Abstract

BackgroundRecent toxicological and epidemiological evidence suggests that chronic psychosocial stress may modify pollution effects on health. Thus, there is increasing interest in refined methods for assessing and incorporating non-chemical exposures, including social stressors, into environmental health research, towards identifying whether and how psychosocial stress interacts with chemical exposures to influence health and health disparities. We present a flexible, GIS-based approach for examining spatial patterns within and among a range of social stressors, and their spatial relationships with air pollution, across New York City, towards understanding their combined effects on health.MethodsWe identified a wide suite of administrative indicators of community-level social stressors (2008–2010), and applied simultaneous autoregressive models and factor analysis to characterize spatial correlations among social stressors, and between social stressors and air pollutants, using New York City Community Air Survey (NYCCAS) data (2008-2009). Finally, we provide an exploratory ecologic analysis evaluating possible modification of the relationship between nitrogen dioxide (NO2) and childhood asthma Emergency Department (ED) visit rates by social stressors, to demonstrate how the methods used to assess stressor exposure (and/or consequent psychosocial stress) may alter model results.ResultsAdministrative indicators of a range of social stressors (e.g., high crime rate, residential crowding rate) were not consistently correlated (rho = - 0.44 to 0.89), nor were they consistently correlated with indicators of socioeconomic position (rho = - 0.54 to 0.89). Factor analysis using 26 stressor indicators suggested geographically distinct patterns of social stressors, characterized by three factors: violent crime and physical disorder, crowding and poor access to resources, and noise disruption and property crimes. In an exploratory ecologic analysis, these factors were differentially associated with area-average NO2 and childhood asthma ED visits. For example, only the ‘violent crime and disorder’ factor was significantly associated with asthma ED visits, and only the ‘crowding and resource access’ factor modified the association between area-level NO2 and asthma ED visits.ConclusionsThis spatial approach enabled quantification of complex spatial patterning and confounding between chemical and non-chemical exposures, and can inform study design for epidemiological studies of separate and combined effects of multiple urban exposures.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-069X-13-91) contains supplementary material, which is available to authorized users.

Highlights

  • Recent toxicological and epidemiological evidence suggests that chronic psychosocial stress may modify pollution effects on health

  • We examined effect modification in the Nitrogen dioxide (NO2)-asthma exacerbation relationship by stressor factors (Figure 6), and found significant (p

  • In conclusion, our city-wide examination of social stressors and air pollution in one U.S city highlight the utility of spatial analysis for disentangling the separate and combined effects of chemical and non-chemical exposures

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Summary

Introduction

Recent toxicological and epidemiological evidence suggests that chronic psychosocial stress may modify pollution effects on health. For investigators interested in understanding the relationship between the social and physical environment, there is a growing need for refined, replicable methods for: a) measuring social stressor exposures across large cohorts, and b) reducing confounding between social and chemical exposures in environmental epidemiology [13] Recent research on this topic has considered psychosocial stress as a possible key factor modifying the relationship between chemical exposures, including air pollution or lead, and adverse health outcomes [14]. Chronic psychosocial stress is associated with negative emotional states and maladaptive behaviors that influence immune, endocrine, and metabolic function to produce cumulative wear-and-tear – often referred to as allostatic load [16] These physiologic changes may alter individuals’ reactivity to chemical exposures (e.g., pathogens, pollutants) and increase risk for multiple disease etiologies [17]. The field of stress measurement primarily relies on individual questionnaire or biomarker data to assess the occurrence of stressful events [18], conditions that might produce stressful experiences [19], recent perceptions of stress [20], or the mental health sequelae of chronic stress (i.e., depression, anxiety)

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