duction. These authors found that among 479 male workers, as the serum concentration of 2,3,7,8-TCDD increased, so did the odds of having a high level of LH or FSH; the odds of having a low testosterone level also increased with the concentration of TCDD. A study of women from Seveso is in progress (Eskenazi et al., 2000). This investigation will examine serum TCDD concentration in relation to (1) endometriosis, (2) menstrual cycle characteristics, (3) age at menarche, (4) birth outcomes, (5) time to conception and infertility, and (6) age at menopause.
The following specific categories of reproductive effects have been reviewed in previous Veterans and Agent Orange (VAO) reports (IOM, 1994, 1996, 1999): fertility, sex ratio, spontaneous abortion, stillbirth and infant mortality, low birthweight and preterm delivery, and birth defects. New data since Update 1998 are available for spontaneous abortion, sex ratio, birth defects, childhood cancer, low birthweight, and early postnatal growth.
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 with birth defects are “congenital anomalies” and “congenital malformations.” Major birth defects are usually defined as those abnormalities that are present at birth and severe enough to interfere with viability or physical well-being. Major birth defects are seen in approximately 2 to 3 percent of live births. An additional 5 percent of birth defects can be detected with follow-up through the first year of life. The cause of most birth defects is unknown. In addition to genetic factors, a number of other factors and exposures including medication, environmental, occupational, and life-style have long been implicated in the etiology of some birth defects (Kalter and Warkany, 1983). Historically, most etiologic research focused on the effect of maternal and fetal exposures, but work on paternal exposures is receiving increased attention. Paternal exposures could exert an effect through direct genetic damage to the male germ cell that is transmitted to the offspring and expressed as a birth defect; through transfer of chemicals via seminal fluid, with subsequent fetal exposure; or by indirect exposure from household contamination.
The committee responsible for VAO found there to be inadequate or insufficient information to determine whether an association existed between exposure to herbicides used in Vietnam or the contaminant dioxin and birth defects among