Congenital anomalies, a leading cause of fetal loss, contribute significantly to preterm birth and childhood and adult morbidity. Serious structural defects are present in 3-8% of newborns worldwide and, while some can readily be attributed to chromosomal or syndromic disorders or known teratogenic or fetotoxic agents, a recent commentary maintained that causes for most anomalies remain a mystery.1 Maternal smoking during pregnancy has long been associated with birth defects2 and numerous biologic pathways have been identified whereby particulate air pollutants might impact the placenta and fetus (reviewed in Kannan3) providing biologic rationale to the assessment of air pollution’s influence on fetal development. Although quantitatively lower than exposure from maternal smoking, exposure to ambient air toxics affects large populations and, importantly, is not modifiable by the individual; and thus of great public health and policy relevance.
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