1,3-Butadiene has been assessed as a Priority Substance under the Canadian Environmental Protection Act. The general population in Canada is exposed to 1,3-butadiene primarily through ambient air. Inhaled 1,3-butadiene is carcinogenic in both mice and rats, inducing tumors at multiple sites at all concentrations tested in all identified studies. In addition, 1,3-butadiene is genotoxic in both somatic and germ cells of rodents. It also induces adverse effects in the reproductive organs of female mice at relatively low concentrations. The greater sensitivity in mice than in rats to induction of these effects by 1,3-butadiene is likely related to species differences in metabolism to active epoxide metabolites. Exposure to 1,3-butadiene in the occupational environment has been associated with the induction of leukemia; there is also some limited evidence that 1,3-butadiene is genotoxic in exposed workers. Therefore, in view of the weight of evidence of available epidemiological and toxicological data, 1,3-butadiene is considered highly likely to be carcinogenic, and likely to be genotoxic, in humans. Estimates of the potency of butadiene to induce cancer have been derived on the basis of both epidemiological investigation and bioassays in mice and rats. Potencies to induce ovarian effects have been estimated on the basis of studies in mice. Uncertainties have been delineated, and, while there are clear species differences in metabolism, estimates of potency to induce effects are considered justifiably conservative in view of the likely variability in metabolism across the population related to genetic polymorphism for enzymes for the critical metabolic pathway.
Ten cases of angiosarcoma of the liver among vinyl chloride workers from a plant in Shawinigan, Québec, are reported. The author insist mostly on the occupational history of these workers and on the morphologic description of the lesions. A pathogenic hypothesis is submitted.
The study population comprised 52 male printers and 52 controls. Each person was interviewed about job history, general health, and work-related symptoms. Symptoms from eyes and airways, neurological symptoms, and general symptoms were recorded. A lung function test and a measurement of the sense of smell were also carried out. The printers had significantly more eye, airway, and neurological symptoms than the controls; the main complaints being irritation of eyes, nose, throat, and a reduced sense of taste. The neurological symptoms were disorders of vision, vertigo, feeling of intoxication, and headache. Furthermore, abdominal pain and flatulence occurred more often among the printers. The symptoms showed no relation to age or job seniority, but neurological and general symptoms were related to shift work. No difference in lung function was found between the two groups. The printers had a slightly lower threshold of smell than the controls. Although the total load due to organic solvents and dust in the air was far below legal limits, the number of magnitude of symptoms experienced by the printers exceeded what is supposed when norms for workroom exposure are set. It is suggested that either the irritative effects of solvents are underestimated or the assumption of additive effects when great numbers of solvents are found does not hold true. A reduction of the number of solvents by eliminating the most toxic solvents or by using dyes without solvents is suggested.
The risk of acute myeloid leukemia (AML) within different occupations was studied, using occupational information obtained from the Swedish 1970 census. Follow-up in the Swedish Cancer Register was carried out from 1971 to 1984. Among male petrol station attendants, 10 cases were observed versus 2.8 expected (observed/expected = 3.6, 95% confidence interval 1.7-6.6). For several decades, Swedish petrol has contained 3-5% of benzene. Thus, a hypothesis was that benzene had contributed to the excess risk. The work histories of the 10 cases were reconstructed through interviews with surviving relatives and were compatible with the hypothesis. However, because the air benzene exposures at petrol stations always have been lower than benzene exposures associated previously with an increased risk of AML, the leukemogenic effect of benzene may have been potentiated by other petrol or vehicle exhaust components.
Comment In: Arch Environ Health. 1996 Nov-Dec;51(6):469-719012330
The contributors provide an analysis of acute occupational poisoning cases basing on the data obtained by the Institute of Occupational Diseases in Leningrad for 1980-1987, investigate the structure of the registered acute poisonings, their occurrence and reasons. A more detailed clinical description of an acute poisoning with trichlorethylene is given with particular emphasis on its cardiotoxic effects.