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IntroductionWildfire smoke (WFS) exposure is a growing threat to human health, and lower socioeconomic position (SEP) has been shown to increase pollution susceptibility. Studies of SEP-related susceptibility, however, are often compromised due to spatial confounding between lower-SEP and pollution. Here we examine outdoor-housed nonhuman primates, living in natural social hierarchy in a common location, born during years of high vs. low WFS, to examine the separate and combined effects of WFS and social rank, an analog to SEP, on lung and immune function.MethodsTwenty-one females were born during extreme WFS events in summer 2008; 22 were born in summer 2009, during low WFS. Pulmonary function and circulating cytokines were measured three years later, in adolescence. We estimated fine particulate (PM2.5) and ozone exposures during each animal's first 90 days and three years of age using regulatory data. Early-life social status was estimated using maternal rank at birth, as rank in females is relatively stable throughout life, and closely approximates mother's rank. We tested associations among WFS exposure, rank, and endpoints using linear regression and ANOVA.ResultsHigher WFS exposure in infancy was, on average, associated with lower functional residual capacity (FRC), residual volume (RV), tissue compliance (Ct), and IL-8 secretion in adolescence. Higher social rank conferred significantly higher expiratory reserve volume (ERV) and functional residual capacity (FRC) solely among those born in the high-WFS year (2008). Differences in effects of rank between years were not significant after adjustment for multiple comparisons.ConclusionsExposure to WFS in infancy generally conferred lower adolescent respiratory volumes and inflammatory cytokines. Higher rank conferred higher respiratory volumes only among females born during WFS, suggesting the possibility that the health benefits of rank may be more apparent under environmental challenge.

BackgroundAir pollution exposure is ubiquitous with demonstrated effects on morbidity and mortality. A growing literature suggests that prenatal air pollution exposure impacts neurodevelopment. We posit that the Environmental influences on Child Health Outcomes (ECHO) program will provide unique opportunities to fill critical knowledge gaps given the wide spatial and temporal variability of ECHO participants.ObjectivesWe briefly describe current methods for air pollution exposure assessment, summarize existing studies of air pollution and neurodevelopment, and synthesize this information as a basis for recommendations, or a blueprint, for evaluating air pollution effects on neurodevelopmental outcomes in ECHO.MethodsWe review peer-reviewed literature on prenatal air pollution exposure and neurodevelopmental outcomes, including autism spectrum disorder, attention deficit hyperactivity disorder, intelligence, general cognition, mood, and imaging measures. ECHO meta-data were compiled and evaluated to assess frequency of neurodevelopmental assessments and prenatal and infancy residential address locations. Cohort recruitment locations and enrollment years were summarized to examine potential spatial and temporal variation present in ECHO.DiscussionWhile the literature provides compelling evidence that prenatal air pollution affects neurodevelopment, limitations in spatial and temporal exposure variation exist for current published studies. As >90% of the ECHO cohorts have collected a prenatal or infancy address, application of advanced geographic information systems-based models for common air pollutant exposures may be ideal to address limitations of published research.ConclusionsIn ECHO we have the opportunity to pioneer unifying exposure assessment and evaluate effects across multiple periods of development and neurodevelopmental outcomes, setting the standard for evaluation of prenatal air pollution exposures with the goal of improving children's health.

In order to develop effective strategies to address noise annoyance, it is essential to develop an explanatory model of the psychological mechanism(s) by which noise becomes annoying. Two online studies were conducted in which a total of 193 participants completed speech perception tasks with varying degrees of background noise. Signal-to-noise ratio levels ranged from −2 to −10 dB. The crucial manipulation in both experiments concerned participants' sense of control over the noise level in the task. Dependent measures were task performance, a self-reported measure of frustration with the task, and self-reported sensitivity (trait) to noise. Results showed small but significant effects of noise sensitivity and sense of control on subjective frustration. In both experiments, more noise-sensitive individuals expressed greater frustration than did those reporting less noise sensitivity. In addition, in experiment 2 there was a significant interaction between sense of control and noise level. Listeners under the higher noise-level conditions expressed relatively similar degrees of frustration irrespective of their sense of control, while those under the lower noise-level condition showed lower frustration with greater sense of control. Results support Stallen's [(1999). Noise Health 1(3), 69–79] theoretical framework of noise annoyance, but also suggest the need for further research under more ecologically plausible conditions. [ABSTRACT FROM AUTHOR]

Introduction Studies in the United States and elsewhere have reported that long-term exposures to air pollution (AP) are associated with increased risk of all-cause (Dockery et al. 1993; Laden et [...], Background: Despite a vast air pollution epidemiology literature to date and the recognition that lower-socioeconomic status (SES) populations are often disproportionately exposed to pollution, there is little research identifying optimal means of adjusting for confounding by SES in air pollution epidemiology, nor is there a strong understanding of biases that may result from improper adjustment. Objective: We aim to provide a conceptualization of SES and a review of approaches to its measurement in the U.S. context and discuss pathways by which SES may influence health and confound effects of air pollution. We explore bias related to measurement and operationalization and identify statistical approaches to reduce bias and confounding. Discussion: Drawing on the social epidemiology, health geography, and economic literatures, we describe how SES, a multifaceted construct operating through myriad pathways, may be conceptualized and operationalized in air pollution epidemiology studies. SES varies across individuals within the contexts of place, time, and culture. Although no single variable or index can fully capture SES, many studies rely on only a single measure. We recommend examining multiple facets of SES appropriate to the study design. Furthermore, investigators should carefully consider the multiple mechanisms by which SES might be operating to identify those SES indicators that may be most appropriate for a given context or study design and assess the impact of improper adjustment on air pollution effect estimates. Last, exploring model contraction and expansion methods may enrich adjustment, whereas statistical approaches, such as quantitative bias analysis, may be used to evaluate residual confounding. https://doi.org/10.1289/EHP7980

Introduction Exposure to airborne fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 [micro]m ([PM.sub.2.5])] has been associated with increased risk of cardiopulmonary diseases, and [...], Background: Chronic exposure to air pollution may prime the immune system to be reactive, increasing inflammatory responses to immune stimulation and providing a pathway to increased risk for inflammatory diseases, including asthma and cardiovascular disease. Although long-term exposure to ambient air pollution has been associated with increased circulating markers of inflammation, it is unknown whether it also relates to the magnitude of inflammatory response. Objectives: The aim of this study was to examine associations between chronic ambient pollution exposures and circulating and stimulated levels of inflammatory mediators in a cohort of healthy adults. Methods: Circulating interleukin (IL)-6, C-reactive protein (CRP) (n = 392), and lipopolysaccharide stimulated production of IL-1[beta], IL-6, and tumor necrosis factor (TNF)-[alpha] (n = 379) were measured in the Adult Health and Behavior II cohort. Fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 [micro]m ([PM.sub.2.5])] and constituents [black carbon (BC), and lead (Pb), manganese (Mn), zinc (Zn), and iron (Fe)] were estimated for each residential address using hybrid dispersion land use regression models. Associations between pollutant exposures and inflammatory measures were examined using linear regression; models were adjusted for age, sex, race, education, smoking, body mass index, and month of blood draw. Results: There were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to [PM.sub.2.5] and BC with stimulated production of IL-6, IL-1[beta], and TNF-[alpha]. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1[beta] and TNF-[alpha]. No pollutants were associated with circulating IL-6 or CRP levels. Discussion: Exposure to [PM.sub.2.5], BC, Pb, Mn, Fe, and Zn was associated with increased production of inflammatory mediators by stimulated immune cells. In contrast, pollutant exposure was not related to circulating markers of inflammation. These results suggest that chronic exposure to some pollutants may prime immune cells to mount larger inflammatory responses, possibly contributing to increased risk for inflammatory disease. https://doi.org/10.1289/EHP7089

Aims. We examine the association between high ambient temperature and acute mental health-related healthcare encounters in New York City for children, adolescents and young adults. Methods. This case-crossover study included emergency department (ED) visits and hospital encounters with a primary diagnosis of any mental health disorder during warm-season months (June-August) in New York City from 2005 to 2011 from patients of three age groups (6-11, 12-17 and 18-25 years). Using a distributed lag non-linear model over 0-5 lag days, by fitting a conditional logistic regression for each age group, we calculated the cumulative odds ratios of mental health encounters associated with an elevated temperature. Analyses were stratified by race/ethnicity, payment source and mental health categories to elucidate vulnerable subpopulations. Results. In New York City, there were 82,982 mental health-related encounters for young people aged 6 to 25 years during our study period months. Elevated temperature days were associated with higher risk of mental health-related ED and hospital encounters for the 6- to 11-year-olds (odds ratio [OR]: 1.28, 95% confidence interval [CI]: 1.13-1.46), for the 12- to 17-year-olds (OR: 1.17, 95% CI: 1.09-1.25) and for the 18- to 25-year-olds (OR: 1.09, 95% CI: 1.04-1.15). Children with reaction disorders, adolescents with anxiety and bipolar disorders, young adults with psychosis and reaction disorders and Black and non-Hispanic children and adolescents showed vulnerability to elevated temperature. Conclusions. We found that elevated ambient temperatures were associated with acute mental health ED or hospital encounters across childhood, adolescence and young adulthood. [ABSTRACT FROM AUTHOR]

The gradient of socioeconomic position (SEP) on health may be explained partly by a combination of increased contaminant exposures and greater susceptibility to their effects. Air pollution, for instance, may [...], BACKGROUND: Disproportionate 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 lowerincome urban communities, where air pollution and social stressors may be elevated. OBJECTIVES: We 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. METHODS: We 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. RESULTS: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in [NO.sub.2] 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 [NO.sub.2] was most predictive of asthma outcomes. CONCLUSIONS: We 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. KEY WORDS: childhood asthma, exposure to violence (ETV), geographic information systems (GIS), intraurban variability, nitrogen dioxide ([NO.sub.2]), social-environmental synergy, stress. Environ Health Perspect 115:1140-1146 (2007). doi:10.1289/ehp.9863 available via http://dx.doi.org/ [Online 22 March 2007]