Dataset Information

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

ABSTRACT:

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.

SUBMITTER: Lelieveld J

PROVIDER: S-EPMC6528157 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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

Lelieveld Jos J Klingmüller Klaus K Pozzer Andrea A Pöschl Ulrich U Fnais Mohammed M Daiber Andreas A Münzel Thomas T

European heart journal 20190501 20

<h4>Aims</h4>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.<h4>Methods and results</h4>The new hazard ratio functions have been combined with ambient air pol ...[more]

PMID: 30860255

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Project description:Background The association between fine particulate matter and cardiovascular disease has been convincingly demonstrated. The role of traffic-related air pollutants is less clear. To better understand the role of traffic-related air pollutants in cardiovascular disease development, we examined associations between NO2, carotid atherosclerotic plaque, and cardiometabolic disorders associated with cardiovascular disease. Methods and Results Cross-sectional analyses were conducted among 2227 patients (62.9±13.8 years; 49.5% women) from the Stroke Prevention and Atherosclerosis Research Centre (SPARC) in London, Ontario, Canada. Total carotid plaque area measured by ultrasound, cardiometabolic disorders, and residential locations were provided by SPARC medical records. Long-term outdoor residential NO2 concentrations were generated by a land use regression model. Associations between NO2, total carotid plaque area, and cardiometabolic disorders were examined using multiple regression models adjusted for age, sex, smoking, and socioeconomic status. Mean NO2 was 5.4±1.6 ppb in London, Ontario. NO2 was associated with a significant increase in plaque (3.4 mm2 total carotid plaque area per 1 ppb NO2), exhibiting a linear dose-response. NO2 was also positively associated with triglycerides, total cholesterol, and the ratio of low- to high-density lipoprotein cholesterol (P<0.05). Diabetes mellitus mediated the relationship between NO2 and total carotid plaque area (P<0.05). Conclusions Our results demonstrate that even low levels of traffic-related air pollutants are linked to atherosclerotic plaque burden, an association that may be partially attributable to pollution-induced diabetes mellitus. Our findings suggest that reducing ambient concentrations in cities with NO2 below current standards would result in additional health benefits. Given the billions of people exposed to traffic emissions, our study supports the global public health significance of reducing air pollution.

Project description:This study was aimed to investigate the air pollutants impact on heart patient's hospital admission rates in Yazd for the first time. Modeling was done by time series, multivariate linear regression, and artificial neural network (ANN). During 5 years, the mean concentrations of PM10, SO2, O3, NO2, and CO were 98.48 μg m-3, 8.57 ppm, 19.66 ppm, 18.14 ppm, and 4.07 ppm, respectively. The total number of cardiovascular disease (CD) patients was 12,491, of which 57% and 43% were related to men and women, respectively. The maximum correlation of air pollutants was observed between CO and PM10 (R = 0.62). The presence of SO2 and NO2 can be dependent on meteorological parameters (R = 0.48). Despite there was a positive correlation between age and CD (p = 0.001), the highest correlation was detected between SO2 and CD (R = 0.4). The annual variation trend of SO2, NO2, and CO concentrations was more similar to the variations trend in meteorological parameters. Moreover, the temperature had also been an effective factor in the O3 variation rate at lag = 0. On the other hand, SO2 has been the most effective contaminant in CD patient admissions in hospitals (R = 0.45). In the monthly database classification, SO2 and NO2 were the most prominent factors in the CD (R = 0.5). The multivariate linear regression model also showed that CO and SO2 were significant contaminants in the number of hospital admissions (R = 0.46, p = 0.001) that both pollutants were a function of air temperature (p = 0.002). In the ANN nonlinear model, the 14, 12, 10, and 13 neurons in the hidden layer were formed the best structure for PM, NO2, O3, and SO2, respectively. Thus, the Rall rate for these structures was 0.78-0.83. In these structures, according to the autocorrelation of error in lag = 0, the series are stationary, which makes it possible to predict using this model. According to the results, the artificial neural network had a good ability to predict the relationship between the effect of air pollutants on the CD in a 5 years' time series.

Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

Dataset Information

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

Aims

Methods and results

Conclusion

Publications

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

Similar Datasets

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