Air pollution and cause-specific mortality: A comparative study of urban and rural areas in China

Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61-4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.

Exposure to ambient nitrogen dioxide (NO2) has been linked to increased mortality in several epidemiological studies but the question remains of whether NO2 is directly responsible for the health effects or is only an indicator of other pollutants, including particulate matter. The aim of the present review was to provide pooled estimates of the long-term effects of NO2 on mortality, which are potentially useful for health impact assessment. We selected 23 papers, published from 2004 to 2013, evaluating the relationship between NO2 and mortality, also including an assessment of the effect of particulate matter exposure. A random-effects meta-analysis was carried out on 19 studies. The pooled effect on mortality was 1.04 (95% CI 1.02-1.06) with an increase of 10 μg · m(-3) in the annual NO2 concentration and 1.05 (95% CI 1.01-1.09) for particulate matter <2.5 μm in diameter (PM2.5) (10 μg · m(-3)). The effect on cardiovascular mortality was 1.13 (95% CI 1.09-1.18) for NO2 and 1.20 (95% CI 1.09-1.31) for PM2.5. The NO2 effect on respiratory mortality was 1.03 (95% CI 1.02-1.03) and 1.05 (95% CI 1.01-1.09) for PM2.5. Four bipollutant analyses with particulate matter and NO2 in the same models showed minimal changes in the effect estimates of NO2. There is evidence of a long-term effect of NO2 on mortality as great as that of PM2.5. An independent effect of NO2 emerged from multipollutant models.

Background: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. Objectives: We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society’s Cancer Prevention Study-II cohort. Methods: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source–associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000–2005. Results: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic–related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-μg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality. Conclusions: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5–mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources. Citation: Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. 2016. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. fine particle air pollution. Environ Health Perspect 124:785–794; http://dx.doi.org/10.1289/ehp.1509777