed pinto bean plants to a range of acrolein concentrations for 35 or 70 minutes, and recorded visible injury to leaf surfaces on the second day after exposure. No visible injury was noted for plants exposed to 140 μg m-3 (60 ppb); plants exposed to 3,000 to 3,700 μg m-3 (1,300-1,600 ppb) and 4,700 to 5,400 μg m-3 (2,000-2,300 ppb) showed injury when exposed for 70 minutes but not 35 minutes. Atmospheric acrolein has been shown to be toxic to pollen, with an estimated EC10 of 900 μg m-3 (390 ppb) based on a study by Masaru (1970). Additional studies of the effects of acrolein on plants were undertaken by Unrau et al. (1965), Ferguson et al. (1965) and Reynolds (1977); however, these studies involved the application of acrolein in an aqueous solution rather than in gaseous form.
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6.0 AIR SAMPLING AND ANALYTICAL METHODS
6.1 Reference Methods
Air sampling and analytical methods for acrolein used by established agencies and laboratories certified by the Canadian Association for Laboratory Accreditation were reviewed. Alberta-based companies involved in air sampling and analysis were also contacted to ensure that current practices in the province were captured. The results of the review indicate that reference air monitoring methods for acrolein are generally limited to those developed by OSHA and the US EPA. Sampling of carbonyl groups such as acrolein is complicated by the formation of unstable derivatives, the presence of similar compounds, and interference from compounds such as ozone (Cahill et al., 2010). Due to the instability of acrolein, most sampling methods require the formation of more stable chemical derivatives in order to prevent substantial loss of analyte; however, even these compounds remain relatively unstable and subject to degradation over the time periods required for sampling ambient air concentrations. High pressure liquid chromatography (HPLC) is the primary method to quantify acrolein derivatives obtained from sorbent matrix samplers (ATSDR, 2007). HPLC may be used in conjunction with UV, ion trap mass spectrometry, and fluorescence detectors (Brombacher et al., 2002; Pal and Kim, 2007) and is currently recommended for US EPA TO-11a and CARB 430 (described below). HPLC-MS can obtain detection limits of 0.001 to 0.015 μg m-3 (0.0004-0.006 ppb) given a sample volume of 750 L (Brombacher et al., 2002), although much smaller sample volumes are generally collected for ambient air monitoring. Gas chromatography (GC) is the primary method to quantify acrolein pre-concentrated in pressurized sampling canisters (Shelow et al., 2009) and is used for US EPA method TO-15a and NIOSH 2501/OSHA 52. The US EPA has developed methods that can attain detection limits as low as 0.12 μg m-3 (0.05 ppb) when using a selective ion mode mass spectrometer (MS) detector (US EPA, 2006). While detectors other than MS can be used, such as flame ionization detectors or electron capture (Aragón et al., 2000), MS is preferred to UV detection to limit issues such as poor chromatographic separation (Cahill et al., 2010). Gas chromatography is the primary analytical method utilized in Alberta for determining acrolein concentrations in ambient air samples.
6.1.1 US EPA Method TO-11a The most common method of sampling acrolein uses a solid sorbent matrix (often within cartridge housing) that chemically binds to acrolein to form a stable derivative. Several absorbent matrices can used including: DNPH, dansylhydrazine, pentafluorophenyl hydrazine (PFPH), 2-(hydroxymethyl)piperidine (2-HMP) (Cahill et al., 2010; Herrington and Zhang, 2007; IARC, 2002).
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US EPA method TO-11a (1999a) is intended for ambient air monitoring of formaldehyde and carbonyl compounds including acrolein, although for many applications it has been replaced by US EPA Method TO-15. This methodology involves reaction of carbonyls on a 2,4-dinotrophenylhydrazine (DNPH)-coated solid absorbent silica gel cartridge that forms a stable hydrazone derivative, which can be extracted and analyzed by HPLC. While DNPH is the most commonly used sorbent, the DNPH-acrolein complex is unstable and is not recommended for collection times greater than 1 hour as it is susceptible to air oxidation (Goelen et al., 1997; Pal and Kim, 2007; Shelow et al., 2009). As ambient air measurement often requires sample times of several hours to detect low concentrations, the validity of this method has been questioned (Cahill et al., 2010). Use of this method was reported by laboratories in Alberta; however, they expressed concerns regarding reliability and elevated background concentrations. The US EPA Method TO-11a procedure involves a known volume of air being drawn through a sampling cartridge at a rate of 100-2000 mL/min. Utilization of sampling cartridges pre-coated with DNHP is recommended. Sampling times of 1-24 hr are required to obtain detection limits at the ppb level, and will be dependant on expected air concentrations and air flow rates. Once sample collection is complete the cartridge is sent to an analytical laboratory for analysis by reverse phase HPLC with an ultraviolet absorption detector operating in linear gradient program mode. Acrolein is identified and quantified by retention time and peak height compared to standard solutions. Concentration results are given as a time-weighted average.
6.1.2 US EPA Method TO-15 US EPA method TO-15 (1999b) is intended for highly volatile hazardous air pollutants, including acrolein. This methodology involves sampling 6 L of ambient air by a pressurized canister followed by analysis using gas chromatography-.mass spectrometry (GC-MS). Canister sampling provides more accurate results for ambient air samples in a shorter time period when compared to using acidified 2,4-dinitrophenylhydrazine cartridges and EPA Method TO-11a (Swift et al., 2007). Detection limits for canister collected samples are generally near 0.69 μg m-3 (0.3 ppb) and US EPA TO-15 is currently the recommended method for ambient air monitoring of acrolein. Other benefits of canister sampling are that it does not require the formation of chemical derivatives and sample preparation is easier. Disadvantages of canister sampling are increased cost and artifacts from ozone can have both positive and negative influences on the measured concentration (Cahill et al., 2010). Ambient air samples are collected within the canisters due to the existence of a pressure gradient between the canister and the exterior atmosphere, and the flow of air into the canister is controlled by a regulator. Sampling volumes are dependant on the canister volume (typically 6L), and sampling time is dependant on the flow rate selected. Sampling times may be up to 24 hours in length. Once sample collection is complete the canister is sent to an analytical laboratory where the sample is transferred to a solid multi-sorbent concentrator. The sample is then analyzed utilizing a high pressure gas chromatograph combined with a mass spectrometer operating in either in scanning or select ion mode. Select ion mode typically allows for higher
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sensitivity, whereas scanning mode allows for determination of complete spectral information of unknown compounds. The gas chromatograph is utilized for separation of organic constituents within the sample, which are then characterized and quantified by fragmentation patterns produced in the mass spectrometer.
6.1.3 NIOSH Method 2501/OSHA Method 52 NIOSH method 2501 (1994) and OSHA method 52 (1989) use a solid sorbent tube with 2-HMP on an XAD-2 substrate, and have working ranges of 130 to 500 μg m-3 (56-1100 ppb) and a reliable quantitation limit of 6.1 μg m-3 (2.7 ppb) when using a gas chromatograph with a nitrogen-specific detector. These methods are intended for use during personal sampling of occupational exposure and are generally not considered to be sufficiently sensitive for detection of acrolein in ambient air (Cahill et al., 2010); however, NIOSH 2501 is currently utilized by analytical laboratories in Alberta for ambient air sampling. NIOSH method 2501 requires that a known volume of air be pumped into a sorbent sampling tube. Sampling rates of 0.01 to 0.1 L/min are recommended, with a total sample volume of 1.5 to 48 L depending on the required detection limit. Sampling times can range from 1-24 hours.
6.1.4 CARB Method 430 Impinger sampling was previously used but has generally been phased out in favour other methods; however, methods such as the California Air Resources Board 430 (CARB, 1991) are still in use due to concerns regarding consistency and high background concentrations with sorbent tubes. One analytical laboratory in Alberta has confirmed that they utilize CARB 430 for testing acrolein in ambient air. Drawbacks of impingers include their labour intensive nature, use of hazardous reagents, lack of sensitivity, susceptibility to interference, and poor reproducibility at low concentrations (US EPA, 1999a). The test is intended for emission sources and requires modification for use in ambient air sampling. CARB 430 involves drawing gaseous emissions through a Teflon sample line and two impingers in series, each of which contain DNHP. The collected sample is then sent to an analytical laboratory where it each impinger is analyzed separately using reverse phase HPLC with an ultraviolet UV absorption detector.
6.2 Alternative Methods
6.2.1 Chromatography Alternative chromatographic methods for analysis of carbonyls, including acrolein, in air were reviewed by Pal and Kim (2007). Liquid-based analytical approaches such as micellar electro-kinetic chromatography and capillary electro-chromatography were considered plausible future
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replacements for current chromatography methods, but further research was needed to determine performance compared to currently available techniques. These methods continued to rely on DNHP for sample collection, and could potentially replace current methods if superior performance compared to conventional GC-MS and HPLC methodologies can be verified.
6.2.2 Mass Spectrometry Use of a portable mass-spectrometer unit for ambient air monitoring of toxic compounds was evaluated by Kell et al. (2008). A sorption trap inlet separated the vacuum chamber of the mass-spectrometer from the atmosphere, which was then evacuated and heated to desorb analyte into the instrument. Initial tests demonstrated that a detection limit of 70 μg m-3 (30 ppb) can be achieved with a sampling time of less than 2 minutes. This methodology operates on principals currently recommended by TO-15, but due to the highly specialized nature of the sampling equipment used, it is unlikely that this method can be implemented for regulatory monitoring. Alternative spectroscopy methods for analysis of carbonyls, including acrolein, in air were reviewed by pal and Kim (2007) including: fourier transform infrared spectroscopy, differential optical absorption spectroscopy, tuneable diode-laser spectroscopy, and atmospheric pressure chemical ionization mass spectrometry. These methods were considered beneficial in that they permitted on-site analysis and continuous monitoring, but were found to have insufficient sensitivity for analysis at the low concentration levels expected in ambient air. Other spectroscopic methods currently in development include cavity ring down spectroscopy, ion trap mass spectrometry, and laser induced fluorescence are currently in development (Shelow et al., 2009). These are considered potential replacements and reliable limits of detection and reference methods have yet to be developed.
6.2.3 Colorimetric Methods Colorimetric methods can be for determination of acrolein concentration in air, but have detection limits in the vicinity of 20 μg m-3 (10 ppb) and are not suitable for ambient air analysis (Feldstein et al., cited in IARC, 2002).
6.2.4 Mist Chambers Mist chambers (also called Cofer scrubbers) have been used to measure acrolein concentrations at the parts-per-trillion level (Cahill et al., 2010; Seaman et al., 2006). This method involves trapping acrolein in solution with sodium bisulphite, and then stabilizing with o-(2,3,4,5,6-pentafluorobenzyl)hydroxylamine for analysis by GC-MS. This method is not currently considered to be useful for regulatory monitoring due to the increased time and effort required compared to other sampling methods.
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7.0 AMBIENT OBJECTIVES IN OTHER JURISDICTIONS Current and/or recommended and proposed ambient air guidelines and objectives for acrolein from other jurisdictions in Canada, the United States, and elsewhere were reviewed. All jurisdictions have specific uses for their guidelines which may include, but are not limited to: Reviewing permit applications for sources that emit pollutants to the atmosphere; Investigating accidental releases or community complaints about adverse air quality for the
purpose of determining follow-up or enforcement activity; and Determining whether to implement temporary emission control actions under persistent
adverse air quality conditions of a short-term nature.
7.1 Air Quality Guidelines and Objectives for Acrolein
The air quality guidelines and objectives available for acrolein are summarized in Table 6, with a detailed summary of each guideline included as Appendix A. Further details on the development and use of these guidelines or objectives by each jurisdiction are provided in Appendix A. Eighteen of the agencies reviewed have a guideline or objective for acrolein. Numerous agencies develop guidelines or objectives for hazardous chemicals using occupational exposure levels (OELs) or results from animal bioassay data and dividing that value by safety or adjustment factors. OELs that are used by state agencies are typically: the American Conference of Governmental Industrial Hygienists (ACGIH) 8-hour time weighted average OEL; the National Institute for Occupational Safety and Health (NIOSH) relative exposure level (REL); or the U.S. Occupational Safety and Health Administration (OSHA) 8-hour Permissible Exposure Limit (PEL).
7.1.1 Canada The Ontario MOE has developed ambient air quality criteria for acrolein of 0.08 μg m-3 (0.03 ppb) for 24-hour exposure and 0.24 μg m-3 (0.10 ppb) for 0.5 hour exposure (Ontario Ministry of the Environment, 2008). The BC MOE Schedule 11 vapour standard for acrolein is 2 μg m-3 (0.9 ppb) based on human health endpoints, but this value is used for contaminated site assessment and not intended for use as an ambient air quality objective.
7.1.2 United States Various US agencies have developed ambient air guidelines or other reference levels for acrolein. US EPA has defined an Acute Exposure Guidance Level (AEGL-1) for acrolein of 70 μg m-3 (30 ppb) that is considered applicable for all exposure durations (US EPA, 2010).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 23
The ATSDR has calculated a minimal risk level for acute inhalation of 7 μg m-3 (3 ppb) and for intermediate inhalation of 0.09 μg m-3 (0.04 ppb) (ATSDR, 2007). The US EPA Integrated Risk Information System (IRIS) recommends a chronic reference concentration for acrolein of 0.002 μg m-3 (0.0009 ppb) based on a LOAEL from a subchronic rat inhalation study (US EPA, 2003b). These ATSDR and US EPA values are not specifically intended as ambient air quality objectives, but rather as health assessment benchmarks; however, they are frequently used as the basis for ambient air quality objectives. Several states have air quality guidelines for acrolein with many of these based on the above US EPA values, or values from other regulatory agencies.
7.1.3 International agencies A maximum permissible concentration of 0.5 μg m-3 (0.2 ppb) for acrolein based on the protection of human health is used by the National Institute for Public Health and the Environment (RIVM) (2008), with a negligible concentration (for environmental risk) of 0.01 μg m-3 (0.004 ppb).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 24
Table 6 Summary of Air Quality Objectives and Guidelines for Acrolein
Objective Value µg m-3 (ppb)
Averaging Time:
Agency Objective Title 1-hour 24-hour Annual
Arizona Department of Health Services Ambient Air Quality Guideline 6.3 (2.7)
2.0 (0.86)
-
California Office of Environmental Health Hazard Assessment
Reference Exposure Level 2.5 (1.1)
0.70 (0.30)
0.35 (0.15)
Louisiana Department of Environmental Health Protection
Ambient Air Standard - 5.4 (3.0)
5.4 (3.0)
Maine Center for Disease Control and Prevention
Ambient Air Guideline - - 0.4 (0.2)
Michigan Department of Environmental Quality
Initial Threshold Screening Level
5 (2)
- 0.02 (0.009)
Minnesota Department of Health Health-Based Value for Air 2 (0.9)
0.2 (0.09)
-
New Jersey Department of Environmental Protection
Inhalation reference concentration
- 0.02 (0.009)
-
New York Department of Environmental Conservation
Guideline Concentration 2.5 (1.1)
- 0.35 (0.15)
New Hampshire Ambient Air Limit - 0.82 (0.35)
0.02 (0.009)
North Carolina Department of Environment and Natural resources
Ambient Air Limit 80 (30)
- -
Ontario Ministry of Environment Ambient Air Quality Criteria 0.24 (0.10)
[0.5-hour]
0.08 (0.03)
-
Rhode Island Department of Environmental Management
Ambient Air Limit 0.2 (0.09)
- 0.02 (0.009)
Texas Commission on Environmental Quality
Air Monitoring Comparison Value
2 (1)
0.2 (0.1)
US EPA Acute Exposure Guidance Level - 1
70 (30)
- -
Vermont Agency of Natural Resources Hazardous Ambient Air Standard
- - 0.02 (0.009)
Wisconsin Department of Natural Resources
Ambient Air Standard 22.9 (9.8)
- -
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 25
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Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 31
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APPENDIX A Air Quality Objectives and Guidelines for Acrolein
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 32
Agency: Agency for Toxic Substances and Disease Registry (ATSDR)
Air Quality Guideline: Minimal Risk Level (MRL) Inhalation Acute – 7 μg m-3 (3 ppb) MRL Inhalation Intermediate – 0.09 μg m-3 (0.04 ppb)
Averaging Time To Which Guideline Applies: unknown
Basis for Development: Based on respiratory endpoints with uncertainty factors of 100 for the acute MRL, and 300 for the intermediate MRL.
Date Guideline Developed: Updated in 2007
How Guideline is Used: MRLs are intended as screening levels to identify contaminants of concern and potential health effects at contaminated sites. An MRL is an estimate of the daily human exposure to a hazardous substance that is not likely to result in appreciable risk of adverse non-cancer health effects over a specified duration of exposure. MRLs are not applied as guidelines.
Additional Comments:
Reference and Supporting Documentation: Agency for Toxic Substances and Disease Registry. 2007. Toxicological Profile for
Acrolein. US Department of Health and Human Services. http://www.atsdr.cdc.gov/toxprofiles/tp124.pdf (accessed February 15, 2011).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 33
Agency: Arizona Department of Health Services (ADHS)
Air Quality Guideline: Arizona Ambient Air Quality Guidelines (AAQG) 1 hour – 6.3 μg m-3 (2.7 ppb) AAQG 24 hour – 2.0 μg m-3 (0.86 ppb)
Averaging Time To Which Guideline Applies: see above
Basis for Development: 1-hour AAQG based on a target lifetime cancer risk of one-in-one million assuming an exposure frequency of 365 days a year for 70 years under a US EPA residential scenario, using toxicity data preferentially from OSHA and NIOSH. 24-hour AAQG based on 8-hour occupational exposure limits from OSHA with conversion factors to account for time and exposure duration, and safety factors to account for sensitive individuals.
Date Guideline Developed: 1999
How Guideline is Used: AAQGs are residential screening values for protection of the general public, including sensitive individuals. Guideline values are not intended for use as standards, and are screening thresholds for use in environmental risk management decisions.
Additional Comments:
Reference and Supporting Documentation: 1999 Update Arizona Ambient Air Quality Guidelines (AAQGs). 1999. Office of Environmental Health, Arizona Department of Environmental Quality Air Programs Division. http://www.maricopa.gov/aq/divisions/permit_engineering/docs/pdf/aaaqgs.pdf (accessed February 15, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 34
Agency: British Columbia Ministry of Environment (MOE)
Air Quality Guideline: Schedule 11 General Numerical Vapour Standards – 2.0 μg m-3 (0.9 ppb)
Averaging Time To Which Guideline Applies: Chronic exposure
Basis for Development: Vapour standards are based on defined exposure scenarios applicable to contaminated sites. The specific basis of the acrolein standard is not detailed, although a footnote suggests it was adjusted to reflect the analytical detection limit.
Date Guideline Developed: 2008
How Guideline is Used: Vapour standards are intended solely for use at contaminated sites (primarily soil vapour and/or indoor air samples) and are not intended to be applied as ambient air quality objectives.
Additional Comments:
Reference and Supporting Documentation: British Columbia Ministry of Environment. 2008. Environmental Management Act Contaminated Sites Regulation – Schedule 11. BC Reg. 343/2008, s. 20. http://www.bclaws.ca/EPLibraries/bclaws_new/document/ID/freeside/375_96_13 (accessed February 5, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 35
Agency: California Office of Environmental Health Hazard Assessment (OEHHA)
Air Quality Guideline: acute reference exposure level (REL) - 1 hour – 2.5 μg/m3 (1.1 ppb) 8-hour REL – 0.70 μg m-3 (0.30 ppb) chronic REL- annual average – 0.35 μg m-3 (0.15 ppb)
Averaging Time To Which Guideline Applies: see above
Basis for Development: Acute REL is based on subjective eye irritation. 8-hour and chronic RELs are based on lesions in respiratory epithelium.
Date Guideline Developed: unknown (reviewed 2008)
How Guideline is Used: Applicable to routine exposures of the general public to hazardous chemicals in order to assess non-cancer health impacts during human health risk assessments.
Additional Comments:
Reference and Supporting Documentation: California Office of Environmental Health Hazard Assessment (OEHHA). 2008. Draft TSD for Noncancer RELs. SRP4. Acrolein Reference Exposure Levels DRAFT. http://www.oehha.org/air/toxic_contaminants/pdf_zip/acrolein_112508.pdf (accessed February 15, 2011).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 36
Agency: Louisiana Department of Environmental Protection (LDEP)
Air Quality Guideline: Ambient Air Standard – 5.4 μg m-3 (2.3 ppb)
Averaging Time To Which Guideline Applies: 8 hour average.
Basis for Development: Unknown
Date Guideline Developed: 1997, updated in 2007
How Guideline is Used: AASs are used by Louisiana DEQ to review permit applications for stationary sources that emit pollutants to the atmosphere.
Additional Comments:
Reference and Supporting Documentation: Louisiana Administrative Code (LAC). Title 33 Environmental Quality, Part III Air, Chapter 51. Comprehensive Toxic Air Pollutant Emission Control Program. Louisiana Department of Environmental Quality. Baton Rouge, LA. LAC 33:III.5112.Table 51.2. http://www.deq.state.la.us/portal/Portals/0/planning/regs/title33/33v03.pdf (accessed February 15, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 37
Agency: Maine Center for Disease Control and Prevention
Air Quality Guideline: Ambient Air Guideline (AAG)– 0.4 μg m-3 (0.2 ppb)
Averaging Time To Which Guideline Applies: Applies only to chronic exposure
Basis for Development: California OEHHA REL
Date Guideline Developed: Updated 2010
How Guideline is Used: The AAGs are intended to be solely health-based guidelines, and do not take into account analytical methods, treatment technology, or economic impacts. AAGs are not legally enforceable and represent recommendations for chemical concentrations in ambient air.
Additional Comments:
Reference and Supporting Documentation: Maine CDC. 2010. Ambient Air Guideline 2010 Update. Environmental and Occupational Health Program, Center for Disease Control and Prevention, Department of Human Services. http://www.maine.gov/dhhs/eohp/air/documents/2010AAGsApril.pdf (accessed February 2011).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 38
Agency: Michigan Department of Environmental Quality (MDEQ)
Air Quality Guideline: Initial Threshold Screening Level (ITSL) – 0.02 μg m-3 (0.009 ppb)
Averaging Time To Which Guideline Applies: Applies to the annually averaged concentration. A second ITSL of 5 μg m-3 (2 ppb) is used for an hourly averaging time.
Basis for Development: Non-carcinogenic health effects
Date Guideline Developed: 1998
How Guideline is Used: Ambient impacts of acrolein may not exceed either the annual or hourly ITSL.
Additional Comments: Intended for use with source emission applications.
Reference and Supporting Documentation: Michigan Air Toxics System. 1998. Initial Threshold Screening level/Initial Risk Screening Level (ITLS/IRSL) Toxics Screening Levels.
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 39
Agency: Minnesota Department of Health
Air Quality Guideline: Acute Health-Based Value for Air – 2 μg m-3 (0.9 ppb) Subchronic Health-Based Value for Air – 0.2 μg m-3 (0.09 ppb)
Averaging Time To Which Guideline Applies: N/A
Basis for Development: Weber-Tschoff et al. (1997) study on effects on human volunteers that determined a LOAEL of 0.09 ppm.
Date Guideline Developed: 2004
How Guideline is Used: Intended for assessing risk from ambient exposures. Used for environmental reviews, issuing air permits, risk assessments and other site-specific assessments.
Additional Comments: Acute value based on one-hour averaged exposure concentration, subchronic value based on 13 week averaged exposure concentration.
Reference and Supporting Documentation: Minnesota Department of Health. 2004. Health-Based Rules and Guidance for Air. http://www.health.state.mn.us/divs/eh/risk/rules/air/index.html (accessed February 15, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 40
Agency: New Jersey Department of Environmental Protection (NJDEP)
Air Quality Guideline: Inhalation reference concentration– 0.02 μg m-3 (0.009 ppb)
Averaging Time To Which Guideline Applies: N/A (chronic)
Basis for Development: Based on assessment by US EPA IRIS.
Date Guideline Developed: 2008
How Guideline is Used: Intended for use as a toxicity reference value in risk assessment.
Additional Comments:
Reference and Supporting Documentation: NJDEP. 2008. Toxicity Factors for Acrolein. http://www.state.nj.us/dep/standards/pdf/107-02-8-tox.pdf (accessed February 15, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 41
Agency: New York Department of Environmental Conservation (NYDEC)
Air Quality Guideline: Annual Guideline Concentration (AGC )– 0.35 μg m-3 (0.15 ppb) Short-term Guideline Concentration (SGC) – 2.5 μg m-3 (1.1 ppb)
Averaging Time To Which Guideline Applies: One year for AGC, one hour for SGC
Basis for Development: AGC based on CalEPA assessment of acute exposure, SGC based on US EPA recommended RfC.
Date Guideline Developed: Last revised in 2007.
How Guideline is Used: Intended for use as screening guidelines for industrial permit applications.
Additional Comments:
Reference and Supporting Documentation: NYDEC. 1997. Policy DAR-1. Guidelines for the Control of Toxic Ambient Air Contaminants. http://www.dec.ny.gov/chemical/30681.html (accessed February 15, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 42
Agency: New Hampshire RSA 125-I:6
Air Quality Guideline: Ambient Air Limit (annual) – 0.020 μg m-3 (0.009 ppb) Ambient Air Limit (24-hour) – 0.82 μg m-3 (0.35 ppb)
Averaging Time To Which Guideline Applies: See above
Basis for Development: Reference concentrations established by the US EPA.
Date Guideline Developed: 1990
How Guideline is Used: Intended for use as ambient air quality guidelines
Additional Comments:
Reference and Supporting Documentation: New Hampshire Code of Administrative Rules. 1990. Chapter Env-A 1400 Regulated Toxic Air Pollutants. http://des.nh.gov/organization/commissioner/legal/rules/documents/env-a1400.pdf (accessed February 15, 2011)
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 43
Agency: North Carolina Department of Environment and Natural Resources
Air Quality Guideline: Ambient Air Limit – 80 μg m-3 (30 ppb)
Averaging Time To Which Guideline Applies: 1 hour.
Basis for Development: Review of multiple human and animal studies, detailed guideline derivation process not described. Final value is based on TLV from ACGIH.
Date Guideline Developed: 1997
How Guideline is Used: Evaluation and regulation of emissions from industrial facilities.
Additional Comments:
Reference and Supporting Documentation: Acrolein Risk Analysis Background Documentation. Toxic Air Pollutant Profile (12-4-1985). North Carolina Department of Environment and Natural Resources – Division of Air Quality. http://www.daq.state.nc.us/toxics/haps-taps/docs/Acrolein_107-02-8.pdf (accessed February 15, 2011)
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Agency: Ontario Ministry of Environment
Air Quality Guideline: Ambient Air Quality Criteria (24-hour) – 0.08 μg m-3 (0.03 ppb) Ambient Air Quality Criteria (0.5 hour) – 0.24 μg m-3 (0.10 ppb)
Averaging Time To Which Guideline Applies: See above
Basis for Development: Human health endpoint based on upper risk thresholds, specifically the prevention of nasal lesions following chronic exposure.
Date Guideline Developed: 2008
How Guideline is Used: Intended for use to assess general air quality in a community and potential for emissions to cause an adverse effect. All averaging time periods for the Ambient Air Quality Criteria must be considered.
Additional Comments:
Reference and Supporting Documentation: Ontario Ministry of Environment. 2008. Summary of Standards and Guidelines to support Ontario Regulation 419: Air Pollution – Local Air Quality. http://www.ene.gov.on.ca/environment/en/resources/STD01_076483.html (February 15, 2011).
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Agency: Rhode Island Department of Environmental Management (Rhode Island DEM)
Air Quality Guideline: Ambient Air Limit (AAL) 1-hour– 0.2 μg m-3 (0.09 ppb) AAL annual – 0.02 μg m-3 (0.009 ppb)
Averaging Time To Which Guideline Applies: see above
Basis for Development: 1-hour limit is based on California Air Resources Board assessment. Annual average limit is based on US ELA RfC for effects on the nasal epithelium.
Date Guideline Developed: 2008
How Guideline is Used: Intended for use in issuing Air Toxics Operating Permits for stationary sources.
Additional Comments:
Reference and Supporting Documentation: Rhode Island Air Toxics Guideline. 2008 revision. Rhode Island Department of Environmental Management. http://www.dem.ri.gov/programs/benviron/air/pdf/airtoxgl.pdf (accessed February 15, 2011).
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Agency: Texas Commission on Environmental Quality (TCEQ)
Air Quality Guideline: Air monitoring Comparison Value (AMCV) odour – 8.4 μg m-3 (3.6 ppb) AMCV short term health – 2 μg m-3 (1 ppb) AMCV long term health – 0.2 μg m-3 (0.1 ppb)
Averaging Time To Which Guideline Applies: none
Basis for Development: Based on review of ambient air monitoring data, no detailed references provided.
Date Guideline Developed: AMCV developed based on procedures described in 2006 guidance document referenced below.
How Guideline is Used: Used for permitting and monitoring of ambient air quality, and is applied for environmental, human health, and aesthetic endpoints.
Additional Comments: Acrolein AMCVs are currently under review.
Reference and Supporting Documentation: TCEQ. 2006.Guidelines to Develop Effects Screening Levels, Reference Values, and Unit Risk Factors. http://www.tceq.texas.gov/publications/rg/rg-442.html/at_download/file (accessed February 15, 2011) TCEQ. undated. Air Monitoring Comparison Values for Evaluating VOCs (ppb-V).
Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 47
Agency: US EPA
Air Quality Guideline: Acute Exposure Guideline Level (AEGL-1) – 70 μg m-3 (30 ppb)
Averaging Time To Which Guideline Applies: Applies for any exposure duration, but are intended for acute exposure
Basis for Development: Based on eye irritation and ‘annoyance’ from Weber-Tschopp et al. (1997) study
Date Guideline Developed: Updated 2010
How Guideline is Used: AEGLs were developed for accidental exposure to the general public
Additional Comments: All AEGLs are intended for the general population, including susceptible individuals. AEGL-1 represents a concentration that may cause transient and reversible discomfort, irritation, or non-sensory effects. AEGL-2 represents concentrations that could cause long-lasting health effects or an impaired ability to escape. AEGL-3 represents concentrations that are life-threatening and could result in death. AEGLs are not always applicable to chronic exposure scenarios.
Reference and Supporting Documentation: Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 8. 2010. Committee on Acute Exposure Guideline Levels; Committee on Toxicology; National Research Council of the National Academies. http://www.epa.gov/opptintr/aegl/pubs/acrolein_final_volume8_2010.pdf (accessed February 15, 20110
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Agency: United States Environmental Protection Agency (US EPA ) Integrated Risk information System (IRIS)
Air Quality Guideline: Reference Concentration (RfC) – 0.02 μg m-3 (0.009 ppb)
Averaging Time To Which Guideline Applies: 1 hour.
Basis for Development: LOAEL from Ferron et al. (1978) study on nasal histopathology in rats.
Date Guideline Developed: 2003
How Guideline is Used: Referenced by several other regulatory agencies as a TRV, not applied as a guideline in practice.
Additional Comments:
Reference and Supporting Documentation: US EPA IRIS. 2003. Toxicological Review of Acrolein (CAS No. 107-02-8). http://www.epa.gov/iris/subst/0364.htm (accessed February 15, 2011).
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Agency: State of Vermont Agency of Natural Resources
Air Quality Guideline: Hazardous Ambient Air Standard– 0.02 μg m-3 (0.009 ppb)
Averaging Time To Which Guideline Applies: Annual
Basis for Development: Systemic toxicity due to long term exposure.
Date Guideline Developed: 2007
How Guideline is Used: Intended for regulation of commercial and industrial emission sources.
Additional Comments:
Reference and Supporting Documentation: State of Vermont Agency of Natural Resources. 2007. Air Pollution Control Regulations, including Amendments to the Regulations Adopted through: April 27, 2007. http://www.anr.state.vt.us/air/docs/apcregs.pdf (accessed February 15, 2011).
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Assessment Report on Acrolein for Developing Ambient Air Quality Objectives 51
Agency: Wisconsin Department of Natural Resources
Air Quality Guideline: Ambient Air Standard – 22.9 μg m-3 (9.8 ppb)
Averaging Time To Which Guideline Applies: 1 hour.
Basis for Development: Acute non-carcinogenic effects; basis not clearly identified.
Date Guideline Developed: 2009
How Guideline is Used: Intended for regulation of stack emissions.
Additional Comments:
Reference and Supporting Documentation: Wisconsin Department of Natural Resources. 2009. Chapter NR445 – Control of Hazardous Pollutants. http://legis.wisconsin.gov/rsb/code/nr/nr445.pdf (accessed February 15, 2011).