China has recently made available hourly air pollution data from over 1500 sites, including airborne particulate matter (PM), SO2, NO2, and O3. We apply Kriging interpolation to four months of data to derive pollution maps for eastern China. Consistent with prior findings, the greatest pollution occurs in the east, but significant levels are widespread across northern and central China and are not limited to major cities or geologic basins. Sources of pollution are widespread, but are particularly intense in a northeast corridor that extends from near Shanghai to north of Beijing. During our analysis period, 92% of the population of China experienced >120 hours of unhealthy air (US EPA standard), and 38% experienced average concentrations that were unhealthy. China’s population-weighted average exposure to PM2.5 was 52 μg/m3. The observed air pollution is calculated to contribute to 1.6 million deaths/year in China [0.7–2.2 million deaths/year at 95% confidence], roughly 17% of all deaths in China.
This paper finds that a 10-μg/m3 increase in airborne particulate matter [particulate matter smaller than 10 μm (PM10)] reduces life expectancy by 0.64 years (95% confidence interval = 0.21–1.07). This estimate is derived from quasiexperimental variation in PM10 generated by China’s Huai River Policy, which provides free or heavily subsidized coal for indoor heating during the winter to cities north of the Huai River but not to those to the south. The findings are derived from a regression discontinuity design based on distance from the Huai River, and they are robust to using parametric and nonparametric estimation methods, different kernel types and bandwidth sizes, and adjustment for a rich set of demographic and behavioral covariates. Furthermore, the shorter lifespans are almost entirely caused by elevated rates of cardiorespiratory mortality, suggesting that PM10 is the causal factor. The estimates imply that bringing all of China into compliance with its Class I standards for PM10 would save 3.7 billion life-years.
Coastal storms can take a devastating toll on the public's health. Urban areas like New York City (NYC) may be particularly at risk, given their dense population, reliance on transportation, energy infrastructure that is vulnerable to flood damage, and high-rise residential housing, which may be hard-hit by power and utility outages. Climate change will exacerbate these risks in the coming decades. Sea levels are rising due to global warming, which will intensify storm surge. These projections make preparing for the health impacts of storms even more important. We conducted a broad review of the health impacts of US coastal storms to inform climate adaptation planning efforts, with a focus on outcomes relevant to NYC and urban coastal areas, and incorporated some lessons learned from recent experience with Superstorm Sandy. Based on the literature, indicators of health vulnerability were selected and mapped within NYC neighborhoods. Preparing for the broad range of anticipated effects of coastal storms and floods may help reduce the public health burden from these events.
The decline of top carnivores has released large herbivore populations around the world, incurring socioeconomic costs such as increased animal–vehicle collisions. Attempts to control overabundant deer in the Eastern United States have largely failed, and deer–vehicle collisions (DVCs) continue to rise at alarming rates. We present the first valuation of an ecosystem service provided by large carnivore recolonization, using DVC reduction by cougars as a case study. Our coupled deer population models and socioeconomic valuations revealed that cougars could reduce deer densities and DVCs by 22% in the Eastern United States, preventing 21,400 human injuries, 155 fatalities, and $2.13 billion in avoided costs within 30 years of establishment. Recently established cougars in South Dakota prevent $1.1 million in collision costs annually. Large carnivore restoration could provide valuable ecosystem services through such socio-ecological cascades, and these benefits could offset the societal costs of coexistence.
ImportanceExposure to ozone has been associated with cardiovascular mortality, but the underlying biological mechanisms are not yet understood.
ObjectiveTo examine the association between ozone exposure and cardiopulmonary pathophysiologic mechanisms.
Design, Setting, and ParticipantsA longitudinal study involving 89 healthy adult participants living on a work campus in Changsha City, China, was conducted from December 1, 2014, to January 31, 2015. This unique quasiexperimental setting allowed for better characterization of air pollutant exposure effects because the participants spent most of their time in controlled indoor environments. Concentrations of indoor and outdoor ozone, along with the copollutants particulate matter, nitrogen dioxide, and sulfur dioxide, were monitored throughout the study period and then combined with time-activity information and filtration conditions of each residence and office to estimate 24-hour and 2-week combined indoor and outdoor mean exposure concentrations. Associations between each exposure measure and outcome measure were analyzed using single-pollutant and 2-pollutant linear mixed models controlling for ambient temperature, secondhand smoke exposure, and personal-level time-varying covariates.
Main Outcomes and MeasuresBiomarkers indicative of inflammation and oxidative stress, arterial stiffness, blood pressure, thrombotic factors, and spirometry were measured at 4 sessions.
ResultsOf the 89 participants, 25 (28%) were women and the mean (SD) age was 31.5 (7.6) years. The 24-hour ozone exposure concentrations ranged from 1.4 to 19.4 parts per billion (ppb), corresponding to outdoor concentrations ranging from 4.3 to 47.9 ppb. Within this range, in models controlling for a second copollutant and other potential confounders, a 10-ppb increase in 24-hour ozone was associated with mean increases of 36.3% (95% CI, 29.9%-43.0%) in the level of platelet activation marker soluble P-selectin, 2.8% (95% CI, 0.6%-5.1%) in diastolic blood pressure, 18.1% (95% CI, 4.5%-33.5%) in pulmonary inflammation markers fractional exhaled nitric oxide, and 31.0% (95% CI, 0.2%-71.1%) in exhaled breath condensate nitrite and nitrate as well as a −9.5% (95% CI, −17.7% to −1.4%) decrease in arterial stiffness marker augmentation index. A 10-ppb increase in 2-week ozone was associated with increases of 61.1% (95% CI, 37.8%-88.2%) in soluble P-selectin level and 126.2% (95% CI, 12.1%-356.2%) in exhaled breath condensate nitrite and nitrate level. Other measured biomarkers, including spirometry, showed no significant associations with either 24-hour ozone or 2-week ozone exposures.
Conclusions and RelevanceShort-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.