Critical Review. The effect of environmental pollutants on human reproduction, including birth defects.
The public has become more and more alarmed in recent years that inadvertent or careless exposure to chemicals in the environment might predispose birth defects or reproductive failure. Focus in this discussion is on chemicals in the workplace chemicals in the environment (from air pollution and from carelessly disposed materials that contaminate the land water supply or food chain) and food additives or contaminants. Attention is initially directed to a review of the concepts in teratology. Air pollutants commonly include those compounds produced by combustion of fossil fuels such as the oxides of nitrogen and sulfur and incompletely oxidized hydrocarbons such as carbon monoxide. The most serious source of air pollution to a pregnant woman is cigarette smoke because it exposes the unborn infant to high levels of carbon monoxide HCN cadmium nicotine and polycyclic aromatic compounds such as benzo (alpha) pyrene which can cross the placenta. Exposure to harmful gases may also follow from occupational exposures such as to ozone anesthetic gases or solvent vapors. Food additives are compounds knowingly added to food products to color preserve or enhance the taste of the product. In a broader context they may also include some natural constituents of food that have teratogenic potential as well as inadvertent additives or contaminants. These may be natural products contaminants of processing or residues either on grains or stored in animal tissues. A study of the effect of Red Dye No. 2 on Osborne Mendel rats reported a dose related embryotoxicity with both early and late deaths. No teratogenic effects were seen but it was also carcinogenic in rats. Subsequent studies in the same and other mammalian species revealed a mild tendency for preimplantation loss and increased embryo resorption. Herbst showed that infants exposed in utero to diethylstilbestrol (DES) suffered carcinogenic and teratogenic effects in the females and teratogenic effects in the males. Scientists reported in 1969 that DDT DDE lindane dieldrin and heptachlorepoxide were present in fetal cord blood and tissues of 10 stillborn infants in levels that were equal to that of adults and confirming the transplacental transfer of these compounds. Male sterility fetal loss and birth defects in their offspring was first recognized in the 1970s with exposure to Kepone and DBCP. To date compounds that decrease male fertility by toxic action on the testes and sperm include lead DBCP Kepone and cholroprene.