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IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Chlorinated Drinking-Water; Chlorination by-Products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds. Lyon (FR): International Agency for Research on Cancer; 1991. (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 52.)

Cover of Chlorinated Drinking-Water; Chlorination by-Products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds

Chlorinated Drinking-Water; Chlorination by-Products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds.

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Bromoethane

1. Chemical and Physical Data

1.1. Synonyms

Chem. Abstr. Services Reg. No.: 74-96-4

Chem. Abstr. Name: Bromoethane

IUPAC Systematic Name: Bromoethane

Synonyms: Bromic ether; ethyl bromide; hydrobromic ether; monobromoethane

1.2. Structural and molecular formulae and molecular weight

Image 006d-1_001

1.3. Chemical and physical properties of the pure substance

  1. Description: Clear, colourless liquid with ethereal odour and burning taste (Great Lakes Chemical Corp., 1981; Budavari, 1989)
  2. Boiling-point: 38.4°C (Weast, 1989)
  3. Melting-point: −118.6°C (Weast, 1989)
  4. Density: 1.4604 at 20/4°C (Weast, 1989)
  5. Spectroscopy data1: Infrared (Sadtler Research Laboratories, 1980, prism [4631, 4632], grating [10951]; Pouchert, 1981, 1985), nuclear magnetic resonance (Sadtler Research Laboratories, 1980, proton [225, V10], C-13 [616]; Pouchert, 1974, 1983) and mass spectral data [331]) have been reported.
  6. Solubility: Soluble in water (1.067 g/100 g at 0°C, 0.914 g/100 g at 20°C), ethanol, chloroform and diethyl ether (Budavari, 1989; Weast, 1989)
  7. Volatility: Vapour pressure, 400 mm Hg at 21.0°C (Weast, 1989); relative vapour density (air = 1), 3.75 (Great Lakes Chemical Corp., 1989a)
  8. Stability: Turns yellow on exposure to air and light (Budavari, 1989)
  9. Reactivity: Reacts rapidly with metals such as sodium, potassium, calcium, powdered aluminium, zinc and magnesium (Sittig, 1985)
  10. Octanol/water partition coefficient (P): log P, 1.61 (Chemical Information Systems, 1990)
  11. Conversion factor1: mg/m3 = 4.46 × ppm

1.4. Technical products and impurities

Bromoethane is available as a commercial-grade liquid with a minimum purity of 99% and maximum acidity of 5.0 ppm (as HBr) (Great Lakes Chemical Corp., 1989b).

2. Production, Use, Occurrence and Analysis

2.1. Production and use

(a) Production

Bromoethane was first synthesized in France in 1827 by Serullas from alcohol and bromine reacted with phosphorus (STN International, 1989). It can be produced commercially by the following methods: reaction of ethanol with hydrogen bromide; distillation of a mixture of hydrogen bromide, ethanol and sulfuric acid; reaction of ethanol with phosphorus and bromine; reaction of ethane with sulfur trioxide and potassium bromide at 300–325 °C; and reaction of ethylene with hydrogen bromide initiated by gamma radiation (Stenger, 1978; Budavari, 1989).

Bromoethane is currently produced by three companies in France, three in the UK, two in Germany, two in Japan, two in the USA and one each in Israel, Italy and the Netherlands (Chemical Information Services, 1988).

(b) Use

Bromoethane has been used as an ethylating agent in organic synthesis and gasoline, as a refrigerant and as an extraction solvent; it has had limited use as a local anaesthetic (Sittig, 1985; Strobel & Grummt, 1987). It has been investigated as a possible substitute for chlorofluorocarbons in compression heat pumps (Narodoslawsky & Moser, 1988).

(c) Regulatory status and guidelines

Occupational exposure limits and guidelines for bromoethane are presented in Table 1.

Table 1.. Occupational exposure limits and guidelines for bromoethane.

Table 1.

Occupational exposure limits and guidelines for bromoethane.

2.2. Occurrence

(a) Natural occurrence

Macroalgae collected near the Bermuda Islands (Fucales sargassum) and at the Cape of Good Hope (Laminariales laminaria) showed a specific pattern of emission of volatile organohalides into the air. The main components were bromoform, bromodichloromethane and chlorodibromomethane; a minor component was bromoethane (Class et al., 1986).

(b) Air

Bromoethane was not found (detection limit, < 1 ppt) in six air samples taken near the surface of the Pacific Ocean at several sites in the northern hemisphere (Hoyt & Rasmussen, 1985).

(c) Water and sediments

Bromoethane was detected (but not quantified) in headspace analysis of seven out of ten seawater samples collected in 1983 (Hoyt & Rasmussen, 1985).

In a two-year study of trace organic compounds in drinking-water in Philadelphia, PA, Suffet et al. (1980) tested samples derived from two surface water (river) sources and collected at four sites. Bromoethane was identified in one of 13 samples collected at the two sites originating from the Delaware River but in neither of the three samples originating from the Schuylkill River. No quantitative analysis was performed.

2.3. Analysis

Selected methods for the analysis of bromoethane in air, breath and water are presented in Table 2.

Table 2.. Methods for the analysis of bromoethane.

Table 2.

Methods for the analysis of bromoethane.

3. Biological Data Relevant to the Evaluation of Carcinogenic Risk to Humans

3.1. Carcinogenicity studies in animals (Table 3)

Table 3.. Summary of carcinogenicity studies of bromoethane in experimental animals.

Table 3.

Summary of carcinogenicity studies of bromoethane in experimental animals.

(a) Inhalation

Mouse: Groups of 50 male and 50 female B6C3F1 mice, nine weeks old, were exposed to 100, 200 or 400 ppm bromoethane (446, 890 or 1780 mg/m3; > 98% pure) by whole-body inhalation for 6 h per day on five days per week for 103 weeks. Survival at 105 weeks was: males—control, 35/50; low-dose, 37/50; mid-dose, 30/50; high-dose, 34/50; females—control, 36/50; low-dose, 37/50; mid-dose, 36/50; high-dose, 22/50. Uterine neoplasms reduced the survival in high-dose female mice. Adenomas of the uterine endometrium occurred in 0/50 control, 1/50 low-dose, 1/47 mid-dose and 6/48 high-dose female mice, and adenocarcinomas occurred in 0/50 control, 2/50 low-dose, 3/47 mid-dose and 19/48 high-dose females; squamous-cell carcinomas of the uterine endometrium occurred in 0/50 control, 1/50 low-dose, 1/47 mid-dose and 3/48 high-dose female mice. The proportion of female mice with uterine endometrium neoplasms (0/50 control, 4/50 low-dose, 5/47 mid-dose, and 27/48 high-dose) was significantly increased over that in controls at all exposure concentrations (low-dose, p = 0.017; mid-dose, p = 0.035; high-dose, p < 0.001, trend test; p < 0.001, incidental tumour test). Alveolar/bronchiolar adenomas occurred in 5/50 control, 6/50 low-dose, 8/50 mid-dose and 9/50 high-dose males, and alveolar/bronchiolar carcinomas occurred in 2/50 control, 0/50 low-dose, 5/50 mid-dose and 6/50 high-dose male mice. The proportion of high-dose male mice with alveolar/bronchiolar neoplasms was significantly increased relative to that in controls (p = 0.049, pairwise comparison; p = 0.012, trend test, incidental tumour test) (National Toxicology Program, 1989).

Rat: Groups of 50 male and 50 female Fischer 344 rats, eight to ten weeks old, were exposed to 100, 200 or 400 ppm bromoethane (446, 890 or 1780 mg/m3 bromoethane; > 98% pure) by whole-body inhalation 6 h per day on five days per week for 104 weeks. Survival at 106 weeks was: males—control, 17/50; low-dose, 26/50; mid-dose, 26/50; high-dose, 21/50; females—control, 19/50; low-dose, 29/50; mid-dose, 24/50; high-dose, 22/50. Adrenal medullary phaeochromocytomas (benign and malignant combined) occurred in 8/48 control, 23/47 low-dose, 18/50 mid-dose and 21/49 high-dose male rats. The proportion of low and high-dose male rats with phaeochromocytoma was significantly greater than that in controls (low-dose, p = 0.013; high-dose, p = 0.007, incidental tumour test); however, there was disproportionate sampling of the adrenal medulla among control and exposure groups (numbers of adrenal medullas examined microscopically: control, 66; low-dose, 82; mid-dose, 85; high-dose, 86). When statistical analyses were performed using as denominators the number of medullas examined microscopically [to reduce observation bias], the p values were 0.022 (low-dose) and 0.027 (high-dose). Granular-cell tumours of the brain occurred in 0/49 control, 3/50 low-dose, 1/50 mid-dose and 1/50 high-dose male rats; these incidences are not significant. The incidences of these tumours in historical controls were 0/297 in the study laboratory and 4/1928 in all National Toxicology Program laboratories. Glial-cell tumours of the brain (glioma, astrocytoma or oligodendroglioma) occurred in 0/49 control and 3/50 low-dose male rats and 0/50 control, 1/50 low-dose, 1/48 mid-dose and 3/50 high-dose female rats (p = 0.045, trend test); the incidences of these tumours in historical controls were: males—study laboratory, 3/297; all National Toxicology Program studies, 13/1928; females—study laboratory, 1/297; all National Toxicology Program laboratories, 23/1969). Gliosis was reported in one rat in each of the low- and high-dose male groups and control and high-dose female groups. The incidence of mammary gland neoplasms (all histological types) was significantly decreased in high-dose female rats (control, 18/50; low-dose, 15/50; mid-dose, 10/48; high-dose, 7/50; p = 0.011, pairwise comparison; p = 0.004, trend test, incidental tumour test). Inflammation, epithelial hyperplasia and squamous metaplasia of the nasal cavity mucosa were increased in frequency in exposed rats (National Toxicology Program, 1989).

(b) Subcutaneous administration

Rat: Groups of 20 female CB hooded rats, six weeks old, were given a single subcutaneous injection of bromoethane [purity unspecified] in trioctanoin at 1.25, 4.2 or 12.5 mmol/kg bw (136, 460 or 1362 mg/kg bw). Twenty female rats given trioctanoin alone were used as controls. Survival at 96 weeks after injection was: low-dose, 18/20; mid-dose, 17/20; high-dose, 17/20 [survival of controls not given]. No sarcoma was seen at the injection sites in either treated or control rats (Dipple et al., 1981). [The Working Group noted that only single injections were given and the small number of animals.]

(c) Intraperitoneal administration

Mouse: In a screening assay based on the enhanced induction of lung tumours, groups of 10 male and 10 female strain A/He mice, six to eight weeks old, were injected intraperitoneally three times per week with three dose levels of bromoethane [purity unspecified] in tricaprylin for a total of 24 injections (total doses, 11, 27.5 or 55 mmol/kg bw [1200, 3000 or 6000 mg/kg bw]). A group of 160 mice given tricaprylin only were used as controls. All surviving animals were killed 24 weeks after the first injection. Survival at that time was 154/160 in the tricaprylin vehicle control, 19/20 in the low-dose, 16/20 in the mid-dose and 20/20 in the high-dose groups. The proportions of mice with lung tumours were 34/154, 4/19, 4/16 and 6/20 in the four groups, respectively; the average numbers of lung tumours per mouse were 0.22 ± 0.07 (SE), 0.21 ± 0.05,0.31 ± 0.08 and 0.35 ± 0.08. In positive control groups given a single intraperitoneal injection of 10 or 20 mg urethane, the numbers of mice with lung tumours were 19/19 and 18/18, respectively and the average numbers of lung tumours per animal were 8.1 ± 2.3 and 17.8 ± 4.32 (Poirier et al., 1975).

3.2. Other relevant data

(a) Experimental systems

(i) Absorption, distribution, metabolism and excretion

Rats given 2.3–11 mmol/kg bw (250–1200 mg/kg bw) bromoethane in olive oil by gavage eliminated 66.7–74.5% of the dose in the expired air within 5–11 h. When rats were given 1.4 mmol/kg bw in five doses of 25 mg/kg at hourly intervals (total dose, 150 mg/kg) or single doses of 4.6 mmol/kg bw (500 mg/kg) or 7.3 mmol/kg bw (800 mg/kg) bromoethane by intraperitoneal injection in olive oil, 73–89% of the dose was eliminated in the expired air by 6 h (Miller & Haggard, 1943).

Williams (1959) reported that 73–89% of a dose of bromoethane injected into rats was eliminated unchanged in the expired air. When bromoethane was given orally in oil at 0.25–1.0 g/kg, 67–76% was eliminated unchanged in the expired air and 34–38% was converted to inorganic bromide.

Enzymatic dehalogenation of bromoethane in the presence of glutathione or cysteine was demonstrated in rat liver extracts (Heppel & Porterfield, 1948).

Bromoethane bound to rat liver cytochrome P450 and inhibited its activity by 27% in microsomes of phenobarbital-induced rats (Ivanetich et al., 1978).

(ii) Toxic effects

The toxicology of bromoethane has been reviewed (Torkelson & Rowe, 1981; National Toxicology Program, 1989).

Intraperitoneal LD50s of 2850 mg/kg bw for mice and 1750 mg/kg bw for rats were reported [vehicle unspecified] (Torkelson & Rowe, 1981). The 1-h LC50s of bromoethane were estimated to be 27 000 ppm [120.42 g/m3] in male Sprague-Dawley rats and 16 200 ppm (72.25 g/m3) in male CF-1 mice (Vernot et al., 1977. The 4-h LC50s in female Fischer 344/N rats and female B6C3F1 mice were 4681 and 2723 ppm (20.88 and 12.1 g/m3), respectively. All male and female Fischer 344/N rats died during or after a 4-h exposure to 10 000 ppm (44.6 g/m3), and exposure concentrations of 10 000 and 5000 ppm (22.3 g/m3) were lethal to all male and female B6C3F1 mice, respectively (National Toxicology Program, 1989). Guinea-pigs died after inhalation of 14% by volume bromoethane for 10 min and 2.4% for 90 min, whereas all survived inhalation of 1.2% for 90 min (Sayers et al., 1929). Signs of toxicity were increased respiration rate, hyperactivity, loss of coordination, dyspnoea, loss of consciousness and lung and liver congestion.

All male and female Fischer 344/N rats and B6C3F1 mice exposed by inhalation to 4000 ppm (17.8 g/m3) and 2000 ppm (8.9 g/m3) bromoethane for 6 h per day on five days per week for two weeks died. Signs of toxicity were prostration, dyspnoea, lachrymation, haemorrhage and congestion in the respiratory tract. Some of these symptoms were also observed after exposure to 1000 ppm (4.46 g/m3). In 14-week studies, male and female Fischer 344/N rats and B6C3F1 mice were exposed to 100–1600 ppm (0.45–7.14 g/m3) bromoethane by inhalation for 6 h per day on five days per week. The high dose resulted in some deaths and reduced body weights of the surviving animals; signs of toxicity in both species included ataxia and atrophy of thigh muscles and uterus. In rats, tremors, paresis, mineralization and degeneration in the brain, atrophy of the testis, haemosiderosis of the spleen and some depletion of bone-marrow haematopoietic cells were also observed Involution of the ovary was observed in mice at the high and mid-doses (see below) (National Toxicology Program, 1989).

(iii) Effects on reproduction and prenatal toxicity

In the 14-week inhalation studies in B6C3F1 mice and Fischer 344 rats described above, severe testicular atrophy was observed in all rats, but not in mice, at 1600 ppm (7.14 g/m3) bromoethane but not at lower concentrations. Four of ten male rats in the 1600-ppm group died. In female mice, but not in rats, the size and number of corpora lutea in the ovary were decreased at 1600 ppm (7/10 animals) and at 800 ppm (3.57 g/m3, 3/9 animals) (National Toxicology Program, 1989).

No data on reproductive or developmental toxicity were available to the Working Group.

(iv) Genetic and related effects (Table 4)
Table 4.. Genetic and related effects of bromoethane.

Table 4.

Genetic and related effects of bromoethane.

Bromoethane was mutagenic to Salmonella typhimurium strains TA100 and TA1535 when tested in closed containers. In single studies, mutations were not induced in Drosophila melanogaster and chromosomal aberrations were not induced in cultured mammalian cells. One study showed an increased incidence of sister chromatid exchange in cultured Chinese hamster ovary (CHO) cells. In a study reported as an abstract, bromoethane tested in a closed container enhanced viral transformation in cultured Syrian hamster embryo cells (Hatch et al., 1983).

(b) Humans

No data were available to the Working Group.

3.3. Case reports and epidemiological studies of carcinogenicity to humans

No data were available to the Working Group.

4. Summary of Data Reported and Evaluation

4.1. Exposure data

Bromoethane has limited commercial use, including that as an ethylating agent. It has been detected in ocean air as a result of emissions by marine algae.

4.2. Experimental carcinogenicity data

Bromoethane was tested for carcinogenicity in a two-year study in male and female Fischer 344 rats and B6C3F1 mice by inhalation. In male rats, there was a significant increase in the incidence of adrenal phaeochromocytomas, which was not dose-related. A marginal increase in the incidence of uncommon brain tumours occurred in treated females. In mice, bromoethane induced neoplasms of the uterine endometrium; a marginal increase in the incidence of lung tumours was observed in males. In a screening study by intraperitoneal injection, bromoethane did not increase the incidence of lung tumours in strain A mice.

4.3. Human carcinogenicity data

No data were available to the Working Group.

4.4. Other relevant data

Bromoethane was mutagenic in bacteria but not in insects in a single study. In other single studies, bromoethane caused sister chromatid exchange but not chromosomal aberrations in mammalian cells.

4.5. Evaluation1

There is limited evidence for the carcinogenicity of bromoethane in experimental animals.

No data were available from studies in humans on the carcinogenicity of bromoethane.

Overall evaluation

Bromoethane is not classifiable as to its carcinogenicity to humans (Group 3).

5. References

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Footnotes

1

In square brackets, spectrum number in compilation

1

Calculated from: mg/m3 = (molecular weight/24.45) × ppm, assuming standard temperature (25°C) and pressure (760 mm Hg)

1

For definition of the italicized terms, see preamble, pp. 30–33.

©International Agency for Research on Cancer, 1991.
Bookshelf ID: NBK506970
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