Oestrogenic and antiandrogenic chemicals in the environment: effects on male reproductive health.
Exposures of human populations to pesticides and industrial pollutants, and to synthetic chemicals present in foods, beverages, and plastics, have raised concern that these substances can interfere with endogenous sex hormone function. Interference with sex hormone action can, in turn, result in a variety of developmental and reproductive anomalies. Compounds in this class are thus referred to as endocrine disruptors (EDs). EDs that affect reproductive processes in vertebrates act primarily by altering oestrogenic and antiandrogenic activities. The recent cloning of a second oestrogen receptor (ER) subtype (ERbeta) and its widespread tissue distribution pattern indicates that the first ER to be cloned, ERalpha, may not be the only, or even the primary, mediator of oestrogen action. It is anticipated that this discovery will lead to development of antagonist compounds specific to either ER subtype, and help to determine the function of each receptor subtype in reproductive and other tissues. Growing evidence suggests that EDs interfere with reproductive function at low exposure levels and cause distinct effects at different concentrations within the same organ. Developing organisms have increased susceptibility to the actions of EDs because differentiating tissues are more vulnerable to changes in hormonal milieu. Thus, children are at greater risk of toxicant-related illnesses than adults. However, most data are collected from laboratory studies, and it remains to be determined that the levels of chemicals in the environment can impair human reproductive health. There is also significant genetic variability between human and animal species in their reactions to chemicals. The effects of low-dose, chronic, and multiple chemical exposures warrant further investigation in order to characterize the risk of environmental agents to humans. The aims of this review, which will focus on male reproduction, are to: 1) identify synthetic chemicals in the environment that fall into the ED class; 2) describe their mechanisms of toxicity in reproductive tissues; and, 3) outline the direction of future research efforts with respect to EDs.
Akingbemi
B T
BT
Center for Biomedical Research, Population Council, New York, NY 10021, USA.
Hardy
M P
MP
D000728:Androgens / Q000502:physiology; D004781:Environmental Exposure; D004967:Estrogens / Q000502:physiology; D005298:Fertility / Q000187:drug effects* / Q000502:physiology*; D005837:Genitalia, Male / Q000187:drug effects; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology; D008297:Male; D011960:Receptors, Estrogen / Q000819:agonists; D012733:Sex Differentiation / Q000502:physiology; D013091:Spermatogenesis / Q000502:physiology; D013736:Testicular Neoplasms / Q000503:physiopathology
D000728:Androgens; D004967:Estrogens; D011960:Receptors, Estrogen