markers. In particular, they also suggest that women have a higher susceptibility than men to lung cancer following exposure to tobacco.

DES has been used as a model of environmental estrogen, and there are reports of reproductive abnormalities in the male offspring of DES subjects, but there has been little tissue-specific study of the effects on the male. It may be that there are "windows of susceptibility" during development, and new studies will address susceptibility at different stages of pregnancy. In general, males appear to be less sensitive to estrogenic compounds, at least initially, but they have a very steep dose-response curve and an abrupt response at higher levels. This may be because androgen is protective in the male, whereas estrogen exaggerates adverse effects.

This review suggests five areas where further research is needed:

  1. inclusion of women in occupational studies and further identification of environmental risk factors;

  2. further clarification of gender differences in frequency of known markers of genetic susceptibility;

  3. evaluation of steroid receptor variants and susceptibility to environmental cancers;

  4. vigorous application of animal models to study underlying regulation of environmental carcinogenesis; and

  5. identification of biological causality between genetic susceptibility markers and gender-related human cancers.

TABLE B-5 Gender Differences in Cancer Susceptibility: Human Studies/Environmental Exposures

Tobacco-related cancers (ORs) (Zang and Wynder, 1996)

Lung (bronchogenic carcinoma)—female: 8.1, male: 4.6

Oral—female: 5.0, male: 2.0

Dioxin-related cancers (Seveso, Italy) (Landi et al., 1997).

—Men: Leukemia, esophageal, rectal

—Women: Liver, stomach, colon (decrease in breast cancer)

—Hodgkin's disease: Women > men

Pesticide exposure (Zahm et al., 1994)

—Non-Hodgkin's lymphoma: Women < men

—Soft-tissue sarcomas: Women < men

Pesticide-breast cancer controversy



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