Search

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 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: 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, 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: Epidemiologic evidence suggests that chronic stress may alter susceptibility to air pollution. However, persistent spatial confounding between these exposures may limit the utility of epidemiologic methods to disentangle these [...]

OBJECTIVE: Epidemiologic studies of air pollution effects on respiratory health report significant modification by sex, although results are not uniform. Importantly, it remains unclear whether modifications are attributable to socially [...]

OBJECTIVE: There is growing interest in disentangling the health effects of spatially clustered social and physical environmental exposures and in exploring potential synergies among them, with particular attention directed to [...]

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], 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: Recent studies have suggested associations between air pollution and various birth outcomes, but the evidence for preterm birth is mixed. OBJECTIVE: We aimed to assess the relationship between air pollution and preterm birth using 2008-2010 New York City (NYC) birth certificates linked to hospital records. METHODS: We analyzed 258,294 singleton births with 22-42 completed weeks gestation to nonsmoking mothers. Exposures to ambient fine particles ([PM.sub.2.5]) and nitrogen dioxide (N[O.sub.2]) during the first, second, and cumulative third trimesters within 300 m of maternal address were estimated using data from the NYC Community Air Survey and regulatory monitors. We estimated the odds ratio (OR) of spontaneous preterm (gestation < 37 weeks) births for the first- and second-trimester exposures in a logistic mixed model, and the third-trimester cumulative exposures in a discrete time survival model, adjusting for maternal characteristics and delivery hospital. Spatial and temporal components of estimated exposures were also separately analyzed. RESULTS: [PM.sub.2.5] was not significantly associated with spontaneous preterm birth. N[O.sub.2] in the second trimester was negatively associated with spontaneous preterm birth in the adjusted model (OR = 0.90; 95% CI: 0.83, 0.97 per 20 ppb). Neither pollutant was significantly associated with spontaneous preterm birth based on adjusted models of temporal exposures, whereas the spatial exposures showed significantly reduced odds ratios (OR = 0.80; 95% CI: 0.67, 0.96 per 10 µg/[m.sup.3] [PM.sub.2.5] and 0.88; 95% CI: 0.79, 0.98 per 20 ppb N[O.sub.2]). Without adjustment for hospital, these negative associations were stronger. CONCLUSION: Neither [PM.sub.2.5] nor N[O.sub.2] was positively associated with spontaneous preterm delivery in NYC. Delivery hospital was an important spatial confounder. http://dx.doi.org/10.1289/ehp.1510266, Introduction Numerous studies have suggested associations between air pollution and various birth outcomes, including preterm birth and low birth weight (Nieuwenhuijsen et al. 2013; Stieb et al. 2012). Maternal exposure [...]

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-1ß, IL-6, and tumor necrosis factor (TNF)-a (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 µm (PM2.5)] 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 PM2.5 and BC with stimulated production of IL-6, IL-1ß, and TNF-a. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1ß and TNF-a. No pollutants were associated with circulating IL-6 or CRP levels. DISCUSSION: Exposure to PM2.5, 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. [ABSTRACT FROM AUTHOR]

The article discusses research which evaluated the impact of the clean heat program (CHP), which was designed to eliminate the use of residual heating oil and move toward cleaner energy forms, on air pollution levels in New York City. Topics covered include air pollution reductions attributable to CHP between 2012 and 2016, how the reductions vary by neighborhood socioeconomic status (SES), and the effects of CHP since its implementation.

The article discusses a study on the significant role of stress processes in mediating impacts of ozone exposures on metabolic function, which references a research paper published within the issue. It tackles the variations in interactions between pollution and stress, the ozone-induced changes in glucose production, and the implications of the lack of response to ozone shown in adrenalectomized rats for understanding biological processes.

Chen et al. (2008) examined the potential for social stressors to influence responsiveness to environmental pollution. Contrary to their initial hypothesis, and to results we reported previously (Clougherty et al. [...]