EFFECTS OF ENVIRONMENTAL SYNTHETIC CHEMICALS ON THYROID-FUNCTION

Authors
Citation
F. Bruckerdavis, EFFECTS OF ENVIRONMENTAL SYNTHETIC CHEMICALS ON THYROID-FUNCTION, Thyroid, 8(9), 1998, pp. 827-856
Citations number
362
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
10507256
Volume
8
Issue
9
Year of publication
1998
Pages
827 - 856
Database
ISI
SICI code
1050-7256(1998)8:9<827:EOESCO>2.0.ZU;2-U
Abstract
Synthetic chemicals are released into the environment by design (pesti cides) or as a result of industrial activity. It is well known that na tural environmental chemicals can cause goiter or thyroid imbalance. H owever, the effects of synthetic chemicals on thyroid function have re ceived little attention, and there is much controversy over their pote ntial clinical impact, because few studies have been conducted in huma ns. This article reviews the literature on possible thyroid disruption in wildlife, humans, and experimental animals and focuses on the most studied chemicals: the pesticides DDT, amitrole, and the thiocarbamat e family, including ethylenethiourea, and the industrial chemicals pol yhalogenated hydrocarbons, phenol derivatives, and phthalates. Wildlif e observations in polluted areas clearly demonstrate a significant inc idence of goiter and/or thyroid imbalance in several species. Experime ntal evidence in rodents, fish, and primates confirms the potentiality for thyroid disruption of several chemicals and illustrates the mecha nisms involved. In adult humans, however, exposure to background level s of chemicals does not seem to have a significant negative effect on thyroid function, while exposure at higher levels, occupational or acc idental, may produce mild thyroid changes. The impact of transgenerati onal, background exposure ill utero on fetal neurodevelopment and late r childhood cognitive function is now under scrutiny. There are severa l studies linking a lack of optimal neurological function in infants a nd children with high background levels of exposure to polychlorinated biphenyls (PCBs), dioxins, and/or co-contaminants, but it is unclear if the effects are caused by thyroid disruption in utero or direct neu rotoxicity.