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BackgroundBoth short- and long-term exposures to fine particulate matter (≤ 2.5 μm; PM2.5) are associated with mortality. However, whether the associations exist at levels below the new U.S. Environmental Protection Agency (EPA) standards (12 μg/m3 of annual average PM2.5, 35 μg/m3 daily) is unclear. In addition, it is not clear whether results from previous time series studies (fit in larger cities) and cohort studies (fit in convenience samples) are generalizable.ObjectivesWe estimated the effects of low-concentration PM2.5 on mortality.MethodsHigh resolution (1 km × 1 km) daily PM2.5 predictions, derived from satellite aerosol optical depth retrievals, were used. Poisson regressions were applied to a Medicare population (≥ 65 years of age) in New England to simultaneously estimate the acute and chronic effects of exposure to PM2.5, with mutual adjustment for short- and long-term exposure, as well as for area-based confounders. Models were also restricted to annual concentrations < 10 μg/m3 or daily concentrations < 30 μg/m3.ResultsPM2.5 was associated with increased mortality. In the study cohort, 2.14% (95% CI: 1.38, 2.89%) and 7.52% (95% CI: 1.95, 13.40%) increases were estimated for each 10-μg/m3 increase in short- (2 day) and long-term (1 year) exposure, respectively. The associations held for analyses restricted to low-concentration PM2.5 exposure, and the corresponding estimates were 2.14% (95% CI: 1.34, 2.95%) and 9.28% (95% CI: 0.76, 18.52%). Penalized spline models of long-term exposure indicated a larger effect for mortality in association with exposures ≥ 6 μg/m3 versus those < 6 μg/m3. In contrast, the association between short-term exposure and mortality appeared to be linear across the entire exposure distribution.ConclusionsUsing a mutually adjusted model, we estimated significant acute and chronic effects of PM2.5 exposure below the current U.S. EPA standards. These findings suggest that improving air quality with even lower PM2.5 than currently allowed by U.S. EPA standards may benefit public health.CitationShi L, Zanobetti A, Kloog I, Coull BA, Koutrakis P, Melly SJ, Schwartz JD. 2016. Low-concentration PM2.5 and mortality: estimating acute and chronic effects in a population-based study. Environ Health Perspect 124:46–52; http://dx.doi.org/10.1289/ehp.1409111

Background The novel human coronavirus disease 2019 (COVID-19) pandemic has claimed more than 600,000 lives worldwide, causing tremendous public health, social, and economic damages. While the risk factors of COVID-19 are still under investigation, environmental factors, such as urban air pollution, may play an important role in increasing population susceptibility to COVID-19 pathogenesis. Methods We conducted a cross-sectional nationwide study using zero-inflated negative binomial models to estimate the association between long-term (2010-2016) county-level exposures to NO 2 , PM 2.5 and O 3 and county-level COVID-19 case-fatality and mortality rates in the US. We used both single and multipollutant models and controlled for spatial trends and a comprehensive set of potential confounders, including state-level test positive rate, county-level healthcare capacity, phase-of-epidemic, population mobility, population density, sociodemographics, socioeconomic status, race and ethnicity, behavioral risk factors, and meteorology. Results 3,659,828 COVID-19 cases and 138,552 deaths were reported in 3,076 US counties from January 22, 2020 to July 17, 2020, with an overall observed case-fatality rate of 3.8%. County-level average NO 2 concentrations were positively associated with both COVID-19 case-fatality rate and mortality rate in single-, bi-, and tri-pollutant models. When adjusted for co-pollutants, per inter-quartile range (IQR) increase in NO 2 (4.6 ppb), COVID-19 case-fatality rate and mortality rate were associated with an increase of 11.3% (95% CI 4.9% to 18.2%) and 16.2% (95% CI 8.7% to 24.0%), respectively. We did not observe significant associations between COVID-19 case-fatality rate and long-term exposure to PM 2.5 or O 3 , although per IQR increase in PM 2.5 (2.6 ug/m 3 ) was marginally associated with 14.9% (95% CI: 0.0% to 31.9%) increase in COVID-19 mortality rate when adjusted for co-pollutants. Discussion Long-term exposure to NO 2 , which largely arises from urban combustion sources such as traffic, may enhance susceptibility to severe COVID-19 outcomes, independent of long-term PM 2.5 and O 3 exposure. The results support targeted public health actions to protect residents from COVID-19 in heavily polluted regions with historically high NO 2 levels. Continuation of current efforts to lower traffic emissions and ambient air pollution may be an important component of reducing population-level risk of COVID-19 case-fatality and mortality.

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Summary Background Accumulating evidence links fine particulate matter (PM 2·5 ) to premature mortality, cardiovascular disease, and respiratory disease. However, less is known about the influence of PM 2·5 on neurological disorders. We aimed to investigate the effect of long-term PM 2·5 exposure on development of Parkinson’s disease or Alzheimer’s disease and related dementias. Methods We did a longitudinal cohort study in which we constructed a population-based nationwide open cohort including all fee-for-service Medicare beneficiaries (aged ≥65 years) in the contiguous United States (2000–16) with no exclusions. We assigned PM 2·5 postal code (ie, ZIP code) concentrations based on mean annual predictions from a high-resolution model. To accommodate our very large dataset, we applied Cox-equivalent Poisson models with parallel computing to estimate hazard ratios (HRs) for first hospital admission for Parkinson’s disease or Alzheimer’s disease and related dementias, adjusting for potential confounders in the health models. Findings Between Jan 1, 2000, and Dec 31, 2016, of 63 038 019 individuals who were aged 65 years or older during the study period, we identified 1·0 million cases of Parkinson’s disease and 3·4 million cases of Alzheimer’s disease and related dementias based on primary and secondary diagnosis billing codes. For each 5 μg/m 3 increase in annual PM 2·5 concentrations, the HR was 1·13 (95% CI 1·12–1·14) for first hospital admission for Parkinson’s disease and 1·13 (1·12–1·14) for first hospital admission for Alzheimer’s disease and related dementias. For both outcomes, there was strong evidence of linearity at PM 2·5 concentrations less than 16 μg/m 3 (95th percentile of the PM 2·5 distribution), followed by a plateaued association with increasingly larger confidence bands. Interpretation We provide evidence that exposure to annual mean PM 2·5 in the USA is significantly associated with an increased hazard of first hospital admission with Parkinson’s disease and Alzheimer’s disease and related dementias. For the ageing American population, improving air quality to reduce PM 2·5 concentrations to less than current national standards could yield substantial health benefits by reducing the burden of neurological disorders.

2Cheng, Z. et al. Status and characteristics of ambient PM2.5 pollution in global megacities.