No abstract

Our results lend support to the hypothesis that occupational PAH exposure causes fatal IHD and demonstrate a consistent exposure-response relation for this association.

Formaldehyde (FA) is a widely produced industrial chemical. Sufficient evidence exists to consider FA as an animal carcinogen. In humans the evidence is not conclusive. DNA-protein crosslinks (DPC) may be one of the early lesions in the carcinogenesis process in cells following exposures to carcinogens. It has been shown in in vitro tests that FA can form DPC. We examined the amount of DPC formation in human white blood cells exposed to FA in vitro and in white blood cells taken from 12 workers exposed to FA and eight controls. We found a significant difference (P = 0.03) in the amount of DPC among exposed (mean +/- SD 28 +/- 5%, minimum 21%, maximum 38%) than among the unexposed controls (mean +/- SD 22 +/- 6%, minimum 16%, maximum 32%). Of the 12 exposed workers, four (33%) showed crosslink values above the upper range of controls. We also found a linear relationship between years of exposure and the amount of DPC. We conclude that our data indicate a possible mechanism of FA carcinogenicity in humans and that DPC can be used as a method for biological monitoring of exposure to FA.

Background: Formaldehyde (FA) is classified as a probable human carcinogen. Aims: To examine DNA protein crosslinks (DPC) and p53, which are generally known to be involved in carcinogenesis, in peripheral blood lymphocytes of workers exposed to FA. Methods: DPC and p53 ("wild type" and mutant) were examined in peripheral blood lymphocytes of 186 workers exposed to FA (mean years of exposure = 16) and 213 unexposed workers. Every worker completed a questionnaire on demographic data, occupational and medical history, smoking, and hygiene. Results: The adjusted mean level of DPC in the exposed and the unexposed workers differed significantly. Adjustment was made for age, sex, years of education, smoking, and origin. Exposure to FA increased the risk of having a higher level of pantropic p53 above 150 pg/ml (OR 1.6, 95% CI 0.8 to 3.1). A significant positive correlation was found between the increase of pantropic p53 protein and mutant p53 protein, as well as between pantropic p53 >150 pg/ml and mutant p53 protein. In the exposed group a significantly higher proportion of p53 >150 pg/ml was found among workers with DPC >0.187 (55.7%) (0.187 = median level of DPC) than among workers with DPC <0.187 (33.3%). The risk of having pantropic p53 protein >150 pg/ml was determined mainly by levels of DPC. Workers with DPC above the median level had a significantly higher risk of having pantropic p53 >150 pg/ml (adjusted OR 2.5, 95% CI 1.2 to 5.4). Conclusions: Results suggest that DPC and mutation in p53 may represent steps in FA carcinogenesis and a possible causal relation between DPC and mutation in p53. These biomarkers can be applied in the assessment of the development of cancer due to FA exposure.

The results of the analysis by bitumen fume exposure do not allow us to conclude on the presence or absence of a causal link between exposure to bitumen fume and risk of cancer of the lung and the head and neck.