Urinary excretion of porphyrins by smelter workers chronically exposed to arsenic dust.

Urinary arsenic (inorganic arsenic and methylated metabolites), uroporphyrin and coproporphyrin I and III isomers were determined in 84 smelter workers exposed to arsenic trioxide and in 22 non-exposed controls. Both 'high' and 'low' exposure groups were defined, based on individual's work area (arsenic recovery plant and maintenance) and mean urinary excretion of arsenic was compared to the control group (257 and 129 micrograms/g creatinine against 9.9 micrograms/g creatinine). Total coproporphyrin (I+III) increased in each exposure group as compared to control (63.3 and 59 micrograms/g creatinine against 27.2 micrograms/g creatinine), as a consequence of a 2-fold increase in each coproporphyrin isomer. The mean concentration of uroporphyrin in each exposure group was very similar to that of the non-exposed controls (9.5 and 8.8 micrograms/g creatinine against 10.7 micrograms/g creatinine). These results suggest that long-term occupational exposure of humans to arsenic is associated with coproporphyrinuria and raise the question of the use of this parameter in addition to urinary arsenic for biological monitoring.

A retrospective mortality study of workers exposed to arsenic in a gold mine and refinery in France.

A historical mortality study of a cohort of employees of a gold mining and refining company was carried out in Salsigne, France. A major goal of the study was to investigate the relationship between lung cancer mortality and exposure to arsenic, radon, silica, and other contaminants of the working environment. A twofold excess of lung cancer was found both among miners and smelters, mainly concentrated among workers who had experienced exposure to past levels of arsenic, radon, and silica. The consistency of the results in the mine and the refinery are suggestive of a carcinogenic risk from both soluble and insoluble arsenic, although the potential role of other factors cannot be dismissed.

Benzene exposure in car mechanics and road tanker drivers.

The purpose of this study was to identify professional factors related to benzene exposure and to deduce suitable safety measures. Atmospheric benzene, urinary muconic acid (tt-MA) and leukocyte alkaline phosphatase activity (LAPA) were evaluated among 66 car mechanics, 34 road tanker drivers, and 28 nonexposed workers. Professional and medical questionnaires were filled in at the same time. Atmospheric benzene was significantly higher among road tanker drivers than among car mechanics. The arithmetic mean +/- SD, median, and geometric mean values were, respectively, 0.48 +/- 1.49, 0.14, and 0.06 mg/m3 among car mechanics and 1.88 +/- 4.18, 0.68, and 0.65 mg/m3 among road tanker drivers. In the latter case the increase was caused by transport of unleaded petrol and correlated with the volume of the tank. Among car mechanics, tobacco smoking, windy conditions, dismantling of petrol filters, and handling of petrol increased atmospheric benzene levels. Urinary muconic acid was increased significantly among car mechanics (148 +/- 137, 127, and 111 micrograms/g) and among road tanker drivers (309 +/- 420, 137, and 151 micrograms/g) as compared with the controls (49 +/- 46, 33, and 33 micrograms/g). Among road tanker drivers, alcohol intake and transportation of unleaded petrol increased the excretion of muconic acid, which was also directly related to the volume of the tank. Among car mechanics, professional factors (dismantling of petrol filters, handling of and washing of hands with petrol) and nonprofessional factors (tobacco smoking and damaged skin on the hands and forearms) increased muconic acid excretion. In the control group, tobacco smoking increased its excretion. LAPA was not significantly modified among exposed workers. There was a weak but significant linear correlation between LAPA and muconic acid. These results suggest that to reduce exposure to benzene in unleaded petrol, individual and collective safety measures should be imposed in both occupations.