Absence of significant genotoxicity in lymphocytes and urine from workers exposed to moderate levels of cobalt-containing dust: A cross-sectional study

Mortality studies have shown that, in the past, lung cancer occurred after exposure to mixtures of cobalt metal and metallic carbide particles, the ma in constituents of hard metals, but apparently not when exposure was to cob alt alone. The major objective of this biomonitoring study was to assess ge notoxic effects as a measure for carcinogenic risk in workers From cobalt r efineries and hard metal plants currently exposed to the threshold limit va lue/time-weighted average (TLV-TWA) for cobalt-containing dust. The study c omprised three groups of workers: 35 workers exposed to cobalt dust From th ree refineries, 29 workers exposed to hard metal dust from two producing pl ants, and 35 matched control subjects recruited from the respective plants. The study design integrated complementary methodologies to assess biomarke rs of effects that represent both initial DNA damage (8-hydroxydeoxyguanosi ne [8-OHdG] in urine and comet assay on lymphocytes) and definitive chromos ome breakage/loss (micronuclei in lymphocytes). Cobalt and cotinine were de termined in urine as a measure for cobalt exposure and recent smoking, resp ectively. No significant increase of genotoxic effects was detected in work ers exposed to cobalt-containing dust as compared to controls. No differenc e in any genotoxicity biomarker was Found between workers exposed to cobalt and hard metal dusts. Multiple regression analysis indicated that workers who smoked and were exposed to hard metal dusts had elevated 8-OHdG and mic ronuclei valves. Because this observation is in line with a previous epidem iological study of an increased risk of dying from lung cancer in workers f rom the hard metal industry who smoked, it is concluded that this specific occupational group needs closer medical surveillance.. (C) 2000 Wiley-Liss, Inc.