The March of Dimes defines a birth defect as “an abnormality of structure, function or metabolism, whether genetically determined or as the result of an environmental influence during embryonic or fetal life” (Bloom, 1981). Other terms, often used interchangeably, are congenital anomaly and congenital malformation. Major birth defects, which occur in 2–3% of live births, are abnormalities that are present at birth that are severe enough to interfere with viability or physical well-being. Birth defects are detected in another 5% of babies during follow-up through the first year of life. The causes of most birth defects are unknown. Genetic factors, exposure to some medications, exposure to environmental contaminants, occupational exposures, and lifestyle factors have been implicated in the etiology of birth defects (Kalter and Warkany, 1983). Most etiologic research has focused on the effect of maternal and fetal exposures, but some work has addressed paternal exposures. Paternally mediated exposures might occur by several routes and exert effects in various ways. One way is through direct genetic damage to the male germ cell transmitted to the offspring and dominantly expressed as a birth defect. A hypothesized route is the transfer of toxic compounds through a man’s body into his seminal fluid, resulting in fetal exposure during gestation (Chia and Shi, 2002). Another more indirect route of paternally mediated exposure could arise from contact of family members with contamination brought into the home from the workplace.

Summary of VAO, Update 1996, Update 1998, Update 2000, and Update 2002

The committee responsible for Veterans and Agent Orange: Health Effects of Herbicides Used in Vietnam (hereafter, VAO; IOM, 1994) determined that there was inadequate or insufficient information to determine an association between exposure to 2,4-dichlorophenoxyacetic acid (2,4-D), 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) or its contaminant TCDD, picloram, or cacodylic acid and birth defects among offspring. Additional information available to the committee responsible for Veterans and Agent Orange: Update 1996 (hereafter, Update 1996; IOM, 1996) led it to conclude that there was limited or suggestive evidence of an association between at least one of the compounds of interest and spina bifida in the children of veterans; there was no change in the conclusions regarding other birth defects. Those findings were not modified further in Veterans and Agent Orange: Update 1998 (hereafter, Update 1998; IOM, 1999), Veterans and Agent Orange: Update 2000 (hereafter, Update 2000; IOM, 2001), or Veterans and Agent Orange: Update 2002 (hereafter, Update 2002; IOM, 2003).

Summaries of the studies of birth defects and neural tube defect specifically that were reviewed here and in earlier reports can be found in the Tables 7-1 and 7-2, respectively.

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