How can chemical compounds alter human fertility?

The effects of environmental toxins, such as pesticides, solvents and industrial waste, on human and animal health have caused much public fear. The suggested mechanism of action for these xenobiotics is their capacity to interact with steroid hormones receptors, in particular those for estrogens an...

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Bibliographic Details
Published in:European Journal of Obstetrics & Gynecology and Reproductive Biology 2002-01, Vol.100 (2), p.127-137
Main Authors: Massaad, Charbel, Entezami, Frida, Massade, Liliane, Benahmed, Mouhamed, Olivennes, François, Barouki, Robert, Hamamah, Samir
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Birth control
Chemical and industrial products toxicology. Toxic occupational diseases
Dioxin
Dioxins - adverse effects
Environmental Pollutants - adverse effects
Ethylene Glycol - adverse effects
Glycol ethers
Gynecology. Andrology. Obstetrics
Hormones - agonists
Humans
Infertility
Infertility - chemically induced
Medical sciences
Nuclear receptors
Propylene Glycol - adverse effects
Receptors, Androgen - drug effects
Receptors, Estrogen - drug effects
Sterility. Assisted procreation
Steroid hormones
Toxicology
Various organic compounds
Xenobiotics - adverse effects
Xenohormones
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Summary:The effects of environmental toxins, such as pesticides, solvents and industrial waste, on human and animal health have caused much public fear. The suggested mechanism of action for these xenobiotics is their capacity to interact with steroid hormones receptors, in particular those for estrogens and androgens. Concern was reinforced by the “historical” example of diethylstilbestrol, an estradiol mimetic causing genital cancer in girls exposed in utero. The real harm of these environmental xenobiotics is controversial. Some authors estimate that they do not reach sufficiently high concentrations to do damage and much experimental work has been done. In this review, we summarise the latest findings on the molecular mechanisms of action of three environmental toxicants, xenohormones, dioxin and glycol ethers and compare animal and cell experimental model data with epidemiological studies.
ISSN:0301-2115
1872-7654
DOI:10.1016/S0301-2115(01)00441-9