Fertility and sterility · 1998
Environmental toxicants and female reproduction.
СтатьяПоддержка исследования: вне правительства СШАОбзорНазвание и аннотация: Перевод в очереди
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Sharara F I, Seifer D B, Flaws J A
Аннотация
OBJECTIVE: To review current knowledge on the potential effects of environmental toxicants on female reproduction in laboratory animals, wildlife, and humans.
DESIGN: Published literature about the effects of endocrine disruptors, heavy metals, solvents, pesticides, plastics, industrial chemicals, and cigarette smoke on female reproduction.
RESULT(S): Published data indicate that chemical exposures may cause alterations in reproductive behavior and contribute to subfecundity, infertility, pregnancy loss, growth retardation, intrauterine fetal demise, birth defect, and ovarian failure in laboratory animals and wildlife. Data on the association of chemical exposures and adverse reproductive outcomes in humans are equivocal and often controversial. Some studies indicate that chemical exposures are associated with infertility, spontaneous abortion, or reproductive cancer in women. In contrast, other studies indicate that there is no association between chemical exposures and adverse reproductive outcomes. The reasons for ambiguous findings in human studies are unknown but likely include the fact that many studies are limited by multiple confounders, inadequate methodology, inappropriate endpoints, and small sample size. The mechanism by which chemicals alter reproductive function in all species is complex and may involve hormonal and/or immune disruption, DNA adduct formation, altered cellular proliferation, or inappropriate cellular death.
CONCLUSION(S): Studies are needed to clarify which toxicants affect human reproduction and by which mechanisms of action. Furthermore, methods should be developed to minimize exposure to known reproductive toxicants such as dioxins and cigarette smoke.
DESIGN: Published literature about the effects of endocrine disruptors, heavy metals, solvents, pesticides, plastics, industrial chemicals, and cigarette smoke on female reproduction.
RESULT(S): Published data indicate that chemical exposures may cause alterations in reproductive behavior and contribute to subfecundity, infertility, pregnancy loss, growth retardation, intrauterine fetal demise, birth defect, and ovarian failure in laboratory animals and wildlife. Data on the association of chemical exposures and adverse reproductive outcomes in humans are equivocal and often controversial. Some studies indicate that chemical exposures are associated with infertility, spontaneous abortion, or reproductive cancer in women. In contrast, other studies indicate that there is no association between chemical exposures and adverse reproductive outcomes. The reasons for ambiguous findings in human studies are unknown but likely include the fact that many studies are limited by multiple confounders, inadequate methodology, inappropriate endpoints, and small sample size. The mechanism by which chemicals alter reproductive function in all species is complex and may involve hormonal and/or immune disruption, DNA adduct formation, altered cellular proliferation, or inappropriate cellular death.
CONCLUSION(S): Studies are needed to clarify which toxicants affect human reproduction and by which mechanisms of action. Furthermore, methods should be developed to minimize exposure to known reproductive toxicants such as dioxins and cigarette smoke.