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1.
Proc Natl Acad Sci U S A ; 116(18): 8775-8780, 2019 04 30.
Artículo en Inglés | MEDLINE | ID: mdl-30962364

RESUMEN

Fine particulate matter (PM2.5) air pollution has been recognized as a major source of mortality in the United States for at least 25 years, yet much remains unknown about which sources are the most harmful, let alone how best to target policies to mitigate them. Such efforts can be improved by employing high-resolution geographically explicit methods for quantifying human health impacts of emissions of PM2.5 and its precursors. Here, we provide a detailed examination of the health and economic impacts of PM2.5 pollution in the United States by linking emission sources with resulting pollution concentrations. We estimate that anthropogenic PM2.5 was responsible for 107,000 premature deaths in 2011, at a cost to society of $886 billion. Of these deaths, 57% were associated with pollution caused by energy consumption [e.g., transportation (28%) and electricity generation (14%)]; another 15% with pollution caused by agricultural activities. A small fraction of emissions, concentrated in or near densely populated areas, plays an outsized role in damaging human health with the most damaging 10% of total emissions accounting for 40% of total damages. We find that 33% of damages occur within 8 km of emission sources, but 25% occur more than 256 km away, emphasizing the importance of tracking both local and long-range impacts. Our paper highlights the importance of a fine-scale approach as marginal damages can vary by over an order of magnitude within a single county. Information presented here can assist mitigation efforts by identifying those sources with the greatest health effects.

2.
Proc Natl Acad Sci U S A ; 115(38): 9592-9597, 2018 09 18.
Artículo en Inglés | MEDLINE | ID: mdl-30181279

RESUMEN

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.


Asunto(s)
Contaminantes Atmosféricos/toxicidad , Exposición a Riesgos Ambientales/efectos adversos , Carga Global de Enfermedades/estadística & datos numéricos , Enfermedades no Transmisibles/mortalidad , Material Particulado/toxicidad , Contaminación del Aire/efectos adversos , Teorema de Bayes , Estudios de Cohortes , Salud Global/estadística & datos numéricos , Humanos , Modelos de Riesgos Proporcionales , Medición de Riesgo , Factores de Tiempo
3.
Environ Sci Technol ; 49(24): 13929-36, 2015 Dec 15.
Artículo en Inglés | MEDLINE | ID: mdl-26535809

RESUMEN

UNLABELLED: The largest U.S. environmental health risk is cardiopulmonary mortality from ambient PM2.5. The concentration-response (C-R) for ambient PM2.5 in the U.S. is generally assumed to be linear: from any initial baseline, a given concentration reduction would yield the same improvement in health risk. Recent evidence points to the perplexing possibility that the PM2.5 C-R for cardiopulmonary mortality and some other major endpoints might be supralinear: a given concentration reduction would yield greater improvements in health risk as the initial baseline becomes cleaner. We explore the implications of supralinearity for air policy, emphasizing U.S. CONDITIONS: If C-R is supralinear, an economically efficient PM2.5 target may be substantially more stringent than under current standards. Also, if a goal of air policy is to achieve the greatest health improvement per unit of PM2.5 reduction, the optimal policy might call for greater emission reductions in already-clean locales-making "blue skies bluer"-which may be at odds with environmental equity goals. Regardless of whether the C-R is linear or supralinear, the health benefits of attaining U.S. PM2.5 levels well below the current standard would be large. For the supralinear C-R considered here, attaining the current U.S. EPA standard, 12 µg m(-3), would avert only ~17% (if C-R is linear: ∼ 25%) of the total annual cardiopulmonary mortality attributable to PM2.5.


Asunto(s)
Contaminación del Aire/prevención & control , Enfermedades Cardiovasculares/mortalidad , Política Ambiental , Enfermedades Pulmonares/mortalidad , Material Particulado , Contaminación del Aire/legislación & jurisprudencia , Enfermedades Cardiovasculares/etiología , Humanos , Enfermedades Pulmonares/etiología , Material Particulado/análisis , Material Particulado/toxicidad , Salud Pública , Estados Unidos/epidemiología
4.
J Air Waste Manag Assoc ; 65(5): 516-22, 2015 May.
Artículo en Inglés | MEDLINE | ID: mdl-25947311

RESUMEN

UNLABELLED: There is strong evidence that fine particulate matter (aerodynamic diameter<2.5 µm; PM2.5) air pollution contributes to increased risk of disease and death. Estimates of the burden of disease attributable to PM2.5 pollution and benefits of reducing pollution are dependent upon the shape of the concentration response (C-R) functions. Recent evidence suggests that the C-R function between PM2.5 air pollution and mortality risk may be supralinear across wide ranges of exposure. Such results imply that incremental pollution abatement efforts may yield greater benefits in relatively clean areas than in highly polluted areas. The role of the shape of the C-R function in evaluating and understanding the costs and health benefits of air pollution abatement policy is explored. There remain uncertainties regarding the shape of the C-R function, and additional efforts to more fully understand the C-R relationships between PM2.5 and adverse health effects are needed to allow for more informed and effective air pollution abatement policies. Current evidence, however, suggests that there are benefits both from reducing air pollution in the more polluted areas and from continuing to reduce air pollution in cleaner areas. IMPLICATIONS: Estimates of the benefits of reducing PM2.5 air pollution are highly dependent upon the shape of the PM2.5-mortality concentration-response (C-R) function. Recent evidence indicates that this C-R function may be supralinear across wide ranges of exposure, suggesting that incremental pollution abatement efforts may yield greater benefits in relatively clean areas than in highly polluted areas. This paper explores the role of the shape of the C-R function in evaluating and understanding the costs and health benefits of PM2.5 air pollution abatement.


Asunto(s)
Contaminación del Aire/prevención & control , Política Ambiental , Estado de Salud , Contaminación del Aire/análisis , Política Ambiental/economía , Humanos , Estados Unidos
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