Appendices of the Screening Assessment Petroleum Sector Stream Approach Petroleum and Refinery Gases [Site-Restricted] Chemical Abstracts Service Registry Numbers 68307-99-3, 68476-26-6, 68476-49-3, 68477-69-0, 68477-71-4, 68477-72-5, 68477-73-6, 68477-75 (2024)

• Back to the Screening Assessment

• Appendix 1: Description of the nine groups of petroleum substances
• Appendix 2: Data tables for site-restricted petroleum and refinery gases
• Appendix 3: Exposure estimate modelling data and results
• Appendix 4: Summary of the toxicological effects of the component classes of petroleum and refinery gases
• Appendix 5: Summary of the critical health effects information on 1,3-butadiene
• Appendix 6: Revisions to Domestic Substances List (DSL) names of site-restricted petroleum and refinery gases

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^[1]Assumptions made in the modelling:

1. All releases of 1,3-butadiene from a petroleum facility are assumed to be attributed to the emissions of site-restricted petroleum and refinery gases and originate from processing areas rather than tank farms.
2. All 40 site-restricted petroleum and refinery gases are flagged as potentially containing 1,3-butadiene.
3. The ratio of 1,3-butadiene to benzene in fugitive emissions is assumed to be constant over different processing units.
4. Fugitive emission heights of 1,3-butadiene are assumed to be 15 m and 3 m, with 80% of total emissions occurring at 15 m and 20% of emissions occurring at 3 m.
5. Considering the fact that the release sources are actually multiple point-sources spatially distributed over the processing area, the effective processing area used for calculation of emission rate is assumed to be 80% of the total process area.
6. Total processing area is assumed to be 300 m × 100 m.
7. Adjustment factor 0.2 is used for estimation of maximum concentration over a year based on the highest 1-hour concentration.

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In experimental animals exposed by inhalation, concentrations of up to 25–70% propene and 15–40% butene induced anesthesia in rats, cats and mice (Brown 1924; Riggs 1925; Virtue 1950), while narcosis was noted in mice exposed to up to 70% isobutene via inhalation (Von Oettingen 1940). Acute toxicity values (LC₅₀) are noted to range from 65000 ppm (111 736 mg/m³)^[5] (propene; molecular weight (MW) = 42.03 g/mol) to 620 mg/L (620 000 mg/m³) (isobutene) (Shugaev 1969; Conolly and Osimitz 1981).

Short-term toxicity studies show that oral exposure to isobutene results in a no-observed-adverse-effect level (NOAEL) of 150 mg/kg body weight (kg-bw) per day, despite the occurrence of significant biochemical changes that fall into the historical control range (Hazleton Laboratories 1986). Short-term exposure by inhalation resulted in changes to hematology in rats exposed for a few days to 60% ethene (approximately 690 000 mg/m³) (Fink 1968) as well as clinical and biochemical changes in rats exposed for 70 days to 100 ppm (115 mg/m³)² ethene (MW of ethene = 28.02 g/mol)(Krasovitskaya and Maliarova 1968). Exposure to propene resulted in a lowest NOEL value of 10 000 ppm (17 190 mg/m³)^[5] for 28-day exposure to multiple concentrations of propene (MW = 42.03 g/mol) up to 17190 mg/m³ (DuPont 2002).

The lowest lowest-observed-effect level (LOEL) identified for sub-chronic toxicity is 500 ppm (1146 mg/m³)^[5] in a 14-week study in which male and female B6C3F1 mice and F344/N rats were exposed by inhalation to isobutene (MW = 54.04 g/mol) at concentrations up to 8000 ppm (18 336 mg/m³)^[5] resulting in significant increases in absolute and relative right kidney weights in female mice. In male mice, the absolute right kidney weight was increased at 1000 and 8000 ppm (2292 and 18 336 mg/m³)^[5]. In female rats, there was a significant increase in relative liver weights from 500 ppm (1146 mg/m³)^[5] and in absolute liver weights from 1000 ppm (2292 mg/m³). In male rats, a significant increase in relative right kidney weight was observed from 500 ppm (1146 mg/m³)^[5] with an increase in absolute right kidney weight at 4000 ppm (9168 mg/m³)^[5] (NTP 1998). In addition, a 90-day continuous inhalation study conducted in newborn rats caused delays in coat appearance, tooth development and eye opening, as well as hypertension, inhibition of cholinesterase activity and behavioural changes, at an ethene (MW = 28.02 g/mol) concentration of 2.62 ppm (3 mg/m³)^[5] (Krasovitskaya and Maliarova 1968).

With regard to developmental toxicity, NOEC values of 5000 ppm (5750 mg/m³) for ethene (MW = 28.02 g/mol), 10 000 ppm (17190 mg/m³)^[5] for propene (MW = 42.03 g/mol) and 5000 ppm (11 460 mg/m³)^[5] for 2-butene (MW = 54.04 g/mol) were identified in rats exposed by inhalation (Waalkens-Berendsen and Arts 1992; Aveyard 1996; BASF 2002). Effects on reproductive organs were observed in male rats exposed to isobutene via inhalation over 14 weeks; these include a significant increase in left epididymal weight and a decrease in epididymal sperm motility at 8000 ppm (18336 mg/m³)^[5]. In addition, female rats were reported to have an increased estrus length with a related decrease in diestrus length; however, the length of the estrus cycle was not noted to change (NTP 1998).

Both propene and ethene have been classified as Group 3 carcinogens (not classifiable as to its carcinogenicity to humans) by IARC (1994 a, 1994c). For propene, a two-year inhalation study (concentrations up to 10000 ppm [17 190 mg/m³; MW for propene = 42.03 g/mol])^[5] showed the occurrence of hemangiosarcoma in male and female mice as well as lung tumours (negative trend with increasing concentration) in male mice. No tumours were observed under the same protocol in rats (Quest et al. 1984; NTP 1985). A second inhalation study in mice (78 weeks) and rats (104 weeks) conducted with up to 5000 ppm (8600 mg/m³)^[5] propylene showed no differences in tumour incidence compared with controls (Ciliberti et al. 1988). For ethene, a two-year study in rats did not result in increased tumour incidence at concentrations up to 3000 ppm (3438 mg/m³; MW of ethene = 28.02 g/mol)^[5] (Hamm et al. 1984). Chronic exposure of male and female F344 rats and B6C3F1 mice to isobutene at levels up to 8000 ppm (18336 mg/m³; MW of isobutene = 54.04 g/mol)^[5] for 104 weeks was noted to cause an increased incidence of thyroid gland follicular cell carcinoma in male rats (NTP 1998). In addition, an increased incidence of hyaline degeneration in the nose of rats and mice was reported (NTP 1998).

Ethene, propene and 1-butene were all noted to cause an increased incidence of DNA adducts in vivo (Segerback 1983; Tornqvist et al. 1989; Filser et al. 1992; Eide et al. 1995; Wu et al. 1995; Zhao et al. 1999; Rusyn et al. 2005; Pottenger et al. 2007), but no micronuclei were induced when rats and mice were exposed to ethene, propene or isobutene (Exxon Biomedical Sciences Inc. 1990; Vergnes and Pritts 1994; NTP 1998; Pottenger et al. 2007). When ethene, 1-butene, 2-butene or isobutene were administered in vitro, negative results were obtained for mutagenicity in bacteria (Landry and Fuerst 1968; Hamm et al. 1984; Hughes et al. 1984; Staab and Sarginson 1984; Shimizu et al. 1985; Victorin and Stahlberg 1988; Thompson 1992; Wagner et al. 1992; Araki et al. 1994; NTP 1998; Japan Chemical Industry Ecology-Toxicology and Information Center 2000), mouse lymphoma cells with and without activation (Staab and Sarginson 1984), micronuclei induction without activation (Jorritsma et al. 1995), chromosomal aberrations with and without activation (Riley 1996; Wright 1992) and cell transformation with and without activation (Staab and Sarginson 1984).

As noted in the health effects section of the screening assessment, a member of the alkadienes, 1,3-butadiene, is classified as both a carcinogen and a mutagen by multiple national and international agencies (Canada 2000a; IARC 2008; US EPA 2002; NTP 2011a; EU RAR 2002; ESIS 2008). A thorough review of the human health effects of 1,3-butadiene was previously done under the Priority Substances List (PSL) 2 assessment (Canada 2000a). 1,3-butadiene was subsequently added to the List of Toxic Substances - Schedule 1 of CEPA 1999. Alkadienes have been observed to have narcotic properties at high concentrations and low general toxicity (Sandmeyer 1981).

Another member of the alkadienes (2-methyl-1,3-butadiene or isoprene) is also classified as a carcinogen (Group 2B: possibly carcinogenic to humans (IARC 1999); Category 2: suspected human carcinogen, may cause cancer (European Commission 2004) and “…reasonably anticipated to be a human carcinogen” (NTP 2011b), as well as a mutagen. (European Commission 2004; ESIS 2008). Isoprene is noted to have reproductive effects in mice (testicular atrophy, similar to those observed after 1,3-butadiene exposure) as well as developmental effects (reduced fetal body weight, increased incidence of supernumerary ribs) (Mast et al. 1989, 1990). As well, isoprene has been reported to have effects on mortality, body weight, organ weight, hematology and histopathology (stomach hyperplasia, olfactory degeneration, thymic atrophy, hepatocellular foci changes, alveolar hyperplasia, spinal cord degeneration) in mice after short- and long-term inhalation exposures (Melnick et al. 1990, 1994, 1996). On the basis of carcinogenicity, for which there may be a probability of harm at any level of exposure, Health Canada concluded that isoprene should be considered as a substance that may be entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health (Canada 2008).

Ethyne or acetylene is noted to be a simple asphyxiant (HSDB 2008), where effects observed in humans after inhalation include intoxication, aggressiveness and unconsciousness at high concentrations (US EPA 2008b).

Acetylene is noted to cause increased mortality in various species of experimental animals, as well as intoxication or anesthesia. Effects in the liver (LOAEC = 266.3 mg/L (266 300 mg/m³), kidneys and spleens of rats were observed following repeated exposure via inhalation. Genotoxic effects were not observed in vitro (US EPA 2008b).

Hydrogen sulphide has been evaluated by the International Programme on Chemical Safety (IPCS) in both an Environmental Health Criteria monograph (IPCS 1981) and a Concise International Chemical Assessment Document (IPCS 2003). In addition, the US Agency for Toxic Substances and Disease Registry (ATSDR 2006) has generated a toxicological profile on hydrogen sulphide. The Government of Canada is currently assessing the potential impacts of hydrogen sulphide on human health from various uses and sources.

Ammonia has been evaluated by the IPCS (1986), ATSDR (2004) and the Organisation for Economic Co-operation and Development (OECD) Screening Information Dataset (SIDS) program (OECD 2007). In addition, ammonia has been evaluated by the Government of Canada under the Priority Substances List program for its presence in the aquatic environment, where “conclusions drawn on the basis of a more robust data set on environmental effects would also be protective of human health” (Canada 2001).

Both nitrogen and carbon dioxide have been noted to be inert pesticide ingredients by the US EPA (2004b). Carbon monoxide has been classified by the European Commission as a Category 1 reproductive toxin (ESIS 2008) and has also been reviewed by IPCS (1999).

Two mercaptans noted to be components of petroleum and refinery gases have been evaluated or reviewed by various international or national agencies; however, for the purposes of this hazard assessment, an evaluation of these component substances will not be included.

Methanethiol or methyl mercaptan has been reviewed by ATSDR (1992) and included in a review of aliphatic and aromatic sulphides and thiols by the Joint Food and Agriculture Organization of the United Nations (FAO)/World Health Organization (WHO) Expert Committee on Food Additives (JECFA) (WHO 2000). In addition, both methanethiol and ethanethiol are substances scheduled for evaluation under the OECD SIDS program, but a final review has not been made available at this time (OECD 2000).

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