Abstract

BackgroundMuch of the current evidence of associations between long-term PM2.5 and health outcomes relies on national or regional analyses using exposures derived directly from regulatory monitoring data. These findings could be affected by limited spatial coverage of monitoring data, particularly for time periods before spatially extensive monitoring began in the late 1990s. For instance, Pope et al. (2009) showed that between 1980 and 2000 a 10 μg/m3 reduction in PM2.5 was associated with an average 0.61 year (standard error (SE) = 0.20) longer life expectancy. That analysis used 1979–1983 averages of PM2.5 across 51 U.S. Metropolitan Statistical Areas (MSAs) computed from about 130 monitoring sites. Our reanalysis re-examines this association using modeled PM2.5 in order to assess population- or spatially-representative exposure. We hypothesized that modeled PM2.5 with finer spatial resolution provides more accurate health effect estimates compared to limited monitoring data.MethodsWe used the same data for life expectancy and confounders, as well as the same analysis models, and investigated the same 211 continental U.S. counties, as Pope et al. (2009). For modeled PM2.5, we relied on a previously-developed point prediction model based on regulatory monitoring data for 1999–2015 and back-extrapolation to 1979. Using this model, we predicted annual average concentrations at centroids of all 72,271 census tracts and 12,501 25-km national grid cells covering the contiguous U.S., to represent population and space, respectively. We averaged these predictions to the county for the two time periods (1979–1983 and 1999–2000), whereas the original analysis used MSA averages given limited monitoring data. Finally, we estimated regression coefficients for PM2.5 reduction on life expectancy improvement over the two periods, adjusting for area-level confounders.ResultsA 10 μg/m3 decrease in modeled PM2.5 based on census tract and national grid predictions was associated with 0.69 (standard error (SE) = 0.31) and 0.81 (0.29) -year increases in life expectancy. These estimates are higher than the estimate of Pope et al. (2009); they also have larger SEs likely because of smaller variability in exposure predictions, a standard property of regression. Two sets of effect estimates, however, had overlapping confidence intervals.ConclusionsOur approach for estimating population- and spatially-representative PM2.5 concentrations based on census tract and national grid predictions, respectively, provided generally consistent findings to the original findings using limited monitoring data. This finding lends additional support to the evidence that reduced fine particulate matter contributes to extended life expectancy.

Highlights

  • Much of the current evidence of associations between long-term ­PM2.5 and health outcomes relies on national or regional analyses using exposures derived directly from regulatory monitoring data

  • Life expectancy reanalysis To compare against results from Pope et al (2009), we examined the association between ­PM2.5 reduction and life expectancy increase for 1980–2000 using the same data for life expectancy and covariates in 211 U.S counties (Additional file 1: Figure S2), and the same seven health analysis models

  • Measured and modeled P­ M2.5 Modeled county- and Metropolitan Statistical Area (MSA)-average P­M2.5 estimated by the historical prediction model tended to be lower than measured MSA-averages derived by P­ M2.5 regulatory monitoring data in both periods

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Summary

Introduction

Much of the current evidence of associations between long-term ­PM2.5 and health outcomes relies on national or regional analyses using exposures derived directly from regulatory monitoring data. As an example of an effort that was restricted to regions with available monitoring data over a long time period, Pope et al (2009) investigated the association between the change in P­ M2.5 from 1980s through 2000s and the change in life expectancy They concluded that improved life expectancy was attributed to decreased ­PM2.5 concentrations [10]. For the 1980s they relied on measurements from the Inhalable Particulate Network (IPN) at only about 130 sites which were located in 51 major metropolitan areas [12, 13] Given these limited monitoring data, P­M2.5 exposure was aggregated to the Metropolitan Statistical Area (MSA) and the analysis was restricted to 211 out of more than 3,000 counties. A recent study expanded Pope et al.’s analysis to all U.S counties by using predicted ­PM2.5 concentrations; because of the unavailability of spatially extensive monitoring data before 1999, they focused on the change during 1999–2015 [14]

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