Cases included in a population-based case-control study of breast cancer in men were recruited from 10 geographic areas of the United States from 1983 to 1986. Controls, matched to cases on age and geographic area, were selected by random digit dialing for men under age 65 years and from Health Care Financing Administration files for older men. Results are based on responses from 227 cases and 300 controls to questions asked in a standardized personal interview. An increased risk of breast cancer was most strongly associated with undescended testes and was also related to orchiectomy, orchitis, testicular injury, late puberty, and infertility; and a decreasing trend in risk was observed with an increasing number of children. Relative risk estimates were also elevated in relation to a history of high blood cholesterol, rapid weight gain, benign breast conditions, and possibly obesity. These findings suggest that breast cancer in men develops in response to androgen deficiency associated with testicular dysfunction and under conditions associated with excess estrogen. Risk was also found to be elevated in men with a history of amphetamine use, diabetes, and cigar smoking and reduced in men with prior head trauma.
Data from a population-based case-control study of breast cancer in men were used to examine the hypothesis that occupational exposure to electromagnetic fields increases the risk of breast cancer. Incident cases (n = 227) diagnosed between 1983 and 1987 were obtained from 10 population-based cancer registries of the Surveillance, Epidemiology, and End Results program of the National Cancer Institute. Controls (n = 300) were selected by random digit dialing and from Medicare eligibility lists. Exposure status, defined as ever having been employed in a job which has been classified as involving potential exposure to electromagnetic fields, was assigned without knowledge of case/control status. An elevated risk was found for any job with exposure (odds ratio (OR) = 1.8, 95 percent confidence interval (CI) 1.0-3.7), and risk was highest among electricians, telephone linemen, and electric power workers (OR = 6.0, 95 percent CI 1.7-21) and radio and communications workers (OR = 2.9, 95 percent CI 0.8-10). Risk did not vary with duration of exposed employment. The risk was highest among subjects who were first employed in jobs with exposure before the age of 30 years and who were initially exposed at least 30 years prior to diagnosis. These results lend support to the theory that electromagnetic fields may be related to breast cancer in men. The hypothesis warrants evaluation in women.
A population-based case-control study of prostate cancer was performed in King County, Washington, in White men and Black men aged 40-64 years, between 1993 and 1996. Incident prostate cancer cases (n = 753) were identified from the Seattle-Puget Sound Surveillance, Epidemiology, and End Results (SEER) cancer registry. Controls (n = 703) were identified through random digit dialing and were frequency matched to cases on age. Sexual behavior, medical history, and other potential prostate cancer risk factors were ascertained through an in-person interview. There was no relation between sexual orientation and prostate cancer, although the number of men who had sex with men was small. Risk estimates increased directly with the lifetime number of female sexual partners (trend p < 0.001) but not with male partners (trend p = 0.62). Risk also increased with decreasing age at first intercourse, but this effect disappeared after adjusting for the number of female partners. Prior infection with gonorrhea was positively associated with risk (odds ratio = 1.50; 95% confidence interval: 1.0, 2.2), but no effect was seen among men with other sexually transmitted diseases. No relation between lifetime frequency of sexual intercourse and risk of prostate cancer was apparent. These findings are consistent with previous studies that support an infectious etiology for prostate cancer.
Previous laboratory investigations, case reports, and a hospital-based case-control study have suggested that marijuana use may be a risk factor for squamous cell head and neck cancer. We conducted a populationbased case-control study to determine whether marijuana use is associated with the development of oral squamous cell carcinoma (OSCC). Case subjects (n ؍ 407) were 18 -65-year-old residents of three counties in western Washington State who were newly diagnosed with OSCC from 1985 through 1995. Control subjects (n ؍ 615), who were similar to the cases with respect to age and sex, were selected from the general population using random-digit telephone dialing. Lifetime histories of marijuana use and exposure to known OSCC risk factors were ascertained using a structured questionnaire. Information on genetic polymorphisms in glutathione S-transferase enzymes was obtained from assays on participant DNA. Odds ratios for associations with features of marijuana use were adjusted for sex, education, birth year, alcohol consumption, and cigarette smoking. A similar proportion of case subjects (25.6%) and control subjects (24.4%) reported ever use of marijuana (adjusted odds ratio, 0.9; 95% confidence interval, 0.6 -1.3). There were no trends in risk observed with increasing duration or average frequency of use or time since first or last use. No subgroup defined by known or suspected OSCC risk factors (age, cigarette smoking, alcohol consumption, and genetic polymorphisms) showed an increased risk. Marijuana use was not associated with OSCC risk in this large, population-based study.
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