Disentangling impacts of multiple pollutants on acute cardiovascular events in New York city: A case-crossover analysis.

BACKGROUND: Ambient air pollution contributes to an estimated 6.67 million deaths annually, and has been linked to cardiovascular disease (CVD), the leading cause of death. Short-term increases in air pollution have been associated with increased risk of CVD event, though relatively few studies have directly compared effects of multiple pollutants using fine-scale spatio-temporal data, thoroughly adjusting for co-pollutants and temperature, in an exhaustive citywide hospitals dataset, towards identifying key pollution sources within the urban environment to most reduce, and reduce disparities in, the leading cause of death worldwide. OBJECTIVES: We aimed to examine multiple pollutants against multiple CVD diagnoses, across lag days, in models adjusted for co-pollutants and meteorology, and inherently adjusted by design for non-time-varying individual and aggregate-level covariates, using fine-scale space-time exposure estimates, in an exhaustive dataset of emergency department visits and hospitalizations across an entire city, thereby capturing the full population-at-risk. METHODS: We used conditional logistic regression in a case-crossover design - inherently controlling for all confounders not varying within case month - to examine associations between spatio-temporal nitrogen dioxide (NO2), fine particulate matter (PM2.5), sulfur dioxide (SO2), and ozone (O3) in New York City, 2005-2011, on individual risk of acute CVD event (n = 837,523), by sub-diagnosis [ischemic heart disease (IHD), heart failure (HF), stroke, ischemic stroke, acute myocardial infarction]. RESULTS: We found significant same-day associations between NO2 and risk of overall CVD, IHD, and HF - and between PM2.5 and overall CVD or HF event risk - robust to all adjustments and multiple comparisons. Results were comparable by sex and race - though median age at CVD was 10 years younger for Black New Yorkers than White New Yorkers. Associations for NO2 were comparable for adults younger or older than 69 years, though PM2.5 associations were stronger among older adults. DISCUSSION: Our results indicate immediate, robust effects of combustion-related pollution on CVD risk, by sub-diagnosis. Though acute impacts differed minimally by age, sex, or race, the much younger age-at-event for Black New Yorkers calls attention to cumulative social susceptibility.

Neighborhood violence and socioeconomic deprivation influence associations between acute air pollution and temperature on childhood asthma in New York city.

Ambient air pollution, temperature, and social stressor exposures are linked with asthma risk, with potential synergistic effects. We examined associations for acute pollution and temperature exposures, with modification by neighborhood violent crime and socioeconomic deprivation, on asthma morbidity among children aged 5-17 years year-round in New York City. Using conditional logistic regression in a time-stratified, case-crossover design, we quantified percent excess risk of asthma event per 10-unit increase in daily, residence-specific exposures to PM2.5, NO2, SO2, O3, and minimum daily temperature (Tmin). Data on 145,834 asthma cases presenting to NYC emergency departments from 2005 to 2011 were obtained from the New York Statewide Planning and Research Cooperative System (SPARCS). Residence- and day-specific spatiotemporal exposures were assigned using the NYC Community Air Survey (NYCCAS) spatial data and daily EPA pollution and NOAA weather data. Point-level NYPD violent crime data for 2009 (study midpoint) was aggregated, and Socioeconomic Deprivation Index (SDI) scores assigned, by census tract. Separate models were fit for each pollutant or temperature exposure for lag days 0-6, controlling for co-exposures and humidity, and mutually-adjusted interactions (modification) by quintile of violent crime and SDI were assessed. We observed stronger main effects for PM2.5 and SO2 in the cold season on lag day 1 [4.90% (95% CI: 3.77-6.04) and 8.57% (5.99-11.21), respectively]; Tmin in the cold season on lag day 0 [2.26% (1.25-3.28)]; and NO2 and O3 in the warm season on lag days 1 [7.86% (6.66-9.07)] and 2 [4.75% (3.53-5.97)], respectively. Violence and SDI modified the main effects in a non-linear manner; contrary to hypotheses, we found stronger associations in lower-violence and -deprivation quintiles. At very high stressor exposures, although asthma exacerbations were highly prevalent, pollution effects were less apparent-suggesting potential saturation effects in socio-environmental synergism.

What Is "Socioeconomic Position (SEP)," and How Might It Modify Air Pollution-Health Associations? Cohering Findings, Identifying Challenges, and Disentangling Effects of SEP and Race in US City Settings.

PURPOSE OF REVIEW: Environmental epidemiology has long considered socioeconomic position (SEP) to be an important confounder of pollution effects on health, given that, in the USA, lower-income and minority communities are often disproportionately exposed to pollution. In recent decades, a growing literature has revealed that lower-SEP communities may also be more susceptible to pollution. Given the vast number of material and psychosocial stressors that vary by SEP, however, it is unclear which specific aspects of SEP may underlie this susceptibility. As environmental epidemiology engages more rigorously with issues of differential susceptibility, it is pertinent to define SEP more clearly, to disentangle its many aspects, and to move towards identifying causal components. Myriad stressors and exposures vary with SEP, with effects accumulating and interacting over the lifecourse. Here, we ask: In the context of environmental epidemiology, how do we meaningfully characterize"SEP"? RECENT FINDINGS: In answering this question, it is critical to acknowledge that SEP, stressors, and pollution are differentially distributed by race in US cities. These distributions have been shaped by neighborhood sorting and race-based residential segregation rooted in historical policies and processes (e.g., redlining), which have served to concentrate wealth and opportunities for education and employment in predominantly-white communities. As a result, it is now profoundly challenging to separate SEP from race in the urban US setting. Here, we cohere evidence from our recent and on-going studies aimed at disentangling synergistic health effects among SEP-related stressors and pollutants. We consider an array of SEP-linked social stressors, and discuss persistent challenges in this epidemiology, many of which are related to spatial confounding among multiple pollutants and stressors. Combining quantitative results with insights from qualitative data on neighborhood perceptions and stress (including violence and police-community relations), we offer a lens towards unpacking the complex interplay among SEP, community stressors, race, and pollution in US cities.

Long-Term Ambient Air Pollution Exposures and Circulating and Stimulated Inflammatory Mediators in a Cohort of Midlife Adults.

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)-α (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-α. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1ß and TNF-α. 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. https://doi.org/10.1289/EHP7089.

Geocoding Error, Spatial Uncertainty, and Implications for Exposure Assessment and Environmental Epidemiology.

Although environmental epidemiology studies often rely on geocoding procedures in the process of assigning spatial exposure estimates, geocoding methods are not commonly reported, nor are consequent errors in exposure assignment explored. Geocoding methods differ in accuracy, however, and, given the increasing refinement of available exposure models for air pollution and other exposures, geocoding error may account for an increasingly larger proportion of exposure misclassification. We used residential addresses from a reasonably large, dense dataset of asthma emergency department visits from all New York City hospitals (n = 21,183; 26.9 addresses/km2), and geocoded each using three methods (Address Point, Street Segment, Parcel Centroid). We compared missingness and spatial patterning therein, quantified distance and directional errors, and quantified impacts on pollution exposure estimates and assignment to Census areas for sociodemographic characterization. Parcel Centroids had the highest overall missingness rate (38.1%, Address Point = 9.6%, Street Segment = 6.1%), and spatial clustering in missingness was significant for all methods, though its spatial patterns differed. Street Segment geocodes had the largest mean distance error (µ = 29.2 (SD = 26.2) m; vs. µ = 15.9 (SD = 17.7) m for Parcel Centroids), and the strongest spatial patterns therein. We found substantial over- and under-estimation of pollution exposures, with greater error for higher pollutant concentrations, but minimal impact on Census area assignment. Finally, we developed surfaces of spatial patterns in errors in order to identify locations in the study area where exposures may be over-/under-estimated. Our observations provide insights towards refining geocoding methods for epidemiology, and suggest methods for quantifying and interpreting geocoding error with respect to exposure misclassification, towards understanding potential impacts on health effect estimates.

Putting Co-Exposures on Equal Footing: An Ecological Analysis of Same-Scale Measures of Air Pollution and Social Factors on Cardiovascular Disease in New York City.

Epidemiologic evidence consistently links urban air pollution exposures to health, even after adjustment for potential spatial confounding by socioeconomic position (SEP), given concerns that air pollution sources may be clustered in and around lower-SEP communities. SEP, however, is often measured with less spatial and temporal resolution than are air pollution exposures (i.e., census-tract socio-demographics vs. fine-scale spatio-temporal air pollution models). Although many questions remain regarding the most appropriate, meaningful scales for the measurement and evaluation of each type of exposure, we aimed to compare associations for multiple air pollutants and social factors against cardiovascular disease (CVD) event rates, with each exposure measured at equal spatial and temporal resolution. We found that, in multivariable census-tract-level models including both types of exposures, most pollutant-CVD associations were non-significant, while most social factors retained significance. Similarly, the magnitude of association was higher for an IQR-range difference in the social factors than in pollutant concentrations. We found that when offered equal spatial and temporal resolution, CVD was more strongly associated with social factors than with air pollutant exposures in census-tract-level analyses in New York City.

Violent crime and socioeconomic deprivation in shaping asthma-related pollution susceptibility: a case-crossover design.

BACKGROUND: The objective of this study was to quantify and compare the relative influence of community violent crime and socioeconomic deprivation in modifying associations between ozone and emergency department (ED) visits for asthma among children. METHODS: We used a spatiotemporal case-crossover analysis for all New York City EDs for the months May-September from 2005 to 2011 from a statewide administrative ED dataset. The data included 11 719 asthmatic children aged 5-18 years, and the main outcome measure was percentage of excess risk of asthma ED visit based on Cox regression analysis. RESULTS: Stronger ozone-asthma associations were observed for both elevated crime and deprivation (eg, on lag day 2, we found 20.0% (95% CI 10.2% to 30.6 %) and 21.0% (10.5% to 32.5%) increased risk per 10 ppb ozone, for communities in the highest vs lowest quartiles of violent crime and deprivation, respectively). However, in varied models accounting for both modifiers, only violence retained significance. CONCLUSIONS: The results suggest stronger spatiotemporal ozone-asthma associations in communities of higher violent crime or deprivation. Notably, violence was the more consistent and significant modifier, potentially mediating a substantial portion of socioeconomic position-related susceptibility.

Not so little differences: variation in hot weather risk to young children in New York City.

OBJECTIVES: High ambient temperatures are associated with significant health risk in the United States. The risk to children has been minimally explored, and often young children are considered as a single age group despite marked physiologic and social variation among this population from infancy through preschool. This study explored the heterogeneity of risk of heat among young children. STUDY DESIGN: Using a time-stratified, case-crossover design, we evaluated associations between maximum daily temperature (Tmax) and ED visits (n = 1,002,951) to New York City (NYC) metropolitan area hospitals for children aged 0-4 years in May-September, 2005-2011. METHODS: Conditional logistic regression analysis estimated risks for an interquartile range of Tmax for 0-6 lag days. Stratified analyses explored age strata by year, race/ethnic groups, and diagnostic codes. Sensitivity analyses controlled for same day ambient ozone, particulate matter <2.5 microns, and relative humidity and, separately, explored race groups without ethnicity and different diagnostic code groupings. RESULTS: Children ages 0-4 years had increased risk of emergency department visits with increased Tmax on lag days 0, 1, and 3. The association was strongest on lag day 0, when an increase in Tmax of 13 °F conferred an excess risk of 2.6% (95% confidence interval [CI]: 2.2-3.0). Stratifying by age, we observed significant positive associations for same-day exposures, for 1-4 year olds. Children less than 1 year of age showed a significant positive association with Tmax only on lag day 3. The race/ethnicity stratified analysis revealed a similar lag pattern for all subgroups. The diagnostic group analysis showed percent excess risk for heat-specific diagnoses (16.6% [95% CI: 3.0-31.9]); general symptoms (10.1% [95% CI: 8.2-11.9]); infectious (4.9% [95% CI: 3.9-5.9]); and injury (5.1% [95% CI: 3.8-6.4]) diagnoses. CONCLUSION: We found a significant risk of ED visits in young children with elevated Tmax. Risk patterns vary based on age with infants showing delayed risk and toddlers and preschoolers with same day risk. In addition, the finding of increased risk of injury associated with higher temperatures is novel. Altogether, these findings suggest a need for a tailored public health response, such as different messages to caregivers of different age children, to protect children from the effects of heat. Next steps include examining specific subcategories of diagnoses to develop protective strategies and better anticipate the needs of population health in future scenarios of climate change.