Accumulating evidence suggests that outdoor air pollution may have a significant impact on central nervous system (CNS) health and disease. To address this issue, the National Institute of Environmental Health Sciences/National Institute of Health convened a panel of research scientists that was assigned the task of identifying research gaps and priority goals essential for advancing this growing field and addressing an emerging human health concern. Here, we review recent findings that have established the effects of inhaled air pollutants in the brain, explore the potential mechanisms driving these phenomena, and discuss the recommended research priorities/approaches that were identified by the panel.

Background Wheezing illnesses cause major morbidity in infants and are frequent precursors to asthma. Objective To examine environmental factors associated with recurrent wheezing in inner-city environments. Methods The Urban Environment and Childhood Asthma (URECA) study examined a birth cohort at high risk for asthma (n=560) in Baltimore, Boston, New York, and St. Louis. Environmental assessments included allergen exposure, and in a nested case-control study of 104 children, the bacterial content of house dust collected in the first year of life. Associations were determined among environmental factors, aeroallergen sensitization, and recurrent wheezing at age three. Results Cumulative allergen exposure over the first three years was associated with allergic sensitization, and sensitization at age three was related to recurrent wheeze. In contrast, first year exposure to cockroach, mouse and cat allergens was negatively associated with recurrent wheeze (OR 0.60, 0.65, and 0.75, p≤0.01). Differences in house-dust bacterial content in the first year, especially reduced exposure to specific Firmicutes and Bacteriodetes, was associated with atopy and atopic wheeze. Exposure to high levels of both allergens and this subset of bacteria in the first year of life was most common among children without atopy or wheeze. Conclusions In inner-city environments, children with the highest exposure to specific allergens and bacteria during their first year were least likely to develop recurrent wheeze and allergic sensitization. These findings suggest that concomitant exposure to high levels of certain allergens and bacteria in early life may be beneficial, and suggest new preventive strategies for wheezing and allergic diseases.

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Mechanisms linking violence and asthma morbidity need to be further explored.

▪ Abstract  The prevalence of asthma in the United States is higher than in many other countries in the world. Asthma, the most common chronic disease of childhood in the United States, disproportionately burdens many socioeconomically disadvantaged urban communities. In this review we discuss hypotheses for between-country disparities in asthma prevalence, including differences in “hygiene” (e.g., family size, use of day care, early-life respiratory infection exposures, endotoxin and other farm-related exposures, microbial colonization of the infant bowel, exposure to parasites, and exposure to large domestic animal sources of allergen), diet, traffic pollution, and cigarette smoking. We present data on socioeconomic and ethnic disparities in asthma prevalence and morbidity in the United States and discuss environmental factors contributing to asthma disparities (e.g., housing conditions, indoor environmental exposures including allergens, traffic air pollution, disparities in treatment and access to care, and cigarette smoking). We discuss environmental influences on somatic growth (low birth weight, prematurity, and obesity) and their relevance to asthma disparities. The relevance of the hygiene hypothesis to the U.S. urban situation is reviewed. Finally, we discuss community-level factors contributing to asthma disparities.

BackgroundDisproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated.ObjectivesWe aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology.MethodsWe developed geographic information systems (GIS)–based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology.ResultsCorrecting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO2 exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14–2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48–3.88). Of multiple exposure periods, year-of-diagnosis NO2 was most predictive of asthma outcomes.ConclusionsWe found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.

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While studies show that ultrafine and fine particles can be translocated from the lungs to the central nervous system, the possible neurodegenerative effect of air pollution remains largely unexplored. The authors examined the relation between black carbon, a marker for traffic particles, and cognition among 202 Boston, Massachusetts, children (mean age = 9.7 years (standard deviation, 1.7)) in a prospective birth cohort study (1986-2001). Local black carbon levels were estimated using a validated spatiotemporal land-use regression model (mean predicted annual black carbon level, 0.56 mug/m(3) (standard deviation, 0.13)). The Wide Range Assessment of Memory and Learning and the Kaufman Brief Intelligence Test were administered for assessment of cognitive constructs. In analysis adjusting for sociodemographic factors, birth weight, blood lead level, and tobacco smoke exposure, black carbon (per interquartile-range increase) was associated with decreases in the vocabulary (-2.2, 95% confidence interval (CI): -5.5, 1.1), matrices (-4.0, 95% CI: -7.6, -0.5), and composite intelligence quotient (-3.4, 95% CI: -6.6, -0.3) scores of the Kaufman Brief Intelligence Test and with decreases on the visual subscale (-5.4, 95% CI: -8.9, -1.9) and general index (-3.9, 95% CI: -7.5, -0.3) of the Wide Range Assessment of Memory and Learning. Higher levels of black carbon predicted decreased cognitive function across assessments of verbal and nonverbal intelligence and memory constructs.