The mutagenicity of butadiene towards salmonella typhimurium

Meester, Conrad De; Poncelet, F.; Roberfroid, Marcel; Mercier, Michel

doi:10.1016/0378-4274(80)90179-4

Cited by 65 publications

(22 citation statements)

References 5 publications

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“…BD was mutagenic in Salmonella typhimurium strain TA 1530 with metabolic activation (7), and BD gas was weakly mutagenic in the mouse lymphoma assay in the presence of rat liver S9 (8). In laboratory animals, BD can induce chromosomal damage and somatic cell mutations.…”

mentioning

confidence: 99%

Assessment of 1,3-Butadiene Exposure in Polymer Production Workers Using HPRT Mutations in Lymphocytes as a Biomarker

Ammenheuser¹,

Bechtold²,

Abdel‐Rahman³

et al. 2001

Environmental Health Perspectives

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mentioning

confidence: 99%

Assessment of 1,3-Butadiene Exposure in Polymer Production Workers Using HPRT Mutations in Lymphocytes as a Biomarker

Ammenheuser¹,

Bechtold²,

Abdel‐Rahman³

et al. 2001

Environmental Health Perspectives

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“…In studies involving bacterial mutagenicity, butadiene has been shown to be a base-pair mutagen in Salmonella typhimurium strains TA1530 and 1535 (23). Its mutagenicity requires metabolic activation (24). Butadiene also causes cytogenetic effects in the whole animal.…”

Section: Toxicitymentioning

confidence: 99%

A brief survey of butadiene health effects: a role for metabolic differences.

Birnbaum

1993

Environ Health Perspect

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1,3-Butadiene is a major monomer in the rubber and plastics industry and is one of the highest-production industrial chemicals in the United States. Although not highly acutely toxic to rodents, inhalation of concentrations as low as 6.25 ppm causes tumors in mice. Butadiene is oncogenic in rats, but much higher exposure concentrations are required than in mice. Chronic toxicity targets the gonads and hematopoetic system. Butadiene is also a potent mutagen and clastogen. Differences in the absorption, distribution, and elimination of butadiene appear to be relatively minor between rats and mice, although mice do retain more butadiene and its metabolites after exposure to the same concentration and have a higher rate of metabolic elimination. Recent studies have demonstrated that major species differences appear to occur in the rate of detoxication of the primary metabolite, 3-epoxybutene (butadiene monoepoxide [BDMO]). Mice have the greatest rate of production of BDMO as compared to other species, but the rate of removal of BDMO appears to be less than in other species. Mice have low levels of epoxide hydrolase; rats have intermediate levels; monkeys and humans appear to have high levels of this detoxifying enzyme. Thus, while only low levels of butadiene exposure may result in an accumulation of BDMO in the mouse, much higher levels would be required to result in an elevation of circulating BDMO in other species. The level of this reactive metabolite may be correlated with the species differences in butadiene sensitivity.

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“…Butadiene monoxide and diepoxybutane have been shown to be mutagenic to Salmonella typhimurium strains, which are sensitive to base pair substitution mutagens (24,25), and to induce local neoplasms when applied to the skin ofmice or when administered to rats or mice by subcutaneous injection (26,27). Since 1,3-butadiene is mutagenic to Salmonella typhimurium only when incubated with liver S-9 activation systems (28), epoxide intermediates may be the ultimate carcinogenic forms of this chemical. Butadiene monoxide has been identified in the expired air of Sprague-Dawley rats exposed to 1,3-butadiene (29).…”

Section: -Week Evaluationmentioning

confidence: 99%

Inhalation Toxicology and Carcinogenicity of 1,3-Butadiene in B6C3F 1 Mice Following 65 Weeks of Exposure

Melnick¹,

Huff²,

Roycroft³

et al. 1990

Environmental Health Perspectives

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1,3-Butadiene, a large-production volume chemical used mainly in the manufacture of synthetic rubber, was found to induce multiple-organ carcinogenicity in male and female B6C3F1 mice at exposure concentrations (625 and 1250 ppm) equivalent to and below the OSHA standard of 1000 ppm. Since this study was terminated after 60 weeks of exposure because of reduced survival due to fatal tumors, and because dose-response relationships for 1,3-butadiene-induced neoplastic and nonneoplastic lesions were not clearly established, a second long-term inhalation study of 1,3-butadiene in B6C3F1 mice was conducted at lower exposure concentrations, ranging from 6.25 to 625 ppm. Both the histopathological findings from animals dying through week 65 and the results of evaluations of animals exposed for 40 and 65 weeks are presented in this report. Exposure to 1,3-butadiene caused a regenerative anemia at concentrations of 62.5 ppm and higher. Testicular atrophy was induced at 625 ppm, and ovarian atrophy was observed at 20 ppm and higher. During the first 50 weeks of the study, lymphocytic lymphoma was the major cause of death of mice exposed to 625 ppm 1,3-butadiene. Neoplasms of the heart, forestomach, lung, Harderian gland, mammary gland, ovary, and liver were frequently observed in 1,3-butadiene-exposed mice that died between week 40 and week 65 of the study. Studies in which exposure to 1,3-butadiene was stopped after limited periods were also included to assess the relationship between exposure levels and duration of exposures on the outcome of 1,3-butadiene-induced carcinogenicity. In these studies, lymphocytic lymphomas were induced in male mice exposed to 625 ppm 1,3-butadiene for only 13 weeks. The incidence of lymphocytic lymphoma in male mice exposed to 625 ppm 1,3-butadiene for 26 weeks was two times that in mice exposed to 625 ppm for 13 weeks. However, when the exposure concentration was reduced by half to 312 ppm and the exposure duration extended to 52 weeks, the incidence of lymphocytic lymphoma was reduced by 90%. Thus, the multiple of the exposure concentration times the exposure duration did not predict the incidence of lymphocytic lymphoma in mice. The early mortalities resulting from lymphocytic lymphomas in male mice exposed to 625 ppm 1,3-butadiene limited the expression of tumors at other sites. A clearer dose-response for 1,3-butadieneinduced neoplasia should be apparent from experiments in mice exposed to lower concentrations of this chemical for 2 years.

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The mutagenicity of butadiene towards salmonella typhimurium

Cited by 65 publications

References 5 publications

Assessment of 1,3-Butadiene Exposure in Polymer Production Workers Using HPRT Mutations in Lymphocytes as a Biomarker

Assessment of 1,3-Butadiene Exposure in Polymer Production Workers Using HPRT Mutations in Lymphocytes as a Biomarker

A brief survey of butadiene health effects: a role for metabolic differences.

Inhalation Toxicology and Carcinogenicity of 1,3-Butadiene in B6C3F 1 Mice Following 65 Weeks of Exposure

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