PubMed · 3853118
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G McMillan. 1985. Meet the welding processes.. https://pubmed.ncbi.nlm.nih.gov/3853118/
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The exposure to polycyclic aromatic hydrocarbons (PAH) was measured in a Finnish coking plant over a 7-year period (1988-1994), since the beginning of production. Hygienic measurements including dust and vapour sampling were performed and the correlations between the concentrations of airborne pyrene with the levels of pyrene metabolite 1-pyrenol in urine were calculated. The profile of measured 12 or 15 PAHs was very similar between mean concentrations of personal samples, which suggests that it is possible to calculate the concentrations of total PAH by using e.g. pyrene as a marker compound. Measurements suggest that the progress of working conditions has been very favourable because the mean exposure level of shift workers to benzo[a]pyrene has decreased from 2.5 micrograms/m3 to 0.3 micrograms/m3. This points to successful measures of technical prevention. The mean concentration of 1-pyrenol in urine has been 0.2-0.6 mumol/mol creatinine. The concentration increases slightly towards the end of the working day, but the correlation urinary pyrenol and air pyrene was weak. Therefore the usefulness of pyrenol level for predicting the pyrene concentration at low exposure level in the ambient air is very limited.
Two large data bases accumulated from the 1980s at the Finnish Institute of Occupational Health, one with results on urinary chromium and nickel analyses and the other with results on total and hexavalent chromium and nickel, were compiled and analysed in order to clarify the occupational exposure during the 1980s, and to reveal possible trends in the exposure of workers in different jobs. The data were processed in three batches: years 1980-1982, 1983-1985 and 1986-1989. The median values of urinary chromium exceeded the biomonitoring action level, BAL, in metal workers, and the mean values exceeded the BAL in both metal workers and plasma cutters. Among all worker groups the median values of urinary chromium remained quite stable during the study period. The median values of urinary nickel concentration did not exceed the BAL in any worker group studied, but an increasing trend was observed among moulders. In the breathing zone of grinders, the median value of total or trivalent chromium exceeded the occupational exposure limit, OEL. The medial of hexavalent chromium concentration in the breathing zone of metal sprayers and spray painters was higher than the OEL. No decreasing trend in exposure could be observed during the 10-year period in breathing zone air.
Previous work suggested that arsine- (AsH3-) induced hemoglobin (HbO2) damage may lead to hemolysis (Hatlelid et al., 1996). The purpose of the work presented here was to determine whether reactive oxygen species are formed by AsH3 in solution, in hemoglobin solutions, or in intact red blood cells, and, if so, to determine whether these species are responsible for the observed hemoglobin damage. Hydrogen peroxide (H2O2) was detected in aqueous solutions containing AsH3 and HbO2 or AsH3 alone but not in intact red blood cells or lysates. Additionally, high-activity catalase (19,200 U/ml) or glutathione peroxidase (68 U/ml) added to solutions of HbO2 and AsH3 had only a minor protective effect against AsH3-induced damage. Further, the differences between the visible spectra of AsH3-treated HbO2 and H2O2-treated HbO2 indicate that two different degradative processes occur. The presence of superoxide anion (O2-) was measured by O2(-)-dependent reduction of nitro blue tetrazolium (NBT). The results were negative for O2-. Exogenous superoxide dismutase (100 micrograms/ml) did not affect AsH3-induced HbO2 spectral changes, nor did the hydroxyl radical scavengers, mannitol, and DMSO (20 mM each). The general antioxidants ascorbate (< or = 10 mM) and glutathione (< or = 1 mM) also had no effect. These results indicate that the superoxide anion and the hydroxyl radical (OH) are not involved in the mechanism of AsH3-induced HbO2 damage. The results also indicate that although AsH3 contributes to H2O2 production in vitro, cellular defenses are adequate to detoxify the amount formed. An alternative mechanism by which an arsenic species is the hemolytic agent is proposed.