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Is maternal smoking during pregnancy a causal environmental risk factor for adolescent antisocial behavior? Testing etiological theories and assumptions

  • B. M. D'Onofrio (a1), C. A. Van Hulle (a2), J. A. Goodnight (a3), P. J. Rathouz (a2) and B. B. Lahey (a4)...

Although many studies indicate that maternal smoking during pregnancy (SDP) is correlated with later offspring antisocial behavior (ASB), recent quasi-experimental studies suggest that background familial factors confound the association. The present study sought to test alternative etiological hypotheses using multiple indices of adolescent ASB, comparing differentially exposed siblings, and testing assumptions in the sibling-comparison design.


The study examined the association between maternal SDP and adolescent-reported ASB, criminal convictions and membership in a group of individuals with early-starting and chronic ASB among 6066 offspring of women from the National Longitudinal Survey of Youth, a representative sample of women in the USA. The analyses controlled for statistical covariates and examined associations while comparing differentially exposed siblings.


At the population level, each additional pack of cigarettes per day predicted greater mean adolescent-reported ASB symptoms [ratio of means 1.15, 95% confidence interval (CI) 1.08–1.22], odds of being in the top 10% of ASB [odds ratio (OR) 1.34, 95% CI 1.10–1.65], hazard of a criminal conviction [hazard ratio (HR) 1.51, 95% CI 1.34–1.68] and odds of chronic ASB (OR 1.57, 95% CI 1.25–1.99). SDP robustly predicted most assessments of ASB while controlling for measured covariates. When siblings exposed to differing levels of SDP were compared, however, all of the associations were attenuated and were not statistically significant: adolescent-reported mean ASB (ratio of means 0.86, 95% CI 0.74–1.01), high ASB (OR 0.67, 95% CI 0.41–1.12), criminal conviction (HR 0.98, 95% CI 0.66–1.44) and chronic ASB (OR 0.80, 95% CI 0.46–1.38).


The results strongly suggest that familial factors account for the correlation between SDP and offspring adolescent ASB, rather than a putative causal environmental influence of SDP.

Corresponding author
*Address for correspondence: B. M. D'Onofrio, Ph.D., Department of Psychological and Brain Sciences, Indiana University, 1101 East 10th Street, Bloomington, IN 47405, USA. (Email:
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