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There is limited evidence regarding the exposure-effect relationship between lung-cancer risk and hexavalent chromium (Cr(VI)) or nickel. We estimated lung-cancer risks in relation to quantitative indices of occupational exposure to Cr(VI) and nickel and their interaction with smoking habits. We pooled 14 case-control studies from Europe and Canada, including 16 901 lung-cancer cases and 20 965 control subjects. A measurement-based job-exposure-matrix estimated job-year-region specific exposure levels to Cr(VI) and nickel, which were linked to the subjects' occupational histories. Odds ratios (OR) and associated 95% confidence intervals (CI) were calculated by unconditional logistic regression, adjusting for study, age group, smoking habits and exposure to other occupational lung carcinogens. Due to their high correlation, we refrained from mutually adjusting for Cr(VI) and nickel independently. In men, ORs for the highest quartile of cumulative exposure to CR(VI) were 1.32 (95% CI 1.19-1.47) and 1.29 (95% CI 1.15-1.45) in relation to nickel. Analogous results among women were: 1.04 (95% CI 0.48-2.24) and 1.29 (95% CI 0.60-2.86), respectively. In men, excess lung-cancer risks due to occupational Cr(VI) and nickel exposure were also observed in each stratum of never, former and current smokers. Joint effects of Cr(VI) and nickel with smoking were in general greater than additive, but not different from multiplicative. In summary, relatively low cumulative levels of occupational exposure to Cr(VI) and nickel were associated with increased ORs for lung cancer, particularly in men. However, we cannot rule out a combined classical measurement and Berkson-type of error structure, which may cause differential bias of risk estimates., (© 2022 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)

It is not clear whether alcohol consumption is associated with lung cancer risk. The relationship is likely confounded by smoking, complicating the interpretation of previous studies. We examined the association of alcohol consumption and lung cancer risk in a large pooled international sample, minimizing potential confounding of tobacco consumption by restricting analyses to never smokers. Our study included 22 case-control and cohort studies with a total of 2548 never-smoking lung cancer patients and 9362 never-smoking controls from North America, Europe and Asia within the International Lung Cancer Consortium (ILCCO) and SYNERGY Consortium. Alcohol consumption was categorized into amounts consumed (grams per day) and also modelled as a continuous variable using restricted cubic splines for potential non-linearity. Analyses by histologic sub-type were included. Associations by type of alcohol consumed (wine, beer and liquor) were also investigated. Alcohol consumption was inversely associated with lung cancer risk with evidence most strongly supporting lower risk for light and moderate drinkers relative to non-drinkers (>0-4.9 g per day: OR = 0.80, 95% CI = 0.70-0.90; 5-9.9 g per day: OR = 0.82, 95% CI = 0.69-0.99; 10-19.9 g per day: OR = 0.79, 95% CI = 0.65-0.96). Inverse associations were found for consumption of wine and liquor, but not beer. The results indicate that alcohol consumption is inversely associated with lung cancer risk, particularly among subjects with low to moderate consumption levels, and among wine and liquor drinkers, but not beer drinkers. Although our results should have no relevant bias from the confounding effect of smoking we cannot preclude that confounding by other factors contributed to the observed associations. Confounding in relation to the non-drinker reference category may be of particular importance., (© 2017 UICC.)

The aim of the work was verification of the hypothesis that weak power frequency (50 Hz) magnetic fields (MF) affected the number of free oxygen radicals in living biological cells and that these changes could be qualitatively explained by the radical pair mechanism. The experiments were performed on rat lymphocytes. One-hour exposure to 50 Hz MF at 20, 40, or 200 microT flux densities was performed inside a pair of Helmholtz coils with axis along or crosswise to the Earth's static MF. Iron ions (FeCl2) were used as a stimulator of the oxidation processes. Oxygen radicals were measured by fluorimetry using a DCF-DA fluorescent probe. Only in the lymphocytes exposed at 40 microT MF directed along the Earth's static MF there was a decrease of fluorescence in relation to non-exposed samples. Our observation seems to confirm the hypothesis that low level power frequency MF affects oxidative processes which occur in living biological cells and that this effect can be explained by the radical pair mechanism., (2004 Wiley-Liss, Inc.)

This study was performed to evaluate the effects of prenatal development of rats. Females were exposed to carbendazim by gavage every day on days 6-15 of gestation at doses 8, 35, 160 mg/kg b.w. Carbendazim administered at doses of 35 and 160 mg/kg was associated with significant maternal toxicity, embryonal lethality, congenital defects, and retarded fetal development. It produced encephalocele, umbilical hernia, missing or shorter tail, and internal malformations of brain, kidneys, and skeletal malformations of ribs, arch, and vertebrae. NOEL for the dam and fetus in our study was 8 mg/kg/day., (Copyright 2001 Wiley-Liss, Inc.)

The alkaline single cell gel electrophoresis (SCGE) or "comet" assay under alkaline conditions was used to measure DNA damage in the liver cells of B6C3F1 male mice exposed to 2,4-dimethylaniline and 2, 4,6-trimethylaniline. Cells embedded in agarose were lysed, subjected briefly to an electric field, stained with a fluorescent DNA-binding stain, and viewed using a fluorescence microscope. The effect of 2,4-dimethylaniline and 2,4,6-trimethylaniline was studied after a single intraperitoneal injections at doses equal to 100, 200 mg/kg and 150, 300 mg/kg b.w., respectively. It was found that 2, 4-dimethylaniline and 2,4,6-trimethylaniline were able to damage DNA in the liver cells of the mice. As has been published elsewhere, the DNA damaging effect of the studied compounds were also observed in bone marrow cells of the mice. In conclusion, taking into account the results mentioned above and the results obtained by other researchers who reported mutagenic activity of 2,4-dimethylaniline and 2,4,6-trimethylaniline in Salmonella typhimurium assay and in a DNA repair test using Chinese hamster hepatocytes, it can be stated that both aromatic amines are genotoxic. Teratogenesis Carcinog. Mutagen. 19:323-327, 1999., (Copyright 1999 Wiley-Liss, Inc.)

N-methylmorpholine, which is used as a catalyst in polyurethane foams producing, in solvents, stabilizing agents, and corrosion inhibitors, was administered to female rats by gavage at 100, 200, 600, and 900 mg/kg during organogenesis. It did not exhibit selective toxicity toward the developing conceptus. This compound administered to pregnant females was fetotoxic and teratogenic in the presence of maternal toxicity. N-methylmorpholine induced anophthalmia, internal hydrocephalus, and hydronephrosis but only at one dose which was also maternotoxic. Teratogenesis Carcinog. Mutagen. 19:369-376, 1999., (Copyright 1999 Wiley-Liss, Inc.)