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.