Faculty Bibliography

To investigate whether hair dye use increases the risk of breast cancer, a case-control study was conducted among patients attending a screening center in New York City. The study group consisted of 398 breast cancer cases identified at the screening center between 1977 and 1981, and 790 randomly selected controls screened during the same period. Subjects were interviewed by telephone to obtain information on known risk factors for breast cancer, along with a complete history of hair dye use detailing type of dye, color, duration, frequency, and temporal periods of use. Most subjects (77%) had used hair dye at least once, 38% of the subjects at least 100 times. However, little increased risk of breast cancer was found among hair dye users. The adjusted odds ratio for ever having used hair dye was 0.8 (95% confidence interval 0.6-1.1), and there was no evidence of a trend in risk with increasing number of hair dye uses. The results were the same whether all past exposures were considered or only exposures more than 10 years before disease. Breast cancer risk did not increase with increasing intensity of exposure, as measured by frequency of use or darkness of color. No effect was seen for different types or colors of dye, or for use during different periods of reproductive life. Although personal hair dye use was unrelated to breast cancer risk, there was an adjusted odds ratio of 3.0 (95% confidence interval 1.1-7.8) for 5 or more years of work as a beautician. Overall, the results of this study, taken in conjunction with the findings of other epidemiologic studies, do not implicate hair dye use as an important cause of human breast cancer

A cohort study is under way in New York City to evaluate how levels of endogenous reproductive hormones influence the risk of breast cancer. The study, in which approximately 15,000 women are being recruited, utilizes a prospective design in which volunteers are asked to provide repeated specimens of serum during the period 1985-1992. A case-control study nested within the cohort is planned by which specimens from all cases arising in the population and from a randomly selected sample of time-matched controls will be analyzed and compared. As of December 31, 1989, 13,609 volunteers had donated blood specimens, about 50% of whom had already donated more than once. Of the 187 incident breast cancer cases who are expected to arise in the cohort before the end of 1992, 77 have been detected thus far

Some derivatives of nickel, cadmium, and cobalt are carcinogenic in humans and/or animals but their mechanisms of action are not known. We show that they are capable of stimulating human polymorphonuclear leukocytes (PMNs), as measured by H2O2 formation, a known tumor promoter. Most effective were the carcinogens nickel subsulfide, which caused a 550% net increase in H2O2 over that formed by resting PMNs, followed by cadmium sulfide, 400%, and nickel disulfide, 200%. Nickel sulfide and cobalt sulfide caused statistically nonsignificant increases of 45 and 20%, respectively. Noncarcinogenic barium and manganese sulfides, and sulfates of nickel, cadmium, and cobalt were inactive. The enhancement of H2O2 formation by CdS and Ni3S2 (1 mumol/2.5 x 10(5) PMNs) was comparable to that mediated by the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate, used at 0.5 and 1 nM, respectively. Concurrent treatment of 12-O-tetradecanoylphorbol-13-acetate-stimulated PMNs with Ni3S2 or NiS caused a decrease in H2O2 accumulation from that expected if the effects were additive. Including catalase in the reaction mixture proved that the oxidant formed by stimulated PMNs was H2O2, whereas adding superoxide dismutase showed that superoxide was also present in PMN samples treated with NiS but not with Ni3S2. Since nickel- and cadmium-containing particulates are deposited in the lungs and cause infiltration of PMNs, the ability to activate those cells and induce H2O2 formation may contribute to their carcinogenicity