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Exposure to multiple air pollutants and the incidence of coronary heart disease: A fine-scale geographic analysis.

ABSTRACT: Geographical variations in cardiovascular disease rates have been linked to individual air pollutants. Investigating the relation between cardiovascular disease and exposure to a complex mixture of air pollutants requires holistic approaches. We assessed the relationship between exposure to multiple air pollutants and the incidence of coronary heart disease (CHD) in a general population sample. We collected data in the Lille MONICA registry (2008-2011) on 3268 incident cases (age range: 35-74). Based on 20 indicators, we derived a composite environmental score (SEnv) for cumulative exposure to air pollution. Poisson regression models were used to analyse associations between CHD rates on one hand and SEnv and each single indicator on the other (considered in tertiles, where T3 is the most contaminated). We adjusted models for age, sex, area-level social deprivation, and neighbourhood spatial structure. The incidence of CHD was a spatially heterogeneous (p=0.006). There was a significant positive association between SEnv and CHD incidence (trend p=0.0151). The relative risks [95%CI] of CHD were 1.08 [0.98-1.18] and 1.16 [1.04-1.29] for the 2nd and 3rd tertile of SEnv exposure. In the single pollutant analysis, PM10, NO2, cadmium, copper, nickel, and palladium were significantly associated with CHD rates. Multiple air pollution was associated with an increased risk of CHD. Single pollutants reflecting road traffic pollution were the most strongly associated with CHD. Our present results are consistent with the literature data on the impact of road traffic on the CHD risk in urban areas.

SUBMITTER: Occelli F

PROVIDER: S-EPMC7112033 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Exposure to multiple air pollutants and the incidence of coronary heart disease: A fine-scale geographic analysis.

Occelli Florent F Lanier Caroline C Cuny Damien D Deram Annabelle A Dumont Julie J Amouyel Philippe P Montaye Michèle M Dauchet Luc L Dallongeville Jean J Genin Michaël M

The Science of the total environment 20200129

Geographical variations in cardiovascular disease rates have been linked to individual air pollutants. Investigating the relation between cardiovascular disease and exposure to a complex mixture of air pollutants requires holistic approaches. We assessed the relationship between exposure to multiple air pollutants and the incidence of coronary heart disease (CHD) in a general population sample. We collected data in the Lille MONICA registry (2008-2011) on 3268 incident cases (age range: 35-74). ...[more]

PMID: 32018947

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Project description:AimsLittle is known about the relation between the long-term joint exposure to various ambient air pollutants and the incidence of heart failure (HF). We aimed to assess the joint association of various air pollutants with HF risk and examine the modification effect of the genetic susceptibility.Methods and resultsThis study included 432 530 participants free of HF, atrial fibrillation, or coronary heart disease in the UK Biobank study. All participants were enrolled from 2006 to 2010 and followed up to 2018. The information on particulate matter (PM) with diameters ≤2.5 µm (PM2.5), ≤10 µm (PM10), and between 2.5 and 10 µm (PM2.5-10) as well as nitrogen oxides (NO2 and NOx) was collected. We newly proposed an air pollution score to assess the joint exposure to the five air pollutants through summing each pollutant concentration weighted by the regression coefficients with HF from single-pollutant models. We also calculated the weighted genetic risk score of HF. During a median of 10.1 years (4 346 642 person-years) of follow-up, we documented 4201 incident HF. The hazard ratios (HRs) [95% confidence interval (CI)] of HF for a 10 µg/m3 increase in PM2.5, PM10, PM2.5-10, NO2, and NOx were 1.85 (1.34-2.55), 1.61 (1.30-2.00), 1.13 (0.80-1.59), 1.10 (1.04-1.15), and 1.04 (1.02-1.06), respectively. We found that the air pollution score was associated with an increased risk of incident HF in a dose-response fashion. The HRs (95% CI) of HF were 1.16 (1.05-1.28), 1.19 (1.08-1.32), 1.21 (1.09-1.35), and 1.31 (1.17-1.48) in higher quintile groups compared with the lowest quintile of the air pollution score (P trend <0.001). In addition, we observed that the elevated risk of HF associated with a higher air pollution score was strengthened by the genetic susceptibility to HF.ConclusionOur results indicate that the long-term joint exposure to various air pollutants including PM2.5, PM10, PM2.5-10, NO2, and NOx is associated with an elevated risk of incident HF in an additive manner. Our findings highlight the importance to comprehensively assess various air pollutants in relation to the HF risk.

Project description:BACKGROUND:Communities need to efficiently estimate the burden from specific pollutants and identify those most at risk to make timely informed policy decisions. We developed a risk-based model to estimate the burden of black carbon (BC) and nitrogen dioxide (NO2) on coronary heart disease (CHD) across environmental justice (EJ) and non-EJ populations in Allegheny County, PA. METHODS:Exposure estimates in census tracts were modeled via land use regression and analyzed in relation to US Census data. Tracts were ranked into quartiles of exposure (Q1-Q4). A risk-based model for estimating the CHD burden attributed to BC and NO2 was developed using county health statistics, census tract level exposure estimates, and quantitative effect estimates available in the literature. RESULTS:For both pollutants, the relative occurrence of EJ tracts (> 20% poverty and/or > 30% non-white minority) in Q2 - Q4 compared to Q1 progressively increased and reached a maximum in Q4. EJ tracts were 4 to 25 times more likely to be in the highest quartile of exposure compared to the lowest quartile for BC and NO2, respectively. Pollutant-specific risk values (mean [95% CI]) for CHD mortality were higher in EJ tracts (5.49 × 10- 5 [5.05 × 10- 5 - 5.92 × 10- 5]; 5.72 × 10- 5 [5.44 × 10- 5 - 6.01 × 10- 5] for BC and NO2, respectively) compared to non-EJ tracts (3.94 × 10- 5 [3.66 × 10- 5 - 4.23 × 10- 5]; 3.49 × 10- 5 [3.27 × 10- 5 - 3.70 × 10- 5] for BC and NO2, respectively). While EJ tracts represented 28% of the county population, they accounted for about 40% of the CHD mortality attributed to each pollutant. EJ tracts are disproportionately skewed toward areas of high exposure and EJ residents bear a greater risk for air pollution-related disease compared to other county residents. CONCLUSIONS:We have combined a risk-based model with spatially resolved long-term exposure estimates to predict CHD burden from air pollution at the census tract level. It provides quantitative estimates of effects that can be used to assess possible health disparities, track temporal changes, and inform timely local community policy decisions. Such an approach can be further expanded to include other pollutants and adverse health endpoints.

Project description:Detrimental effects of air pollution with fine dust (particulate matter ?2.5 ?m in aerodynamic diameter, or PM2.5) on the systemic circulation and the left heart have been studied intensely during the past decade. In comparison, knowledge regarding the effects of exposure to air pollution with PM2.5 on the pulmonary vasculature and the right heart lags far behind. A report on severe lung disease and right heart failure in coal miners was published nearly 170 years ago. However, today, we still do not have a clear picture of how the effect of air pollution on the pulmonary circulation or the right heart should be viewed from a clinical, mechanistic biological, therapeutic, or economic angle. In the laboratory, we have established a model of immune response–induced vascular remodeling that is significantly worsened by adding PM2.5 to the intranasal antigen challenge solution. Importantly, the PM2.5 is given at a concentration that by itself does not induce significant inflammation or pulmonary vascular remodeling. However, when added to antigen, this low-dose PM2.5 exposure induces severe pulmonary vascular remodeling, significantly increased right ventricular pressures, and significant molecular changes in the right heart. Our data also show that these PM2.5-exaggerated responses are dependent on interleukin-13, interleukin-17A, and antigen-specific antibody. The experimental model is being used to address a few questions:1. Which mechanism protects the animals from severe right ventricular failure despite the severity of the pulmonary artery remodeling?2. What is the mechanism by which PM2.5 worsens the response to antigen?3. How does PM2.5 exert its effects across the small airways to the small blood vessels? In conclusion, further investigation is urgently needed to understand the effects of exposure to ambient or occupational air pollution on the pulmonary vasculature, because better knowledge could lead to immediate beneficial actions for patients with pulmonary hypertension and persons at risk.

Project description:BackgroundLong-term exposure to air pollution and noise is detrimental to health; but studies that evaluated both remain limited. This study explores associations with natural and cause-specific mortality for a range of air pollutants and transportation noise.MethodsOver 4 million adults in Switzerland were followed from 2000 to 2014. Exposure to PM2.5, PM2.5 components (Cu, Fe, S and Zn), NO2, black carbon (BC) and ozone (O3) from European models, and transportation noise from source-specific Swiss models, were assigned at baseline home addresses. Cox proportional hazards models, adjusted for individual and area-level covariates, were used to evaluate associations with each exposure and death from natural, cardiovascular (CVD) or non-malignant respiratory disease. Analyses included single and two exposure models, and subset analysis to study lower exposure ranges.ResultsDuring follow-up, 661,534 individuals died of natural causes (36.6% CVD, 6.6% respiratory). All exposures including the PM2.5 components were associated with natural mortality, with hazard ratios (95% confidence intervals) of 1.026 (1.015, 1.038) per 5 µg/m3 PM2.5, 1.050 (1.041, 1.059) per 10 µg/m3 NO2, 1.057 (1.048, 1.067) per 0.5 × 10-5/m BC and 1.045 (1.040, 1.049) per 10 dB Lden total transportation noise. NO2, BC, Cu, Fe and noise were consistently associated with CVD and respiratory mortality, whereas PM2.5 was only associated with CVD mortality. Natural mortality associations persisted < 20 µg/m3 for PM2.5 and NO2, < 1.5 10-5/m BC and < 53 dB Lden total transportation noise. The O3 association was inverse for all outcomes. Including noise attenuated all outcome associations, though many remained significant. Across outcomes, noise was robust to adjustment to air pollutants (e.g. natural mortality 1.037 (1.033, 1.042) per 10 dB Lden total transportation noise, after including BC).ConclusionLong-term exposure to air pollution and transportation noise in Switzerland contribute to premature mortality. Considering co-exposures revealed the importance of local traffic-related pollutants such as NO2, BC and transportation noise.

Dataset Information

Exposure to multiple air pollutants and the incidence of coronary heart disease: A fine-scale geographic analysis.

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Exposure to multiple air pollutants and the incidence of coronary heart disease: A fine-scale geographic analysis.

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