Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015

Air Pollution and Cardiovascular Disease: JACC State-of-the-Art Review

Aims Ambient air pollution is a major health risk, leading to respiratory and cardiovascular mortality. A recent Global Exposure Mortality Model, based on an unmatched number of cohort studies in many countries, provides new hazard ratio functions, calling for re-evaluation of the disease burden. Accordingly, we estimated excess cardiovascular mortality attributed to air pollution in Europe. Methods and results The new hazard ratio functions have been combined with ambient air pollution exposure data to estimate the impacts in Europe and the 28 countries of the European Union (EU-28). The annual excess mortality rate from ambient air pollution in Europe is 790 000 [95% confidence interval (95% CI) 645 000-934 000], and 659 000 (95% CI 537 000-775 000) in the EU-28. Between 40% and 80% are due to cardiovascular events, which dominate health outcomes. The upper limit includes events attributed to other non-communicable diseases, which are currently not specified. These estimates exceed recent analyses, such as the Global Burden of Disease for 2015, by more than a factor of two. We estimate that air pollution reduces the mean life expectancy in Europe by about 2.2 years with an annual, attributable per capita mortality rate in Europe of 133/100 000 per year. Conclusion We provide new data based on novel hazard ratio functions suggesting that the health impacts attributable to ambient air pollution in Europe are substantially higher than previously assumed, though subject to considerable uncertainty. Our results imply that replacing fossil fuels by clean, renewable energy sources could substantially reduce the loss of life expectancy from air pollution.

/pdf/cardiovascular-disease-burden-from-ambient-air-pollution-in-4ntgurb18s.pdf

Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions.

Background Type 2 diabetes mellitus (T2DM) is a global epidemic associated with increased health expenditure, and low quality of life. Many non-genetic risk factors have been suggested, but their overall epidemiological credibility has not been assessed. Methods We searched PubMed to capture all meta-analyses and Mendelian randomization studies for risk factors of T2DM. For each association, we estimated the summary effect size, its 95% confidence and prediction interval, and the I2 metric. We examined the presence of small-study effects and excess significance bias. We assessed the epidemiological credibility through a set of predefined criteria. Results We captured 86 eligible papers (142 associations) covering a wide range of biomarkers, medical conditions, and dietary, lifestyle, environmental and psychosocial factors. Adiposity, low hip circumference, serum biomarkers (increased level of alanine aminotransferase, gamma-glutamyl transferase, uric acid and C-reactive protein, and decreased level of adiponectin and vitamin D), an unhealthy dietary pattern (increased consumption of processed meat and sugar-sweetened beverages, decreased intake of whole grains, coffee and heme iron, and low adherence to a healthy dietary pattern), low level of education and conscientiousness, decreased physical activity, high sedentary time and duration of television watching, low alcohol drinking, smoking, air pollution, and some medical conditions (high systolic blood pressure, late menarche age, gestational diabetes, metabolic syndrome, preterm birth) presented robust evidence for increased risk of T2DM. Conclusions A healthy lifestyle pattern could lead to decreased risk for T2DM. Future randomized clinical trials should focus on identifying efficient strategies to modify harmful daily habits and predisposing dietary patterns.

/pdf/risk-factors-for-type-2-diabetes-mellitus-an-exposure-wide-3spd5o49ly.pdf

Risk factors for type 2 diabetes mellitus: An exposure-wide umbrella review of meta-analyses.

Air pollution is well recognized as a major risk factor for chronic non-communicable diseases and has been estimated to contribute more to global morbidity and mortality than all other known environmental risk factors combined. Although air pollution contains a heterogeneous mixture of gases, the most robust evidence for detrimental effects on health is for fine particulate matter (particles ≤2.5 µm in diameter (PM2.5)) and ozone gas and, therefore, these species have been the main focus of environmental health research and regulatory standards. The evidence to date supports a strong link between the risk of cardiovascular events and all-cause mortality with PM2.5 across a range of exposure levels, including to levels below current regulatory standards, with no ‘safe’ lower exposure levels at the population level. In this comprehensive Review, the empirical evidence supporting the effects of air pollution on cardiovascular health are examined, potential mechanisms that lead to increased cardiovascular risk are described, and measures to reduce this risk and identify key gaps in our knowledge that could help address the increasing cardiovascular morbidity and mortality associated with air pollution are discussed. A strong relationship exists between exposure to air pollution and cardiovascular events. In this Review, Rajagopalan and colleagues summarize the evidence supporting the detrimental effects of air pollution on cardiovascular health and describe the potential mechanisms involved in air pollution-mediated cardiovascular mortality.

Environmental determinants of cardiovascular disease: lessons learned from air pollution.

Objective: To assess the effect of long-term exposure to air pollution on type 2 diabetes risk, a meta-analysis of prospective cohort studies was performed. Methods: Literature search was conducted with Pubmed, Embase, and Web of Science for prospective cohort studies investigating the association of type 2 diabetes risk with increments in particulate matter (PM, diameter !2.5 mm (PM2.5) or !10 mm (PM10)) or nitrogen dioxide (NO2). We used a random-effects model to calculate the overall relative risk (RR) with 95% CI. Results: Of 808 identified articles, ten cohort studies were finally included, which involved a total of 2 371 907 participants and 21 095 incident cases of type 2 diabetes. Elevated risk of type 2 diabetes was significantly associated with long-term exposures to high levels of PM2.5 (RRZ1.28, 95% CI 1.06‐1.55, PZ0.009, I 2 Z83.5%), PM10 (RRZ1.15, 95% CI 1.02‐1.30, PZ0.022, I 2 Z0%), and NO2 (RRZ1.12, 95% CI 1.02‐1.23, PZ0.015, I 2 Z63.5%). When using standardized risk estimates, the RRs of type 2 diabetes were significant for increments in concentrations of PM2.5 (1.39 per 10 mg/m 3 increment, 95% CI 1.14‐1.68, PZ0.001), PM10 (1.34 per 10 mg/m 3 increment, 95% CI 1.22‐1.47, P!0.001), and NO2 (1.11 per 10 mg/m 3 increment, 95% CI 1.07‐1.16, P!0.001). No obvious evidence of publication bias was observed. Conclusion: Long-term exposure to high levels of main air pollutants is significantly associated with elevated risk of type 2 diabetes mellitus.

/pdf/effect-of-long-term-exposure-to-air-pollution-on-type-2-1m14wdeey3.pdf

Effect of long-term exposure to air pollution on type 2 diabetes mellitus risk: a systemic review and meta-analysis of cohort studies

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Effect of long-term exposure to air pollution on type 2 diabetes mellitus risk: a systemic review and meta-analysis of cohort studies