Several authors have considered the importance of exposure timing and how this affects the outcomes observed, but no one has systematically compiled preconceptional, prenatal, and postnatal developmental exposures and subsequent outcomes. Efforts were undertaken to examine the information available and to evaluate implications for risk assessment for several areas: a) respiratory and immune systems, b) reproductive system, c) nervous system, d) cardiovascular system, endocrine system, and general growth, and e) cancer. Major conclusions from a workshop on "Critical Windows of Exposure for Children's Health" included a) broad windows of sensitivity can be identified for many systems but detailed information is limited; b) cross-species comparisons of dose to target tissue and better data on the exposure-dose-outcome continuum are needed; c) increased interaction among scientific disciplines can further understanding by using laboratory animal results in designing epidemiological studies and human data to suggest specific laboratory studies on mechanisms and agent-target interactions; and d) thus far, only limited attention has been given to peripubertal/adolescent exposures, adult consequences of developmental exposures, and genome-environment interactions. More specific information on developmental windows will improve risk assessment by identifying the most sensitive window(s) for evaluation of dose-response relationships and exposure, evaluation of biological plausibility of research findings in humans, and comparison of data across species. In public health and risk management, information on critical windows may help identify especially susceptible subgroups for specific interventions.

Black girls on average enter puberty first, followed by Mexican American and then white girls.

A population-based case-control study investigated the association between maternal exposure to air pollutants, carbon monoxide, nitrogen dioxide, ozone, sulfur dioxide, and particulate matter <10 microm in aerodynamic diameter during weeks 3-8 of pregnancy and the risk of selected cardiac birth defects and oral clefts in livebirths and fetal deaths between 1997 and 2000 in seven Texas counties. Controls were frequency matched to cases on year of birth, vital status, and maternal county of residence at delivery. Stationary monitoring data were used to estimate air pollution exposure. Logistic regression models adjusted for covariates available in the vital record. When the highest quartile of exposure was compared with the lowest, the authors observed positive associations between carbon monoxide and tetralogy of Fallot (odds ratio = 2.04, 95% confidence interval: 1.26, 3.29), particulate matter <10 microm in aerodynamic diameter and isolated atrial septal defects (odds ratio = 2.27, 95% confidence interval: 1.43, 3.60), and sulfur dioxide and isolated ventricular septal defects (odds ratio = 2.16, 95% confidence interval: 1.51, 3.09). There were inverse associations between carbon monoxide and isolated atrial septal defects and between ozone and isolated ventricular septal defects. Evidence that air pollution exposure influences the risk of oral clefts was limited. Suggestive results support a previously reported finding of an association between ozone exposure and pulmonary artery and valve defects.