Environmental birth defects

Definition: Problems in fetal development related to environmental pollutants to which parents are exposed before conception or to which mothers are exposed during pregnancy

Embryotoxic agents encountered through environmental exposure can cause a variety of birth defects, ranging from growth retardation to malformations and death. The severity of any particular birth defect results from a combination of factors, including the gestational age at which the fetus is exposed to the agent and the effective dose of the toxic substance.

According to a 2006 report issued by the March of Dimes Foundation, roughly eight million of the world’s children are born with birth defects every year. The U.S. Centers for Disease Control and Prevention reports that birth defects affect about one in every thirty-three babies born in the United States annually, and that these babies account for more than 20 percent of the country’s infant deaths. Some birth defects are caused by environmental exposure to teratogens (substances that cause developmental malformations). According to the U.S. National Research Council, environmental exposures cause 3 percent of all birth defects and developmental disabilities; an interaction between genes and the environment may account for at least another 25 percent.

In the United States, the National Birth Defect Registry, assembled through responses to a questionnaire designed by Birth Defect Research for Children (formerly the Association of Birth Defect Children), details maternal and paternal exposure to environmental agents, including chemicals, radiation, pesticides, lead, and mercury. In March, 1998, the U.S. Congress passed the Birth Defects Prevention Act, which continued the National Birth Defects Prevention Study, a research project begun in 1996 to gather data on birth defects, including possible environmental causes.

Teratogenic Agents

Chemical agents known to cause environmental birth defects in animals and humans include compounds of heavy metals (especially mercury, lead, and thallium), urethane, dioxin-like chemicals, various steroids, sex hormones (including xenoestrogens and antiandrogenic pesticides), and trypan blue, an agent once used to treat mange. Chemical agents disturb intracellular chemistry; embryonic changes usually precede placental changes.

Testing of some agents has shown increases in the frequency of common malformations. For example, dioxin and similar chemicals have been observed to increase cleft palate and hydronephrosis (a swelling of the kidneys caused by obstructed urine flow) in mice. A minimum of two species of animals, studied at a minimum of three dose levels, is essential for teratogenic testing. Strong teratogenic agents usually produce similar malformations in different species. Agents that produce demonstrable birth defects in animals, especially in higher primates such as baboons, are presumed capable of producing birth defects in a human fetus.

Prenatal exposure to ionizing radiation is another environmental factor known to cause birth defects. For this reason, pregnant women are asked to inform radiologic technicians of their condition before X-ray sessions so that the technicians can minimize risk to the fetuses. Exposure to large, fluctuating electromagnetic fields (EMFs) has also been a suspected cause of environmental birth defects. Speculation that high-voltage electric power transmission lines might cause environmental birth defects or childhood cancer has led to many epidemiological studies using small mammals. Animal studies conducted over a number of years have not established any link between high-voltage lines and birth defects. Studies into the genotoxic potential (ability to alter genetic material) of EMFs have been conducted with bacteria, fruit flies, and mice. Although some cell research has suggested that EMF exposure may negatively affect the ability of cells to repair normal damage to genetic material, most evidence has suggested that EMF exposure is not genotoxic.

Examples

Clusters of environmental birth defects within human populations sometimes arise as a result of exposure of multiple persons to a release of a teratogenic agent, especially when the food chain is contaminated. When consumed by pregnant women, organic mercury is a potent teratogen. The best-known widespread occurrence of organic mercury poisoning took place in the 1950’s and early 1960’s in Japan’s Minamata Bay, where industrial effluents containing high levels of mercury were pumped into the ocean for many years. This mercury was assimilated into seafood consumed by the local population, resulting in many cases of congenital Minamata disease.

In contrast to the environmental health problems at Minamata Bay, which took years to emerge, damage to human health was immediately apparent in Bhopal, India, after the catastrophic December, 1984, industrial accident that released a lethal cloud of methyl isocyanate gas over a crowded shantytown. Some pregnant women spontaneously aborted upon exposure to the gas. A 1987 study found that, of a sample of 865 surviving pregnant women who lived within a kilometer (0.6 mile) of the accident site when the incident occurred, only 57 percent gave birth to live children. Of those babies, 14 percent died within a month of delivery, an infant mortality rate about five times greater than what was common in the community before the accident. Many were monstrously deformed. In the decades after the release, birth defects were common in children born to gas victims. These defects included cleft palate, joined or extra fingers, retarded growth, and mental problems. Soil and groundwater contamination from chemicals abandoned at the industrial site continues to poison area residents, giving rise to still more birth defects.

Use of chemical agents during wartime is also associated with widespread birth defects. Birth Defect Research for Children has collected data since 1990 concerning an elevated incidence of birth defects and developmental disabilities in the children of U.S. veterans of the Vietnam War. Heavy use of the dioxin-tainted defoliantAgent Orange in Vietnam is associated with a suite of deformities and ailments among the children of veterans. These include spina bifida; oral clefts; learning, attention, and behavioral disorders; and increased susceptibility to chronic childhood infections and to cancers later in life. Vietnamese researchers have found that, in comparison with background levels in their country, rates of birth defects are four times higher in areas that were sprayed with Agent Orange during the war.

Bibliography

Hansen, Deborah Kay, and Barbara D. Abbott, eds. Developmental Toxicology. 3d ed. New York: Informa Healthcare, 2009.

Moore, Keith L., and T. V. N. Persaud. Before We Are Born: Essentials of Embryology and Birth Defects. 7th ed. Philadelphia: Saunders/Elsevier, 2008.

Schardein, James L. Chemically Induced Birth Defects. 3d ed. New York: Marcel Dekker, 2000.

Shenoy, Rathika, and Nutan Kamath. “Teratogenicity of Environmental Pollutants: An Overview.” In Focus on Birth Defects Research, edited by Janet V. Engels. New York: Nova Science, 2006.

Yu, Ming-Ho. “Environmental Change and Health.” In Environmental Toxicology: Impacts of Environmental Toxicants on Living Systems. Boca Raton, Fla.: CRC Press, 2001.