Lead and cancer in humans: Where are we now?

Background Lead is only weakly mutagenic, but in vitro it inhibits DNA repa ir and acts synergistically with other mutagens. Lead acetate administered orally, cutaneously, or intraperitoneally causes kidney cancel; brain cance r (gliomas), and lung cancer in rodents, and acts synergistically with othe r carcinogens. Most cytogenetic studies of exposed workers have shown incre ases in chromosome aberrations or sister chromatid exchange, including some studies with positive-exposure response trends. There are eight studies of cancer mortality or incidence among highly exposed workers; most are cohor t studies of lead smelter or battery workers exposed decades ago. Methods We reviewed the epidemologic studies with regard to cancel: Results These studies provide some evidence of increased risk of lung cance r (RR = 1.30, 1.15-1.46, 675 observed deaths) and stomach cancer (combined RR = 1.34 1.14-1.57, 181 observed). However; the lung cancer findings are n ot consistent across studies, and confounding by arsenic may affect the stu dy with the highest lung cancer RR. Exclusion of that study yields a combin ed lung cancer RR of 1.14 (1.04-1.73). There is little evidence of increase d risk of kidney cancer (combined RR = 1.01, 0.72-1.42, 40 observed) or bra in cancer (combined RR = 1.06, 0.81-1.40, 69 observed). However two studies show a two-fold increase in kidney cancer and one study shows a significan t excess of gliomas. IARC classified lead as a "possible human carcinogen" based on sufficient animal data and insufficient human data in 1987 Six of the eight studies cited above have been published since 1987 Conclusion Overall, there is only weak evidence associating lend with cance r; the most likely candidates are lung cancer stomach cancel; and gliomas. Am. J. Ind. Med. 38:295-299, 2000. Published 2000 Wiley-Liss, Inc.(dagger)