Paternal occupational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and birth outcomes of offspring: birth weight, preterm delivery, and birth defects.
Agent Orange is a phenoxy herbicide that was contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). We studied pregnancy outcomes among wives of male chemical workers who were highly exposed to chemicals contaminated with TCDD and among wives of nonexposed neighborhood referents. For exposed pregnancies, we estimated serum TCDD concentration at the time of conception using a pharmacokinetic model. The mean TCDD concentration for workers' births was 254 pg/g lipid (range, 3-16,340 pg/g). The mean referent concentration of 6 pg/g was assigned to pregnancies fathered by workers before exposure. A total of 1,117 live singleton births of 217 referent wives and 176 worker wives were included. Only full-term births were included in the birth weight analysis (greater than or equal to 37 weeks of gestation). Mean birth weight among full-term babies was similar among referents' babies (n = 604), preexposure workers' babies (n = 221), and exposed workers' babies (n = 292) (3,420, 3,347, and 3,442 g, respectively). Neither continuous nor categorical TCDD concentration had an effect on birth weight for term infants after adjustment for infant sex, mother's education, parity, prenatal cigarette smoking, and gestation length. An analysis to estimate potential direct exposure of the wives during periods of workers' exposure yielded a nonstatistically significant increase in infant birth weight of 130 g in the highest exposure group (TCDD concentration > 254 pg/g) compared with referents (p = 0.09). Mothers' reports of preterm delivery showed a somewhat protective association with paternal TCDD (log) concentration (odds ratio = 0.8; 95% confidence interval, 0.6-1.1). We also include descriptive information on reported birth defects. Because the estimated TCDD concentrations in this population were much higher than in other studies, the results indicate that TCDD is unlikely to increase the risk of low birth weight or preterm delivery through a paternal mechanism. Key words: birth defects, birth weight, congenital anomalies, dioxin, occupation, paternal exposure, preterm birth, TCDD.
Lawson
Christina C
CC
National Institute for Occupational Safety and Health, 4676 Columbia Parkway (R-15), Cincinnati, OH 45226, USA. CJL(@cdc.gov
Schnorr
Teresa M
TM
Whelan
Elizabeth A
EA
Deddens
James A
JA
Dankovic
David A
DA
Piacitelli
Laurie A
LA
Sweeney
Marie H
MH
Connally
L Barbara
LB
D000328:Adult; D001724:Birth Weight; D016022:Case-Control Studies; D000013:Congenital Abnormalities / Q000209:etiology*; D004785:Environmental Pollutants / Q000493:pharmacokinetics / Q000506:poisoning*; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D016273:Occupational Exposure; D016017:Odds Ratio; D018812:Paternal Exposure; D000072317:Polychlorinated Dibenzodioxins / Q000493:pharmacokinetics / Q000506:poisoning*; D011247:Pregnancy; D047928:Premature Birth; D018570:Risk Assessment
D004785:Environmental Pollutants; D000072317:Polychlorinated Dibenzodioxins