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Priority Substances List Assessment Report for Acrylonitrile
3.0 Assessment of "Toxic" Under CEPA 1999
3.1 CEPA 1999 64(a): Environment
The environmental risk assessment of a PSL substance is based on the procedures outlined in Environment Canada (1997a). Analysis of exposure pathways and subsequent identification of sensitive receptors are used to select environmental assessment endpoints (e.g., adverse reproductive effects on sensitive fish species in a community). For each endpoint, a conservative Estimated Exposure Value (EEV) is selected and an Estimated No-Effects Value (ENEV) is determined by dividing a Critical Toxicity Value (CTV) by an application factor. A hyperconservative or conservative quotient (EEV/ENEV) is calculated for each of the assessment endpoints in order to determine whether there is potential ecological risk in Canada. If these quotients are less than one, it can be concluded that the substance poses no significant risk to the environment, and the risk assessment is completed. If, however, the quotient is greater than one for a particular assessment endpoint, then the risk assessment for that endpoint proceeds to an analysis where more realistic assumptions are used and the probability and magnitude of effects are considered. This latter approach involves a more thorough consideration of sources of variability and uncertainty in the risk analysis.
3.1.1 Assessment endpoints
Acrylonitrile enters the Canadian environment from anthropogenic sources, primarily from industrial on-site releases. Almost all releases in the environment are to air, with small amounts released to water.
Based on its physical-chemical properties, acrylonitrile undergoes various degradation processes in air, with very small amounts transferring to water. When released into water, it is expected to remain primarily in water, where it undergoes biodegradation after an acclimation period. Acrylonitrile does not bioaccumulate in organisms.
Based on the sources and fate of acrylonitrile in the environment, biota are expected to be exposed to acrylonitrile primarily in air and to a much lesser extent in water. Little exposure to soil or benthic organisms is expected. Therefore, the focus of the environmental risk characterization will be on terrestrial and aquatic organisms exposed directly to ambient acrylonitrile in air and water.
3.1.1.1 Terrestrial organisms
Terrestrial toxicity data are available for invertebrates (particularly grain insect pests) (Section 2.4.1.1) as well as from mammalian toxicology (Section 2.4.3). Identified sensitive endpoints via fumigation or inhalation routes of exposure include mortality of insect eggs (Adu and Muthu, 1985), decreased number of insect offspring (Rajendran and Muthu, 1981a), maternal and fetal toxicity in rats (Saillenfait et al., 1993a) and histopathological changes in the nasal turbinates in rats (Quast et al., 1980b). The single most sensitive response for these endpoints will be used as the CTV for the risk characterization for terrestrial effects.
3.1.1.2 Aquatic organisms
Aquatic toxicity data are available for a variety of plants, invertebrates, fish and amphibians (Section 2.4.1.2). Identified sensitive endpoints include growth inhibition in aquatic plants (Zhang et al., 1996), mortality in pond snails (Erben and Beader, 1983), mortality and reduced growth in fish (Henderson et al., 1961; ABCL, 1980a) and reduction in growth of frogs (Zhang et al., 1996).
The single most sensitive response for all these endpoints will be used as the CTV for the risk characterization for aquatic effects.
3.1.2 Environmental risk characterization
3.1.2.1 Terrestrial organisms
Environmental exposure to acrylonitrile in air is expected to be greatest near industrial point sources. Levels of acrylonitrile in ambient air in Canada are generally below detection. The highest concentration of acrylonitrile in outdoor air in a half-hour period in Canada is predicted to be 9.3 µg/m3(Michelin, 1999) at an 11-m distance from an industrial stack. The value 9.3 µg/m3will be used as the EEV in the hyperconservative analysis for terrestrial organisms.
For the exposure of terrestrial organisms to acrylonitrile in air, the CTV is the LOEL of 55 mg/m3causing decreased maternal weight and fetal toxicity in rats exposed for nine days during gestation (Saillenfait et al., 1993a). This LOEL was the most sensitive effect identified from a data set composed of acute and chronic toxicity studies conducted on 14 species of insects and mammals. Saillenfait et al. (1993a) reported that none of these effects were observed at 26.4 mg/m3. For the hyperconservative analysis, the ENEV is derived by dividing the CTV by a factor of 100. This factor accounts for the extrapolation from laboratory to field conditions, conversion of the LOEL to a long-term no-effects value, interspecies and intraspecies variations in sensitivity and the moderate dataset. As a result, the ENEV is 0.55 mg/m3(550 µg/m3).
The hyperconservative quotient is calculated by dividing the EEV of 9.3 µg/m3by the ENEV as follows:
Since the hyperconservative quotient is less than one, it is unlikely that acrylonitrile causes adverse effects on populations of terrestrial organisms in Canada.
Table 8 summarizes the risk quotients for the environmental media of concern.
3.1.2.2 Aquatic organisms
Environmental exposure to acrylonitrile is expected to be greatest near point sources. In general, releases to water are low (0.529 tonnes, or 2.7% of all releases). All known releases of acrylonitrile to water in Canada occur to freshwater environments.
In general, levels of acrylonitrile in ambient surface water and groundwater are low. A large study of Canadian municipal water supplies conducted in 1987 detected no acrylonitrile in 84 samples at nine municipalities around the Great Lakes at the detection limit of 0.005 mg/L. Similarly, the level of acrylonitrile in 207 samples of intake water taken in 1989-90 at 26 Ontario organic chemical manufacturing plants was below the detection limit of 0.0042 mg/L.
Measurable levels of acrylonitrile were found in industrial effluents discharged to the environment in 1989-90. In 1997, however, only two companies in Ontario and one in Quebec used acrylonitrile in manufacturing. There have been significant changes to the effluent treatment process in these remaining facilities, such that levels in effluent are very low, below the recommended method detection limit of 0.0042 mg/L. Therefore, the value 0.0042 mg/L will be used as the EEV in the hyperconservative analysis for aquatic organisms.
For exposure of aquatic biota to acrylonitrile in water, the CTV is 0.4 mg/L, based on the lower chronic level around the EC50 of foreleg development after a 28-day exposure in the frog, Bufo bufo gargarizans (Zhange et al., 1996). This was the most sensitive value identified from the primary and secondary data composed of acute and chronic studies conducted on 16 species of aquatic invertebrates, plants, fish and amphibians.
For a hyperconservative analysis, the ENEV is derived by dividing this CTV by a factor of 10. This factor accounts for extrapolation from field to laboratory conditions and interspecies and intraspecies variations in sensitivity. The resulting ENEV is 0.04 mg/L.
The hyperconservative quotient is calculated by dividing the EEV of 0.0042 mg/L by the ENEV as follows:
Since the hyperconservative quotient is less than one, it is unlikely that acrylonitrile causes adverse effects on populations of aquatic organisms in Canada.
3.1.2.3 Discussion of uncertainty
There are a number of potential sources of uncertainty in this environmental risk assessment. Regarding environmental exposure, there could be concentrations of acrylonitrile in Canada that are higher than those identified and used in this assessment. While no data or limited data were found for Canadian soils and sediments, significant concentrations of acrylonitrile are not expected because of the unlikely partitioning of acrylonitrile to these compartments from air. Levels of acrylonitrile in ambient air and water are not widely monitored in Canada. Concentrations of acrylonitrile in water have been measured in connection with point sources. Improvements to industrial effluent treatment systems over the last decade to take advantage of the biodegradability of acrylonitrile by acclimatized microorganisms appear to have resulted in acrylonitrile levels being below detection. Few data were available on acrylonitrile concentrations in air near industrial point sources, and these data indicate that in rare occasions, for small time periods, acrylonitrile is discharged from some stacks. The largest of these gave a "theoretical" point of impingement concentration of 9.3 µg/m3and was associated with a total annual discharge of 31 g of acrylonitrile. No acrylonitrile was detected off the industrial site property. However, the few measured data support the predicted concentrations in air, which are used to determine point of impingement concentrations for site registration permits.
Regarding effects of acrylonitrile on terrestrial and aquatic organisms, uncertainty inevitably surrounds the extrapolation from available toxicity data to potential ecosystem effects. Somewhat surprisingly, the data set lacks information on the toxicity of acrylonitrile in air to plant species. Studies of acrylonitrile in air have focussed on the effects via inhalation and fumigation on laboratory mammals (particularly rats) and pest insect species. There has been considerable examination of a wide range of effects in rats. It is not known to what extent the physiological effects observed in the rat are representative of long-term ecological effects. Regarding effects of acrylonitrile on aquatic organisms, the data set includes studies on organisms from a variety of ecological niches and taxa for both the short and long term. To counter these uncertainties, appropriate application factors were used in the environmental risk analysis to derive ENEVs.
Despite some data gaps regarding the environmental effects and exposure of acrylonitrile, the data available at this time are considered adequate for making a conclusion on the environmental risk of acrylonitrile in Canada.
3.2 CEPA 1999 64(b): Environment on which life depends
Once released into the atmosphere, reaction of acrylonitrile with hydroxyl radicals is the primary removal mechanism and yields formaldehyde, formic acid and formyl cyanide. Worst-case calculations were made to determine whether acrylonitrile has the potential to contribute to (ground-level) photochemical ozone formation, depletion of stratospheric ozone or climate change (Bunce, 1996).
Because of its reactivity in the atmosphere, acrylonitrile's potential contribution to photochemical ozone creation (and also smog) is moderate; however, quantities available for reaction (18.75 tonnes in Canada in 1996) make the contribution low relative to those of other smog-forming substances. Reaction with ozone and nitrate are negligible, and the absence of chlorine and bromine atoms in the molecule means that the potential contributions to stratospheric ozone depletion (ODP = 0) and climate change (GWP = 4.3 X 10-4) are both negligible (Bunce, 1996).
It is therefore concluded that acrylonitrile is not "toxic" in the abiotic atmosphere as defined in Section 64(b) of CEPA 1999.
3.3 CEPA 1999 64(c): Human health
3.3.1 Estimated population exposure
Data on levels of acrylonitrile in environmental media in Canada to serve as a basis for development of estimates of population exposure are restricted to an almost complete lack of detection in limited surveys of outdoor and indoor air, similar lack of detection in a more extensive survey of drinking water and an early report of levels in a limited number of foodstuffs packaged in acrylonitrile-based plastic containers. Point estimates of average daily intake (per kilogram body weight), based on these few data (Section 2.3.2) and reference values for body weight, inhalation volume and amounts of food and drinking water consumed daily, are presented for six age groups in Table 9. These estimates, which should be considered to be bounding only, as a result of the limitations of the data on which they are based, range from 0.01 to 0.65 µg/kg-bw per day.
| Route of exposure | Estimated intake (µg/kg-bw per day) of acrylonitrile by various age groups | ||||||
|---|---|---|---|---|---|---|---|
| 0-6 months1 | 6 months -4 years4 | 5-11 years5 | 12-19 years6 | 20-59 years7 | 60+ years8 | ||
| formula fed2 |
not formula fed3 |
||||||
| Ambient air9 | <0.01-0.07 | <0.01-0.07 | <0.01-0.14 | <0.01-0.11 | <0.01-0.06 | <0.01-0.05 | <0.01-0.05 |
| Indoor air10 | <0.01-0.22 | <0.01-0.22 | <0.01-0.47 | <0.01-0.37 | <0.01-0.21 | <0.01-0.18 | <0.01-0.16 |
| Drinking water11 | 0.05-0.07 | 0.01-0.02 | 0.01 | 0.01 | <0.01 | <0.01 | <0.01 |
| Food12 | <0.01 | 0.01-0.03 | 0.01-0.02 | 0.01-0.02 | <0.01-0.01 | <0.01-0.01 | |
| Soil13 | |||||||
| Total intake | 0.05-0.36 | 0.01-0.31 | 0.02-0.65 | 0.02-0.51 | 0.01-0.29 | <0.01-0.24 | <0.01-0.22 |
1Assumed to weigh 7.6 kg and breathe 2.1 m3/day (EHD, 1997).
2Assumed to ingest 0.8 L/day (reconstituted formula) (EHD, 1997). For formula-fed infants, intake from water is synonymous with intake from food.
3 Assumed to ingest 0.2 L water per day and to consume on a daily basis 0.01 g natural cheese, 0.10 g margarine, 0.91 g butter, 0.073 g peanut butter and 0.24 g chocolate bar (EHD, 1997).
4Assumed to weigh 15.6 kg, breathe 9.3 m3/day, ingest 0.2 L water per day and consume on a daily basis 2.59 g natural cheese, 5.69 g cold cuts, 0.94 g canned luncheon meat, 0.24 g ham luncheon meat, 2.66 g margarine, 7.32 g butter, 2.57 g peanut butter and 3.18 g chocolate bar (EHD, 1997).
5 Assumed to weigh 31.2 kg, breathe 14.5 m3/day, ingest 0.4 L water per day and consume on a daily basis 3.18 g natural cheese, 7.57 g cold cuts, 0.97 g canned luncheon meat, 0.24 g ham luncheon meat, 6.10 g margarine, 12.93 g butter, 4.99 g peanut butter and 5.45 g chocolate bar (EHD, 1997).
6Assumed to weigh 59.7 kg, breathe 15.8 m3/day, ingest 0.4 L water per day and consume on a daily basis 5.68 g natural cheese, 9.61 g cold cuts, 2.22 g canned luncheon meat, 1.33 g ham luncheon meat, 8.25 g margarine, 16.35 g butter, 4.84 g peanut butter and 8.07 g chocolate bar (EHD, 1997).
7 Assumed to weigh 70.7 kg, breathe 16.2 m3/day, ingest 0.4 L water per day and consume on a daily basis 8.83 g natural cheese, 9.63 g cold cuts, 2.39 g canned luncheon meat, 0.38 g ham luncheon meat, 5.11 g margarine, 15.19 g butter, 1.55 g peanut butter and 4.31 g chocolate bar (EHD, 1997).
8Assumed to weigh 70.6 kg, breathe 14.3 m3/day, ingest 0.4 L water per day and consume on a daily basis 7.17 g natural cheese, 6.26 g cold cuts, 1.70 g canned luncheon meat, 0.39 g ham luncheon meat, 8.10 g margarine, 10.18 g butter, 1.20 g peanut butter and 1.92 g chocolate bar (EHD, 1997).
9 In monitoring of ambient air at six urban stations in Ontario in 1990, concentrations of acrylonitrile were below the limit of detection (0.0003 µg/m3) in 10 of 11 samples. The maximum and only detectable concentration was 1.9 µg/m3in one sample (OMOE, 1992a,b). Canadians are assumed to spend three of 24 hours outdoors (EHD, 1997). The limit of detection (0.0003 µg/m3) and the highest reported concentration (1.9 µg/m3) were used to calculate the range of exposures in ambient air.
10Acrylonitrile was not detected (limit of detection 0.9 µg/m3) in limited monitoring of indoor air in Toronto in 1990 (Bell et al., 1991). Canadians are assumed to spend 21 of 24 hours indoors (EHD, 1997). Concentrations of 0 and 0.9 µg/m3(limit of detection) were used to calculate the range of exposures from indoor air.
11The range of exposure from drinking water is calculated from the lowest limit of detection (0.5 µg/L, for minimum estimate) and the highest concentration reported, 0.7 µg/L (Environment Canada, 1989a).
12 Page and Charbonneau (1983) measured concentrations of acrylonitrile in five types of food packaged in acrylonitrile-based plastic containers, purchased from several stores in Ottawa, Ontario. Average concentrations of acrylonitrile (measured in three duplicate samples of each food type) ranged from 8.4 to 38.1 ng/g:
8.4-31.0 ng/g in honey butter (natural or cinnamon)
23.8-31.5 ng/g in cold pack cheese
<10-38.1 ng/g in peanut butter
<2.5 ng/g in soft butter and creamed coconut
Concentrations in other foods were assumed to be zero.
13Concentrations of acrylonitrile in soil in Canada were not identified
Although it is uncertain, based on this limited information, indoor air is likely the principal medium of exposure to acrylonitrile, followed by ambient air. Intakes from food and drinking water are likely to be negligible in comparison. This is consistent with the physical/chemical properties of acrylonitrile, which has moderate vapour pressure and a low log Kow, and the results of fugacity modelling (Section 2.3.1.5). Indeed, that air is likely the principal medium of exposure has been confirmed by point estimates of average daily intake based on concentrations of acrylonitrile predicted in various media by fugacity modelling and reference values for body weight, inhalation volume and amounts of food and drinking water consumed daily for six age groups (Table 10). On this basis, intake from ambient and indoor air ranges from 96% to 100% of total intake.
| Route of exposure |
Estimated relative intake of acrylonitrile (%) | |||||||
|---|---|---|---|---|---|---|---|---|
| 0-6 months1 | 6 months - 4 years4 | 5-11 years5 | 12-19 years6 | 20-59 years7 | 60+ years8 | |||
| formula fed2 |
not formula fed3 |
|||||||
| Ambient air9 | 12 | 12 | 12 | 12 | 12 | 12 | 12 | |
| Indoor air | 84 | 84 | 87 | 86 | 88 | 86 | 86 | |
| Drinking water | 3 | 0.01 | 0.2 | 0.2 | 0.2 | 0.2 | 0.2 | |
| Food10 | 4 | 2 | 1 | 1 | 1 | 1 | ||
| Soil | ||||||||
1Assumed to weigh 7.6 kg, breathe 2.1 m3/day and ingest 30 mg soil per day (EHD, 1997).
2For formula-fed infants, intake from water is synonymous with intake from food.
3 Assumed to consume 1010 g food/day (EHD, 1997).
4Assumed to weigh 15.6 kg, breathe 9.3 m3/day, ingest 0.2 L water per day, ingest 100 mg soil per day and consume 1413 g food/day (EHD, 1997).
5 Assumed to weigh 31.2 kg, breathe 14.5 m3/day, ingest 0.4 L water per day, ingest 65 mg soil per day and consume 1834 g food/day (EHD, 1997).
6Assumed to weigh 59.7 kg, breathe 15.8 m3/day, ingest 0.4 L water per day, ingest 30 mg soil per day and consume 2074 g food/day (EHD, 1997).
7Assumed to weigh 70.7 kg, breathe 16.2 m3/day, ingest 0.4 L water per day, ingest 30 mg soil per day and consume 2353 g food/day (EHD, 1997).
8 Assumed to weigh 70.6 kg, breathe 14.3 m3/day, ingest 0.4 L water per day, ingest 30 mg soil per day and consume 1969 g food/day (EHD, 1997).
9The results of the ChemCAN3 model (Section 2.3.1.5) indicate that when all Canadian releases are assumed to occur in southern Ontario, release over the long term may result in very low levels across the region. The predicted levels are: air: 2.1 X 10-4µg/m3water: 1.6 X 10-8mg/L soil: 2.0 X 10-8µg/g; calculated intakes from soil were negligible.
10 The concentration of acrylonitrile in foods was assumed to be the same as that in soil.
Exposures from ambient air may be substantially higher for populations in the vicinity of point sources. Based upon the limit of detection in sampling at the site of nitrile-butadiene rubber production in Sarnia, Ontario, the maximum concentration would be <52.9 µg/m3. Assuming the same reference values and intake in other media as for the general population, worst-case upper-bound estimates of exposure in the vicinity of industrial sources range from 10.7 to 31.6 µg/kg-bw per day (Table 11). The only other (earlier) data on concentrations in the vicinity of point sources indicate that populations in the area might be exposed to levels considerably less than these (in the range of tenths of µg/m3) (Ng and Karellas, 1994; Ortech Corporation, 1994). Additional data from the United States indicate that levels vary considerably in the vicinity of various point sources.6
Table 11 Estimated daily intake of acrylonitrile by the population of Canada: worst-case upper-bound estimates
Limitations of the data preclude development of meaningful probabilistic estimates of exposure to acrylonitrile in the general population.
6 Table 6.3.3 in the supporting documentation (Health Canada, 1999)
