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.
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.
The contributors provide an analysis of the conditions and reasons accounting for the acute occupational intoxications in closed environments, which occurred in Moscow in 1986-1989 and resulted in 18 deaths. Proposals are made with regard to a state standard act on the safety rules for working in closed environments with the texts of some paragraphs to this act.
A study was performed of acute pneumonia (AP) morbidity among the workers exposed to respiratory irritation inducing chemical substances, which revealed a marked AP prevalence in these professional groups. A qualitative analysis of the AP cases severity helped to establish some peculiarities of the disease course in workers exposed to minor concentrations of the chemical substances, which should be taken into account in diagnosis, prognosis, treatment and out-patient observation.
Occupational asthma is an avoidable form of asthma. In Finland, the diagnosis of occupational asthma entitles substantial compensation to the employee. The diagnostics are based on symptoms, exposure assessment, allergologic investigations, follow-up of peak expiratory flow (PEF) at work and at home and, in many cases, specific challenge tests.
To study the causative agents of occupational asthma in Finland.
The causative agents and the numbers of new occupational asthma cases notified to the Finnish Register of Occupational Diseases (FROD) during 1986-2002 are reported.
The number of occupational asthma cases increased from 1986 until 1995, after which a downward trend, stabilizing during the last few years, has been observed. The majority of the cases (59%) in the beginning of the period (1986-1990) were associated with agriculture, but the percentage has fallen thereafter (42% of the cases in 1998-2002) along with the fall in the total number of cases. Since 1995, indoor moulds from water-damaged buildings have caused an increasing number of cases and have become the most important causative agents (0.5% cases, in 1986-1990 and 18% of the cases in 1998-2002). Chemicals have caused 10-30% of the cases, a decreasing number since 1990. The most important chemicals causing occupational asthma have been diisocyanates and welding fumes, followed by hairdressing chemicals and formaldehyde.
The number of occupational asthma cases in Finland reached its height in the mid-1990s. The decrease in the number of total cases is because of the decrease in agriculture-associated cases, reflecting the number of employees in agriculture-associated occupations, which has greatly decreased since Finland joined the EU in 1995. An epidemic of mould-induced asthma, affecting mostly white-collar employees working in moisture-damaged buildings, has taken place since 1995.
Clinical and epidemiologic study of chronic somatic discases in workers engaged into thorium production (main group) in short-term period revealed significantly higher prevalence of vegetative neurosis, asthenic state, chronic gastritis, arterial hypotension, chronic nasopharyngitis and higher risk of those conditions, if compared to reference group over the period since 1947 to 1959. These findings are caused by combined exposure to occupational hazards: outer and inner radiation due to long-lived thorium, thoron and their radioactive products, associated exposure to toxic chemicals. Chronic radiation sickness was diagnosed only in individuals who worked over the period since 1947 to 1959 and demonstrated hemopoietic disorders associated with functional neural system impairment. Better sanitary and hygienic work conditions and more efficient individual protective means ("Lepestok" respirator) resulted in reliably decreased risk of chronic somatic diseases among thorium production workers employed since 1960 to 1972.
The aim of this study was to compare, by stratification, subgroups of hairdressers. Three groups were considered: Group I (102 persons) consisted of hairdressers reporting skin affection at the time of completing an earlier mailed questionnaire (point prevalence). Group II reported exanthema prior to completing, while group III reported not having had exanthema at all (51 and 50 persons, respectively). No significant difference was found between these groups with regard to age and duration in work. The mean number of months since start of disease was significantly higher for group I (64 (range: 0.5-552)) than group II (7 (range: 0.6-38)). The frequency of atopic dermatitis was 12.7% (C.I: 6.3-19.2) in group I, compared with 3.9% (C.I: 0.0-9.2) in group II and none in group III. This difference between groups was significant. A significantly higher extent of sick leave was found in group I, compared to group II.