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Background: Early life exposure to air pollution has been linked with cognitive impairment in children, but the results have not been conclusive. We analyzed the association between traffic-related air pollution and cognitive function in a prospective birth cohort in Rome., Methods: A cohort of 719 newborns was enrolled in 2003-2004 as part of the GASPII project. At age 7 years, 474 children took the Wechsler Intelligence Scale for Children-III to assess their cognitive development in terms of IQ composite scores. Exposure to air pollutants (NO2, PMcoarse, PM2.5, PM2.5 absorbance) at birth was assessed using land use regression models. We also considered variables indicating traffic intensity. The effect of environmental pollution on IQ was evaluated performing a linear regression model for each outcome, adjusting for gender, child age at cognitive test, maternal age at delivery, parental educational level, siblings, socio-economic status, maternal smoking during pregnancy, and tester. To account for selection bias at enrollment and during follow-up, the regression models were weighted for the inverse probabilities of participation and follow-up., Results: A 10 μg/m³ higher NO2 exposure during pregnancy was associated with 1.4 fewer points (95% confidence interval = -2.6, -0.20) of verbal IQ, and 1.4 fewer points (95% confidence interval = -2.7, -0.20) of verbal comprehension IQ. Similar associations were found for traffic intensity in a 100 m buffer around home. Other pollutants showed negative associations with larger confidence intervals., Conclusions: Consistent with previous evidence, this study suggests an association of exposure to NO2 and traffic intensity with the verbal area of cognitive development.See Video Abstract at http://links.lww.com/EDE/B12.

Stress is the main non-genetic source of psychopathology. Therefore, the identification of neurobiological bases of resilience, the resistance to pathological outcomes of stress, is a most relevant topic of research. It is an accepted view that resilient individuals are those who do not develop helplessness, or other depression-like phenotypes, following a history of stress. In the present review, we discuss the phenotypic differences between mice of the inbred C57BL/6J and DBA/2J strains that could be associated with the strain-specific resistance to helplessness observable in DBA/2J mice. The reviewed results support the hypothesis that resilience to stress-promoted helplessness develops through interactions between a specific genetic makeup and a history of stress, and is associated with an active coping style, a bias toward the use of stimulus-response learning, and specific adaptive changes of mesoaccumbens dopamine transmission under stress. Finally, evidence that compulsivity represents a side effect of the neuroadaptive processes fostering resistance to develop depressive-like phenotypes under stress is discussed.