Ambient fine particulate matter (PM2.5) has a large and well-documented global burden of disease. Our analysis uses high-resolution (10 km, global-coverage) concentration data and cause-specific ...integrated exposure-response (IER) functions developed for the Global Burden of Disease 2010 to assess how regional and global improvements in ambient air quality could reduce attributable mortality from PM2.5. Overall, an aggressive global program of PM2.5 mitigation in line with WHO interim guidelines could avoid 750 000 (23%) of the 3.2 million deaths per year currently (ca. 2010) attributable to ambient PM2.5. Modest improvements in PM2.5 in relatively clean regions (North America, Europe) would result in surprisingly large avoided mortality, owing to demographic factors and the nonlinear concentration-response relationship that describes the risk of particulate matter in relation to several important causes of death. In contrast, major improvements in air quality would be required to substantially reduce mortality from PM2.5 in more polluted regions, such as China and India. Moreover, forecasted demographic and epidemiological transitions in India and China imply that to keep PM2.5-attributable mortality rates (deaths per 100 000 people per year) constant, average PM2.5 levels would need to decline by ∼20–30% over the next 15 years merely to offset increases in PM2.5-attributable mortality from aging populations. An effective program to deliver clean air to the world’s most polluted regions could avoid several hundred thousand premature deaths each year.
To assess the value of exosomal miRNAs as biomarkers for Alzheimer disease (AD), the expression of microRNAs was measured in a plasma fraction enriched in exosomes by differential centrifugation, ...using Illumina deep sequencing. Samples from 35 persons with a clinical diagnosis of AD dementia were compared to 35 age and sex matched controls. Although these samples contained less than 0.1 microgram of total RNA, deep sequencing gave reliable and informative results. Twenty miRNAs showed significant differences in the AD group in initial screening (miR-23b-3p, miR-24-3p, miR-29b-3p, miR-125b-5p, miR-138-5p, miR-139-5p, miR-141-3p, miR-150-5p, miR-152-3p, miR-185-5p, miR-338-3p, miR-342-3p, miR-342-5p, miR-548at-5p, miR-659-5p, miR-3065-5p, miR-3613-3p, miR-3916, miR-4772-3p, miR-5001-3p), many of which satisfied additional biological and statistical criteria, and among which a panel of seven miRNAs were highly informative in a machine learning model for predicting AD status of individual samples with 83-89% accuracy. This performance is not due to over-fitting, because a) we used separate samples for training and testing, and b) similar performance was achieved when tested on technical replicate data. Perhaps the most interesting single miRNA was miR-342-3p, which was a) expressed in the AD group at about 60% of control levels, b) highly correlated with several of the other miRNAs that were significantly down-regulated in AD, and c) was also reported to be down-regulated in AD in two previous studies. The findings warrant replication and follow-up with a larger cohort of patients and controls who have been carefully characterized in terms of cognitive and imaging data, other biomarkers (e.g., CSF amyloid and tau levels) and risk factors (e.g., apoE4 status), and who are sampled repeatedly over time. Integrating miRNA expression data with other data is likely to provide informative and robust biomarkers in Alzheimer disease.
Summary Background Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and ...burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels. Methods We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM2·5 ) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure. Findings Ambient PM2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2·5 caused 4·2 million (95% uncertainty interval UI 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015. Interpretation Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction. Funding Bill & Melinda Gates Foundation and Health Effects Institute.
Exposure to traffic-related air pollutants is an important public health issue. Here, we present a systematic review and meta-analysis of research examining the relationship of measures of nitrogen ...oxides (NOx) and of various measures of traffic-related air pollution exposure with lung cancer.
We conducted random-effects meta-analyses of studies examining exposure to nitrogen dioxide (NO2) and NOx and its association with lung cancer. We identified 20 studies that met inclusion criteria and provided information necessary to estimate the change in lung cancer per 10-μg/m3 increase in exposure to measured NO2. Further, we qualitatively assessed the evidence of association between distance to roadways and traffic volume associated with lung cancer.
The meta-estimate for the change in lung cancer associated with a 10-μg/m3 increase in exposure to NO2 was 4% (95% CI: 1%, 8%). The meta-estimate for change in lung cancer associated with a 10-μg/m3 increase in NOx was similar and slightly more precise, 3% (95% CI: 1%, 5%). The NO2 meta-estimate was robust to different confounding adjustment sets as well as the exposure assessment techniques used. Trim-and-fill analyses suggest that if publication bias exists, the overall meta-estimate is biased away from the null. Forest plots for measures of traffic volume and distance to roadways largely suggest a modest increase in lung cancer risk.
We found consistent evidence of a relationship between NO2, as a proxy for traffic-sourced air pollution exposure, with lung cancer. Studies of lung cancer related to residential proximity to roadways and NOx also suggest increased risk, which may be attributable partly to air pollution exposure. The International Agency for Research on Cancer recently classified outdoor air pollution and particulate matter as carcinogenic (Group 1). These meta-analyses support this conclusion, drawing particular attention to traffic-sourced air pollution.
Hamra GB, Laden F, Cohen AJ, Raaschou-Nielsen O, Brauer M, Loomis D. 2015. Lung cancer and exposure to nitrogen dioxide and traffic: a systematic review and meta-analysis. Environ Health Perspect 123:1107-1112; http://dx.doi.org/10.1289/ehp.1408882.
Abstract
Air pollution is now recognized by governments, international institutions and civil society as a major global public health risk factor. This is the result of the remarkable growth of ...scientific knowledge enabled by advances in epidemiology and exposure assessment. There is now a broad scientific consensus that exposure to air pollution increases mortality and morbidity from cardiovascular and respiratory disease and lung cancer and shortens life expectancy. Although air pollution has markedly declined in high-income countries, it was still responsible for some 4.9 million deaths in 2017, largely in low- and middle-income countries, where air pollution has increased over the past 25 y. As governments act to reduce air pollution there is a continuing need for research to strengthen the evidence on disease risk at very low and very high levels of air pollution, identify the air pollution sources most responsible for disease burden and assess the public health effectiveness of actions taken to improve air quality.
Exposure to ambient fine particulate matter (PM2.5) air pollution is a major risk for premature death. Here, we systematically quantify the global impact of PM2.5 on life expectancy. Using data from ...the Global Burden of Disease project and actuarial standard life table methods, we estimate global and national decrements in life expectancy that can be attributed to ambient PM2.5 for 185 countries. In 2016, PM2.5 exposure reduced average global life expectancy at birth by ∼1 year with reductions of ∼1.2–1.9 years in polluted countries of Asia and Africa. If PM2.5 in all countries met the World Health Organization Air Quality Guideline (10 μg m–3), we estimate life expectancy could increase by a population-weighted median of 0.6 year (interquartile range of 0.2–1.0 year), a benefit of a magnitude similar to that of eradicating lung and breast cancer. Because background disease rates modulate the effect of air pollution on life expectancy, high age-specific rates of cardiovascular disease in many polluted low- and middle-income countries amplify the impact of PM2.5 on survival. Our analysis adds to prior research by illustrating how mortality from air pollution substantially reduces human longevity.
Particulate matter <2.5 micrometer (PM2.5) is associated with adverse perinatal outcomes, but the impact on disease burden mediated by this pathway has not previously been included in the Global ...Burden of Disease (GBD), Mortality, Injuries, and Risk Factors studies. We estimated the global burden of low birth weight (LBW) and preterm birth (PTB) and impacts on reduced birth weight and gestational age (GA), attributable to ambient and household PM2.5 pollution in 2019.
We searched PubMed, Embase, and Web of Science for peer-reviewed articles in English. Study quality was assessed using 2 tools: (1) Agency for Healthcare Research and Quality checklist; and (2) National Institute of Environmental Health Sciences (NIEHS) risk of bias questions. We conducted a meta-regression (MR) to quantify the risk of PM2.5 on birth weight and GA. The MR, based on a systematic review (SR) of articles published through April 4, 2021, and resulting uncertainty intervals (UIs) accounted for unexplained between-study heterogeneity. Separate nonlinear relationships relating exposure to risk were generated for each outcome and applied in the burden estimation. The MR included 44, 40, and 40 birth weight, LBW, and PTB studies, respectively. Majority of the studies were of retrospective cohort design and primarily from North America, Europe, and Australia. A few recent studies were from China, India, sub-Saharan Africa, and South America. Pooled estimates indicated 22 grams (95% UI: 12, 32) lower birth weight, 11% greater risk of LBW (1.11, 95% UI: 1.07, 1.16), and 12% greater risk of PTB (1.12, 95% UI: 1.06, 1.19), per 10 μg/m3 increment in ambient PM2.5. We estimated a global population-weighted mean lowering of 89 grams (95% UI: 88, 89) of birth weight and 3.4 weeks (95% UI: 3.4, 3.4) of GA in 2019, attributable to total PM2.5. Globally, an estimated 15.6% (95% UI: 15.6, 15.7) of all LBW and 35.7% (95% UI: 35.6, 35.9) of all PTB infants were attributable to total PM2.5, equivalent to 2,761,720 (95% UI: 2,746,713 to 2,776,722) and 5,870,103 (95% UI: 5,848,046 to 5,892,166) infants in 2019, respectively. About one-third of the total PM2.5 burden for LBW and PTB could be attributable to ambient exposure, with household air pollution (HAP) dominating in low-income countries. The findings should be viewed in light of some limitations such as heterogeneity between studies including size, exposure levels, exposure assessment method, and adjustment for confounding. Furthermore, studies did not separate the direct effect of PM2.5 on birth weight from that mediated through GA. As a consequence, the pooled risk estimates in the MR and likewise the global burden may have been underestimated.
Ambient and household PM2.5 were associated with reduced birth weight and GA, which are, in turn, associated with neonatal and infant mortality, particularly in low- and middle-income countries.
Acute lower respiratory infections (ALRI) account for nearly one fifth of mortality in young children worldwide and have been associated with exposures to indoor and outdoor sources of ...combustion-derived air pollution. A systematic review was conducted to identify relevant articles on air pollution and ALRI in children. Using a Bayesian approach to meta-analysis, a summary estimate of 1.12 (1.03, 1.30) increased risk in ALRI occurrence per 10 μg/m
3
increase in annual average PM
2.5
concentration was derived from the longer-term (subchronic and chronic) effects studies. This analysis strengthens the evidence for a causal relationship between exposure to PM
2.5
and the occurrence of ALRI and provides a basis for estimating the global attributable burden of mortality due to ALRI that is not influenced by the wide variation in regional case fatality rates. Most studies, however, have been conducted in settings with relatively low levels of PM
2.5
. Extrapolating their results to other, more polluted, regions will require a model that is informed by evidence from studies of the effects on ALRI of exposure to PM
2.5
from other combustion sources, such as secondhand smoke and household solid fuel use.
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•Exposure to PM2.5 increased CVD mortality in a nationally representative cohort.•We provided one of the very few evidence on long-term CVD effects of PM2.5 constituents.•BC, OM, ...NO3–, NH4+ and SO42− showed appreciably larger risks than PM2.5 total mass.•Soil dust showed no cardiovascular risks.
Few studies have evaluated long-term cardiovascular effects of fine particulate matter (PM2.5) and its constituents in countries with high air pollution levels. We aimed to investigate the associations of long-term exposure to PM2.5 and constituents with cardiovascular mortality in China.
We conducted a prospective cohort study of 90,672 adults ≥ 18 years from 2010 to 2017 in 161 districts/counties across China. The residential annual-average exposure to PM2.5 and 6 main components from 2011 to 2017 were estimated by satellite-based and chemical transport models. Associations of PM2.5 and constituents with cardiovascular mortality were analyzed by competing-risk Cox proportional hazards regression.
The average PM2.5 exposure throughout the whole period was 46 ± 22 μg/m3. The hazard ratios of mortality (95% confidence intervals) per 10 μg/m3 increase in PM2.5 concentrations were 1.02 (1.00, 1.05) for overall cardiovascular disease, 1.05 (1.01, 1.09) for ischemic heart disease, 1.03 (1.00, 1.06) for overall stroke, 0.99 (0.94, 1.04) for hemorrhagic stroke, and 1.11 (1.04, 1.19) for ischemic stroke. PM2.5 constituents from fossil fuel combustion (i.e., black carbon, organic matter, nitrate, ammonium, and sulfate) showed larger hazard ratios than PM2.5 total mass, while soil dust showed no risks.
This nationwide cohort study demonstrated associations of long-term exposure to PM2.5 and its constituents with increased risks of cardiovascular mortality in the general population of China. Our study highlighted the importance of PM2.5 constituents from fossil fuel combustion in the long-term cardiovascular effects of PM2.5 in China.
Outdoor air pollution is a major contributor to the burden of disease worldwide. Most of the global population resides in places where air pollution levels, because of emissions from industry, power ...generation, transportation, and domestic burning, considerably exceed the World Health Organization's health‐based air‐quality guidelines. Outdoor air pollution poses an urgent worldwide public health challenge because it is ubiquitous and has numerous serious adverse human health effects, including cancer. Currently, there is substantial evidence from studies of humans and experimental animals as well as mechanistic evidence to support a causal link between outdoor (ambient) air pollution, and especially particulate matter (PM) in outdoor air, with lung cancer incidence and mortality. It is estimated that hundreds of thousands of lung cancer deaths annually worldwide are attributable to PM air pollution. Epidemiological evidence on outdoor air pollution and the risk of other types of cancer, such as bladder cancer or breast cancer, is more limited. Outdoor air pollution may also be associated with poorer cancer survival, although further research is needed. This report presents an overview of outdoor air pollutants, sources, and global levels, as well as a description of epidemiological evidence linking outdoor air pollution with cancer incidence and mortality. Biological mechanisms of air pollution‐derived carcinogenesis are also described. This report concludes by summarizing public health/policy recommendations, including multilevel interventions aimed at individual, community, and regional scales. Specific roles for medical and health care communities with regard to prevention and advocacy and recommendations for further research are also described.
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