4.7 Article

Fine Particle Exposure and Clinical Aggravation in Neurodegenerative Diseases in New York State

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ENVIRONMENTAL HEALTH PERSPECTIVES
卷 129, 期 2, 页码 -

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US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/EHP7425

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资金

  1. National Institutes of Health/National Institute of Environmental Health Sciences [R21 ES028472, R01 ES028805, R01 ES030616, P30 ES000002, P30 ES009089]
  2. NIA [R01 AG066793, T32 ES007322, T32 ES007142]

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The study examined the potential association between long-term exposure to particulate matter <= 2.5 mu m in aerodynamic diameter and disease aggravation in neurodegenerative diseases. Findings suggest that annual increase in county-level PM2.5 concentrations may contribute to clinical aggravation of Parkinson's disease and amyotrophic lateral sclerosis, with evidence that the current national standards may not adequately protect the aging population.
BACKGROUND: Adult-onset neurodegenerative diseases affect millions and negatively impact health care systems worldwide. Evidence suggests that air pollution may contribute to aggravation of neurodegeneration, but studies have been limited. OBJECTIVE: We examined the potential association between long-term exposure to particulate matter <= 2.5 mu m in aerodynamic diameter [fine particulate matter (PM2.5)] and disease aggravation in Alzheimer's (AD) and Parkinson's (PD) diseases and amyotrophic lateral sclerosis (ALS), using first hospitalization as a surrogate of clinical aggravation. METHODS: We used data from the New York Department of Health Statewide Planning and Research Cooperative System (SPARCS 2000-2014) to construct annual county counts of first hospitalizations with a diagnosis of AD, PD, or ALS (total, urbanicity-, sex-, and age-stratified). We used annual PM2.5 concentrations estimated by a prediction model at a 1-km(2) resolution, which we aggregated to population-weighted county averages to assign exposure to cases based on county of residence. We used outcome-specific mixed quasi-Poisson models with county-specific random intercepts to estimate rate ratios (RRs) for a 1-y PM2.5 exposure. We allowed for nonlinear exposure-outcome relationships using penalized splines and accounted for potential confounders. RESULTS: We found a positive nonlinear PM2.5-PD association that plateaued above 11 mu g/m(3) (RR = 1.09, 95% CI: 1.04, 1.14 for a PM2.5 increase from 8.1 to 10.4 mu g/m(3)). We also found a linear PM2.5 -ALS positive association (RR =1.05, 95% CI: 1.01, 1.09 per 1-mu g/m(3) PM2.5 increase), and suggestive evidence of an association with AD. We found effect modification by age for PD and ALS with a stronger positive association in patients <70 years of age but found insufficient evidence of effect modification by sex or urbanization level for any of the outcomes. CONCLUSION: Our findings suggest that annual increase in county-level PM2.5 concentrations may contribute to clinical aggravation of PD and ALS. Importantly, the average annual PM2.5 concentration in our study was 8.1 mu g/m(3), below the current American national standards, suggesting the standards may not adequately protect the aging population.

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