Active travel (cycling, walking) is beneficial for the health due to increased physical activity (PA). However, active travel may increase the intake of air pollution, leading to negative health consequences. We examined the risk-benefit balance between active travel related PA and exposure to air pollution across a range of air pollution and PA scenarios. The health effects of active travel and air pollution were estimated through changes in all-cause mortality for different levels of active travel and air pollution. Air pollution exposure was estimated through changes in background concentrations of fine particulate matter (PM2.5), ranging from 5 to 200μg/m3. For active travel exposure, we estimated cycling and walking from 0 up to 16h per day, respectively. These refer to long-term average levels of active travel and PM2.5 exposure. For the global average urban background PM2.5 concentration (22μg/m3) benefits of PA by far outweigh risks from air pollution even under the most extreme levels of active travel. In areas with PM2.5 concentrations of 100μg/m3, harms would exceed benefits after 1h 30min of cycling per day or more than 10h of walking per day. If the counterfactual was driving, rather than staying at home, the benefits of PA would exceed harms from air pollution up to 3h 30min of cycling per day. The results were sensitive to dose-response function (DRF) assumptions for PM2.5 and PA. PA benefits of active travel outweighed the harm caused by air pollution in all but the most extreme air pollution concentrations.
Preterm birth (PTB) rates (11.4% in 2013) in the United States (US) remain high and are a substantial cause of morbidity. Studies of prenatal exposure have associated particulate matter <2.5microns in diameter (PM2.5) and other ambient air pollutants with adverse birth outcomes, yet, to our knowledge, burden and costs of PM 2.5-attributable PTB have not been estimated in the US.
Reduction of preterm births (<37 completed weeks of gestation) would substantially reduce neonatal and infant mortality, and deleterious health effects in survivors. Maternal fine particulate matter (PM2.5) exposure has been identified as a possible risk factor contributing to preterm birth. The aim of this study was to produce the first estimates of ambient PM2.5-associated preterm births for 183 individual countries and globally. To do this, national, population-weighted, annual average ambient PM2.5 concentration, preterm birth rate and number of livebirths were combined to calculate the number of PM2.5-associated preterm births in 2010 for 183 countries. Uncertainty was quantified using Monte-Carlo simulations, and analyses were undertaken to investigate the sensitivity of PM2.5-associated preterm birth estimates to assumptions about the shape of the concentration-response function at low and high PM2.5 exposures, inclusion of provider-initiated preterm births, and exposure to indoor air pollution. Globally, in 2010, the number of PM2.5-associated preterm births was estimated as 2.7 million (1.8-3.5 million, 18% (12-24%) of total preterm births globally) with a low concentration cut-off (LCC) set at 10μgm(-3), and 3.4 million (2.4-4.2 million, 23% (16-28%)) with a LCC of 4.3μgm(-3). South and East Asia, North Africa/Middle East and West sub-Saharan Africa had the largest contribution to the global total, and the largest percentage of preterm births associated with PM2.5. Sensitivity analyses showed that PM2.5-associated preterm birth estimates were 24% lower when provider-initiated preterm births were excluded, 38-51% lower when risk was confined to the PM2.5 exposure range in the studies used to derive the effect estimate, and 56% lower when mothers who live in households that cook with solid fuels (and whose personal PM2.5 exposure is likely dominated by indoor air pollution) were excluded. The concentration-response function applied here derives from a meta-analysis of studies, most of which were conducted in the US and Europe, and its application to the areas of the world where we estimate the greatest effects on preterm births remains uncertain. Nevertheless, the substantial percentage of preterm births estimated to be associated with anthropogenic PM2.5 (18% (13%-24%) of total preterm births globally) indicates that reduction of maternal PM2.5 exposure through emission reduction strategies should be considered alongside mitigation of other risk factors associated with preterm births.
Epidemiologic studies have consistently reported associations between outdoor fine particulate matter (PM2.5) air pollution and adverse health effects. Although Asia bears the majority of the public health burden from air pollution, few epidemiologic studies have been conducted outside of North America and Europe due in part to challenges in population exposure assessment. We assessed the feasibility of two current exposure assessment techniques, land use regression (LUR) modeling and mobile monitoring, and estimated the mortality attributable to air pollution in Ulaanbaatar, Mongolia. We developed LUR models for predicting wintertime spatial patterns of NO2 and SO2 based on 2-week passive Ogawa measurements at 37 locations and freely available geographic predictors. The models explained 74% and 78% of the variance in NO2 and SO2, respectively. Land cover characteristics derived from satellite images were useful predictors of both pollutants. Mobile PM2.5 monitoring with an integrating nephelometer also showed promise, capturing substantial spatial variation in PM2.5 concentrations. The spatial patterns in SO2 and PM, seasonal and diurnal patterns in PM2.5, and high wintertime PM2.5/PM10 ratios were consistent with a major impact from coal and wood combustion in the city’s low-income traditional housing (ger) areas. The annual average concentration of PM2.5 measured at a centrally located government monitoring site was 75 μg/m3 or more than seven times the World Health Organization’s PM2.5 air quality guideline, driven by a wintertime average concentration of 148 μg/m3. PM2.5 concentrations measured in a traditional housing area were higher, with a wintertime mean PM2.5 concentration of 250 μg/m3. We conservatively estimated that 29% (95% CI, 12-43%) of cardiopulmonary deaths and 40% (95% CI, 17-56%) of lung cancer deaths in the city are attributable to outdoor air pollution. These deaths correspond to nearly 10% of the city’s total mortality, with estimates ranging to more than 13% of mortality under less conservative model assumptions. LUR models and mobile monitoring can be successfully implemented in developing country cities, thus cost-effectively improving exposure assessment for epidemiology and risk assessment. Air pollution represents a major threat to public health in Ulaanbaatar, Mongolia, and reducing home heating emissions in traditional housing areas should be the primary focus of air pollution control efforts.
Mammographic breast density is a well-established strong risk factor for breast cancer. The environmental contributors to geographic variation in breast density in urban and rural areas are poorly understood. We examined the association between breast density and exposure to ambient air pollutants (particulate matter <2.5 μm in diameter (PM2.5) and ozone (O3)) in a large population-based screening registry.
Fine particulate matter (PM2.5) has been linked to cardiovascular disease, possibly via accelerated atherosclerosis. We examined associations between the progression of the intima-medial thickness (IMT) of the common carotid artery, as an indicator of atherosclerosis, and long-term PM2.5 concentrations in participants from the Multi-Ethnic Study of Atherosclerosis (MESA).
- Proceedings of the National Academy of Sciences of the United States of America
- Published over 2 years ago
Sulfate aerosols exert profound impacts on human and ecosystem health, weather, and climate, but their formation mechanism remains uncertain. Atmospheric models consistently underpredict sulfate levels under diverse environmental conditions. From atmospheric measurements in two Chinese megacities and complementary laboratory experiments, we show that the aqueous oxidation of SO2 by NO2 is key to efficient sulfate formation but is only feasible under two atmospheric conditions: on fine aerosols with high relative humidity and NH3 neutralization or under cloud conditions. Under polluted environments, this SO2 oxidation process leads to large sulfate production rates and promotes formation of nitrate and organic matter on aqueous particles, exacerbating severe haze development. Effective haze mitigation is achievable by intervening in the sulfate formation process with enforced NH3 and NO2 control measures. In addition to explaining the polluted episodes currently occurring in China and during the 1952 London Fog, this sulfate production mechanism is widespread, and our results suggest a way to tackle this growing problem in China and much of the developing world.
BACKGROUND: Environmental pollution is a known risk factor for multiple diseases and furthermore increases rate of hospitalisations. We investigated the correlation between emergency room admissions (ERAs) of the general population for respiratory diseases and the environmental pollutant levels in Milan, a metropolis in northern Italy. METHODS: We collected data from 45770 ERAs for respiratory diseases. A time-stratified case-crossover design was used to investigate the association between air pollution levels and ERAs for acute respiratory conditions. The effects of air pollutants were investigated at lag 0 to lag 5, lag 0–2 and lag 3–5 in both single and multi-pollutant models, adjusted for daily weather variables. RESULTS: An increase in ozone (O3) levels at lag 3–5 was associated with a 78% increase in the number of ERAs for asthma, especially during the warm season. Exposure to carbon monoxide (CO) proved to be a risk factor for pneumonia at lag 0–2 and in the warm season increased the risk of ERA by 66%. A significant association was found between ERAs for COPD exacerbation and levels of sulphur dioxide (SO2), CO, nitrate dioxide (NO2), and particulate matter (PM10 and PM2.5). The multipollutant model that includes all pollutants showed a significant association between CO (26%) and ERA for upper respiratory tract diseases at lag 0–2. For chronic obstructive pulmonary disease (COPD) exacerbations, only CO (OR 1.19) showed a significant association. CONCLUSIONS: Exposure to environmental pollution, even at typical low levels, can increase the risk of ERA for acute respiratory diseases and exacerbation of obstructive lung diseases in the general population.
A gap in emission inventories of urban volatile organic compound (VOC) sources, which contribute to regional ozone and aerosol burdens, has increased as transportation emissions in the United States and Europe have declined rapidly. A detailed mass balance demonstrates that the use of volatile chemical products (VCPs)-including pesticides, coatings, printing inks, adhesives, cleaning agents, and personal care products-now constitutes half of fossil fuel VOC emissions in industrialized cities. The high fraction of VCP emissions is consistent with observed urban outdoor and indoor air measurements. We show that human exposure to carbonaceous aerosols of fossil origin is transitioning away from transportation-related sources and toward VCPs. Existing U.S. regulations on VCPs emphasize mitigating ozone and air toxics, but they currently exempt many chemicals that lead to secondary organic aerosols.
Environmental exposure to chemicals has been considered a potential factor contributing to deteriorated semen quality. However, previous literature on exposure to air pollution and semen quality is inconsistent. We therefore investigated the health effects of short-term and long-term exposure to fine particulate matter (PM2.5) on semen quality in Taiwanese men from the general population.