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Christina C. Lawson,¹ Teresa M. Schnorr,¹ Elizabeth A. Whelan,¹ James A. Deddens,¹ David A. Dankovic,¹ Laurie A. Piacitelli,¹ Marie H. Sweeney,² and L. Barbara Connally¹

¹National Institute for Occupational Safety and Health, Cincinnati, Ohio, USA; ²Office of Global Health Affairs, Department of Health and Human Services, Hanoi, Vietnam

Abstract
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 ( 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. Environ Health Perspect 112:1403-1408 (2004) . doi:10.1289/ehp.7051 available via http://dx.doi.org/ [Online 23 June 2004]

Address correspondence to C.C. Lawson, National Institute for Occupational Safety and Health, 4676 Columbia Parkway (R-15) , Cincinnati, OH 45226 USA. Telephone: (513) 841-4171. Fax: (513) 841-4486. E-mail: CJL9@cdc.gov

We thank M. Fingerhut and J. Reefhuis for their scientific contributions and expertise. We also thank B. Jenkins and C. Gersic for their assistance in data collection and data management.

The authors declare they have no competing financial interests.

Received 23 February 2004 ; accepted 23 June 2004.