Jane E. Clougherty

Synergistic Effects of Traffic-Related Air Pollution and Exposure to Violence on Urban Asthma Etiology

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 lower-income 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 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. 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.

A Growing Role for Gender Analysis in Air Pollution Epidemiology

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 derived gendered exposures, to sex-linked physiological differences, or to some interplay thereof. Gender analysis, which aims to disaggregate social from biological differences between males and females, may help to elucidate these possible sources of effect modification. Data sources and data extraction A PubMed literature search was performed in July 2009, using the terms “respiratory” and any of “sex” or “gender” or “men and women” or “boys and girls” and either “PM2.5” (particulate matter ≥ 2.5 μm in aerodynamic diameter) or “NO2” (nitrogen dioxide). I reviewed the identified studies, and others cited therein, to summarize current evidence of effect modification, with attention to authors’ interpretation of observed differences. Owing to broad differences in exposure mixes, outcomes, and analytic techniques, with few studies examining any given combination thereof, meta-analysis was not deemed appropriate at this time. Data synthesis More studies of adults report stronger effects among women, particularly for older persons or where using residential exposure assessment. Studies of children suggest stronger effects among boys in early life and among girls in later childhood. Conclusions The qualitative review describes possible sources of difference in air pollution response between women and men, which may vary by life stage, coexposures, hormonal status, or other factors. The sources of observed effect modifications remain unclear, although gender analytic approaches may help to disentangle gender and sex differences in pollution response. A framework for incorporating gender analysis into environmental epidemiology is offered, along with several potentially useful methods from gender analysis.

A Framework for Examining Social Stress and Susceptibility to Air Pollution in Respiratory Health

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 the combined effects of psychosocial stress and air pollution. Both exposures may be elevated in lower-income urban communities, and it has been hypothesized that stress, which can influence immune function and susceptibility, may potentiate the effects of air pollution in respiratory disease onset and exacerbation. In this paper, we attempt to synthesize the relevant research from social and environmental epidemiology, toxicology, immunology, and exposure assessment to provide a useful framework for environmental health researchers aiming to investigate the health effects of environmental pollution in combination with social or psychological factors. Data synthesis We review the existing epidemiologic and toxicologic evidence on synergistic effects of stress and pollution, and then describe the physiologic effects of stress and key issues related to measuring and evaluating stress as it relates to physical environmental exposures and susceptibility. Finally, we identify some of the major methodologic challenges ahead as we work toward disentangling the health effects of clustered social and physical exposures and accurately describing the interplay among these exposures. Conclusions There is still tremendous work to be done toward understanding the combined and potentially synergistic health effects of stress and pollution. As this research proceeds, we recommend careful attention to the relative temporalities of stress and pollution exposures, to nonlinearities in their independent and combined effects, to physiologic pathways not elucidated by epidemiologic methods, and to the relative spatial distributions of social and physical exposures at multiple geographic scales.

Work and its role in shaping the social gradient in health

Adults with better jobs enjoy better health: job title was, in fact, the social gradient metric first used to study the relationship between social class and chronic disease etiology, a core finding now replicated in most developed countries. What has been less well proved is whether this correlation is causal, and if so, through what mechanisms. During the past decade, much research has been directed at these issues. Best evidence in 2009 suggests that occupation does affect health. Most recent research on the relationship has been directed at disentangling the pathways through which lower‐status work leads to adverse health outcomes. This review focuses on six areas of recent progress: (1) the role of status in a hierarchical occupational system; (2) the roles of psychosocial job stressors; (3) effects of workplace physical and chemical hazard exposures; (4) evidence that work organization matters as a contextual factor; (5) implications for the gradient of new forms of nonstandard or “precarious” employment such as contract and shift work; and (6) emerging evidence that women may be impacted differently by adverse working conditions, and possibly more strongly, than men.

Land use regression modeling of intra-urban residential variability in multiple traffic-related air pollutants

BackgroundThere is a growing body of literature linking GIS-based measures of traffic density to asthma and other respiratory outcomes. However, no consensus exists on which traffic indicators best capture variability in different pollutants or within different settings. As part of a study on childhood asthma etiology, we examined variability in outdoor concentrations of multiple traffic-related air pollutants within urban communities, using a range of GIS-based predictors and land use regression techniques.MethodsWe measured fine particulate matter (PM2.5), nitrogen dioxide (NO2), and elemental carbon (EC) outside 44 homes representing a range of traffic densities and neighborhoods across Boston, Massachusetts and nearby communities. Multiple three to four-day average samples were collected at each home during winters and summers from 2003 to 2005. Traffic indicators were derived using Massachusetts Highway Department data and direct traffic counts. Multivariate regression analyses were performed separately for each pollutant, using traffic indicators, land use, meteorology, site characteristics, and central site concentrations.ResultsPM2.5 was strongly associated with the central site monitor (R2 = 0.68). Additional variability was explained by total roadway length within 100 m of the home, smoking or grilling near the monitor, and block-group population density (R2 = 0.76). EC showed greater spatial variability, especially during winter months, and was predicted by roadway length within 200 m of the home. The influence of traffic was greater under low wind speed conditions, and concentrations were lower during summer (R2 = 0.52). NO2 showed significant spatial variability, predicted by population density and roadway length within 50 m of the home, modified by site characteristics (obstruction), and with higher concentrations during summer (R2 = 0.56).ConclusionEach pollutant examined displayed somewhat different spatial patterns within urban neighborhoods, and were differently related to local traffic and meteorology. Our results indicate a need for multi-pollutant exposure modeling to disentangle causal agents in epidemiological studies, and further investigation of site-specific and meteorological modification of the traffic-concentration relationship in urban neighborhoods.

Predictors of concentrations of nitrogen dioxide, fine particulate matter, and particle constituents inside of lower socioeconomic status urban homes

Air pollution exposure patterns may contribute to known spatial patterning of asthma morbidity within urban areas. While studies have evaluated the relationship between traffic and outdoor concentrations, few have considered indoor exposure patterns within low socioeconomic status (SES) urban communities. In this study, part of a prospective birth cohort study assessing asthma etiology in urban Boston, we collected indoor and outdoor 3–4 day samples of nitrogen dioxide (NO2) and fine particulate matter (PM2.5) in 43 residences across multiple seasons from 2003 to 2005. Homes were chosen to represent low SES households, including both cohort and non-cohort residences in similar neighborhoods, and consisted almost entirely of multiunit residences. Reflectance analysis and X-ray fluorescence spectroscopy were performed on the particle filters to determine elemental carbon (EC) and trace element concentrations, respectively. Additionally, information on home characteristics (e.g. type, age, stove fuel) and occupant behaviors (e.g. smoking, cooking, cleaning) were collected via a standardized questionnaire. The contributions of outdoor and indoor sources to indoor concentrations were quantified with regression analyses using mass balance principles. For NO2 and most particle constituents (except outdoor-dominated constituents like sulfur and vanadium), the addition of selected indoor source terms improved the models predictive power. Cooking time, gas stove usage, occupant density, and humidifiers were identified as important contributors to indoor levels of various pollutants. A comparison between cohort and non-cohort participants provided another means to determine the influence of occupant activity patterns on indoor–outdoor ratios. Although the groups had similar housing characteristics and were located in similar neighborhoods, cohort members had significantly higher indoor concentrations of PM2.5 and NO2, associated with indoor activities. We conclude that the effect of indoor sources may be more pronounced in high-density multiunit dwellings, and that future epidemiological studies in these populations should explicitly consider these sources in assigning exposures.

Lung function, asthma symptoms, and quality of life for children in public housing in Boston: a case-series analysis

BackgroundChildren in urban public housing are at high risk for asthma, given elevated environmental and social exposures and suboptimal medical care. For a multifactorial disease like asthma, design of intervention studies can be influenced by the relative prevalence of key risk factors. To better understand risk factors for asthma morbidity in the context of an environmental intervention study, we conducted a detailed baseline evaluation of 78 children (aged 4–17 years) from three public housing developments in Boston.MethodsAsthmatic children and their caregivers were recruited between April 2002 and January 2003. We conducted intake interviews that captured a detailed family and medical history, including questions regarding asthma symptom severity, access to health care, medication usage, and psychological stress. Quality of life was evaluated for both the child and caregiver with an asthma-specific scale. Pulmonary function was measured with a portable spirometer, and allergy testing for common indoor and outdoor allergens was conducted with skin testing using the prick puncture method. Exploratory linear and logistic regression models evaluating predictors of respiratory symptoms, quality of life, and pulmonary function were conducted using SAS.ResultsWe found high rates of obesity (56%) and allergies to indoor contaminants such as cockroaches (59%) and dust mites (59%). Only 36% of children with persistent asthma reported being prescribed any daily controller medication, and most did not have an asthma action plan or a peak flow meter. One-time lung function measures were poorly correlated with respiratory symptoms or quality of life, which were significantly correlated with each other. In multivariate regression models, household size, body mass index, and environmental tobacco smoke exposure were positively associated with respiratory symptom severity (p < 0.10). Symptom severity was negatively associated with asthma-related quality of life for the child and the caregiver, with caregiver (but not child) quality of life significantly influenced by caregiver stress and whether the child was in the intensive care unit at birth.ConclusionGiven the elevated prevalence of multiple risk factors, coordinated improvements in the social environment, the built environment, and in medical management would likely yield the greatest health benefits in this high-risk population.

Monitoring intraurban spatial patterns of multiple combustion air pollutants in New York City: Design and implementation

Routine air monitoring provides data to assess urban scale temporal variation in pollution concentrations in relation to regulatory standards, but is not well suited to characterizing intraurban spatial variation in pollutant concentrations from local sources. To address these limitations and inform local control strategies, New York City developed a program to track spatial patterns of multiple air pollutants in each season of the year. Monitor locations include 150 distributed street-level sites chosen to represent a range of traffic, land-use and other characteristics. Integrated samples are collected at each distributed site for one 2-week session each season and in every 2-week period at five reference locations to track city-wide temporal variation. Pollutants sampled include PM2.5 and constituents, nitrogen oxides, black carbon, ozone (summer only) and sulfur dioxide (winter only). During the first full year of monitoring more than 95% of designed samples were completed. Agreement between colocated samples was good (absolute mean % difference 3.2–8.9%). Street-level pollutant concentrations spanned a much greater range than did concentrations at regulatory monitors, especially for oxides of nitrogen and sulfur dioxide. Monitoring to characterize intraurban spatial gradients in ambient pollution usefully complements regulatory monitoring data to inform local air quality management.

Intra-urban spatial variability in wintertime street-level concentrations of multiple combustion-related air pollutants: the New York City Community Air Survey (NYCCAS).

Although intra-urban air pollution differs by season, few monitoring networks provide adequate geographic density and year-round coverage to fully characterize seasonal patterns. Here, we report winter intra-urban monitoring and land-use regression (LUR) results from the New York City Community Air Survey (NYCCAS). Two-week integrated samples of fine particles (PM2.5), black carbon (BC), nitrogen oxides (NOx) and sulfur dioxide (SO2) were collected at 155 city-wide street-level locations during winter 2008–2009. Sites were selected using stratified random sampling, randomized across sampling sessions to minimize spatio-temporal confounding. LUR was used to identify GIS-based source indicators associated with higher concentrations. Prediction surfaces were produced using kriging with external drift. Each pollutant varied twofold or more across sites, with higher concentrations near midtown Manhattan. All pollutants were positively correlated, particularly PM2.5 and BC (Spearman’s r=0.84). Density of oil-burning boilers, total and truck traffic density, and temporality explained 84% of PM2.5 variation. Densities of total traffic, truck traffic, oil-burning boilers and industrial space, with temporality, explained 65% of BC variation. Temporality, built space, bus route location, and traffic density described 67% of nitrogen dioxide variation. Residual oil-burning units, nighttime population and temporality explained 77% of SO2 variation. Spatial variation in combustion-related pollutants in New York City was strongly associated with oil-burning and traffic density. Chronic exposure disparities and unique local sources can be identified through year-round saturation monitoring.

Chronic Social Stress and Susceptibility to Concentrated Ambient Fine Particles in Rats

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 effects and cannot identify physiologic mechanisms for potential differential susceptibilities. Objectives Using a rat model of social stress, we compared respiratory responses to fine concentrated ambient particles (CAPs) and examined biological markers of inflammation. Methods Twenty-four 12-week-old male Sprague-Dawley rats were randomly assigned to four groups [stress/CAPs, stress/filtered air (FA), nonstress/CAPs, nonstress/FA]. Stress-group animals were individually introduced into the home cage of a dominant male twice weekly. Blood drawn at sacrifice was analyzed for immune and inflammatory markers. CAPs were generated using the Harvard ambient particle concentrator, which draws real-time urban ambient fine particles, enriching concentrations approximately 30 times. CAPs/FA exposures were delivered in single-animal plethysmographs, 5 hr/day for 10 days, and respiratory function was continuously monitored using a Buxco system. Results Stressed animals displayed higher average C-reactive protein, tumor necrosis factor-α, and white blood cell counts than did nonstressed animals. Only among stressed animals were CAPs exposures associated with increased respiratory frequency, lower flows, and lower volumes, suggesting a rapid, shallow breathing pattern. Conversely, in animals with elevated CAPs exposures alone, we observed increased inspiratory flows and greater minute volumes (volume of air inhaled or exhaled per minute). Conclusions CAPs effects on respiratory measures differed significantly, and substantively, by stress group. Higher CAPs exposures were associated with a rapid, shallow breathing pattern only under chronic stress. Blood measures provided evidence of inflammatory responses. Results support epidemiologic findings that chronic stress may alter respiratory response to air pollution and may help elucidate pathways for differential susceptibility.