Cardiovascular Effects Of Air Pollution Research Articles

Long-term exposure to ambient air pollution and risk of microvascular complications among patients with type 2 diabetes: a prospective study.

Patients with type 2 diabetes (T2D) may disproportionately suffer the adverse cardiovascular effects of air pollution, but relevant evidence on microvascular outcome is lacking. We aimed to examine the association between air pollution exposure and the risk of microvascular complications among patients with T2D. This prospective study included 17 995 participants with T2D who were free of macro- and micro-vascular complications at baseline from the UK Biobank. Annual average concentrations of particulate matter (PM) with diameters <2.5 μm (PM2.5), <10 μm (PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOx) were assessed using land use regression models. Cox proportional hazards regression was used to estimate the associations of air pollution exposure with incident diabetic microvascular complications. The joint effects of the air pollutant mixture were examined using quantile-based g-computation in a survival setting. In single-pollutant models, the adjusted hazard ratios (95% confidence intervals) for composite diabetic microvascular complications per interquartile range increase in PM2.5, PM10, NO2 and NOx were 1.09 (1.04-1.14), 1.06 (1.01-1.11), 1.07 (1.02-1.12) and 1.04 (1.00-1.08), respectively. Similar significant results were found for diabetic nephropathy and diabetic neuropathy, but not for diabetic retinopathy. The associations of certain air pollutants with composite microvascular complications and diabetic nephropathy were present even at concentrations below the World Health Organization limit values. Multi-pollutant analyses demonstrated that PM2.5 contributed most to the elevated risk associated with the air pollutant mixture. In addition, we found no interactions between air pollution and metabolic risk factor control on the risk of diabetic microvascular complications. Long-term individual and joint exposure to PM2.5, PM10, NO2 and NOx, even at low levels, was associated with an increased risk of diabetic microvascular complications, with PM2.5 potentially being the main contributor.

A bibliometric and visualized analysis of research on air pollution and cardiovascular diseases

A large number of studies have shown that air pollution has a great impact on cardiovascular diseases (CVD). However, there are few bibliometric studies or visual analyses in this field. The objective of this study was to research trends and hotspots of air pollution and CVD. We used CiteSpace and VOSviewer software to retrieve relevant studies from the Web of Science Core Collection (WoSCC) over the past decade. Amount to 4284 documents on air pollution and CVD were included in this study. The past decade saw an upward trend in the number of studies. The analysis of national publications showed that the United States had the highest academic contribution in this field. Peking University, the University of Washington and Harvard University were the main institutions studying the effect of air pollution on CVD. The cooperation among institutions with high publications was very close. Cluster analysis of the keywords listed four categories as follow: (1) oxidative stress and the cardiovascular effects of air pollution; (2) the cardiovascular effects of pollution exposure sources; (3) the relationship between environmental stressors and CVD; (4) personal-level interventions. This study puts forward a comprehensive summary of the trends and development of air pollution and CVD, confirms the research frontier and hotspot direction and could give a meaningful reference for researchers in this field.

Air pollution and cardiovascular heath in a changing climate

Air pollution and cardiovascular heath in a changing climate

Proinflammatory lipid signals trigger the health effects of air pollution in individuals with prediabetes

Individuals with metabolic disorders exhibit enhanced susceptibility to the cardiovascular health effects of particulate air pollution, but the underlying mechanisms are not yet understood. We aim to assess whether changes in proinflammatory lipid signals are associated with fine particulate matter (PM2.5) exposure in individuals with and without prediabetes. A longitudinal panel study was conducted in Beijing, China, and included 120 participants followed up over 589 clinical visits from August 2013 to February 2015. We measured 12 lipids derived from arachidonic acid pathways in blood samples of the participants via targeted lipidomic analyses. Ambient PM2.5 concentrations were continuously monitored at a station for associations with the lipids. Among the 120 participants, 110 (mean [SD] age at recruitment, 56.5 [4.2] years; 31 prediabetics) who visited the clinic at least twice over the follow-up period were assigned exposure values of the outdoor residential PM2.5 concentrations during the 1–14 days preceding each clinical visit. With an interquartile range increase in the 1-day-lag PM2.5 exposure (64.0 μg/m3), the prediabetic group had consistently greater increases in the concentration of arachidonate metabolites derived from the cytochrome P450 (CYP450) pathway (5,6-DHET, 15.8% [95% CI, 3.5–29.7%]; 8,9-DHET, 9.7% [95% CI, 0.6–19.6%]; 11,12-DHET, 8.3% [95% CI, 1.9–15.1%]; 14,15-DHET, 7.4% [95% CI, 0.9–14.4%]; and 20-HETE, 8.9% [95% CI, 1.0–17.5%]), compared with the healthy group. Among CYP450-derived lipids, 14,15-DHET and 20-HETE significantly mediated 8% and 8% of the PM2.5-associated increase in white blood cells, 10% and 13% of that in neutrophils, and 20% and 23% of that in monocytes, respectively, in the prediabetic group. In conclusion, proinflammatory lipid signals from CYP450 pathways triggered the health effects of particulate air pollution in individuals with prediabetes, suggesting that targeting lipid metabolism has therapeutic potential to attenuate or prevent the cardiovascular effects of air pollution in susceptible populations.

Air pollution and cardiovascular disease: Can the Australian bushfires and global COVID-19 pandemic of 2020 convince us to change our ways?

Air pollution is a major global challenge for a multitude of reasons. As a specific concern, there is now compelling evidence demonstrating a causal relationship between exposure to airborne pollutants and the onset of cardiovascular disease (CVD). As such, reducing air pollution as a means to decrease cardiovascular morbidity and mortality should be a global health priority. This review provides an overview of the cardiovascular effects of air pollution and uses two major events of 2020—the Australian bushfires and COVID‐19 pandemic lockdown—to illustrate the relationship between air pollution and CVD. The bushfires highlight the substantial human and economic costs associated with elevations in air pollution. Conversely, the COVID‐19‐related lockdowns demonstrated that stringent measures are effective at reducing airborne pollutants, which in turn resulted in a potential reduction in cardiovascular events. Perhaps one positive to come out of 2020 will be the recognition that tough measures are effective at reducing air pollution and that these measures have the potential to stop thousands of deaths from CVD.

Effects of short-term personal exposure to air pollution on platelet mitochondrial DNA methylation levels and the potential mitigation by L-arginine supplementation

The potential effect of short-term exposure to air pollution on mitochondrial DNA (mtDNA) methylation remains to be explored. This study adopted an experimental exposure protocol nested with an intervention study on L-arginine (L-Arg) supplementation among 118 participants. Participants walked along a traffic road for 2 hours in the last day of a 14-day intervention to investigate the effects of short-term personal exposure to air pollution on platelet mtDNA methylation and the possible modifying effects of L-Arg supplementation. Results showed that short-term personal exposure to air pollutants was associated with hypomethylation in platelet mtDNA in 110 participants who completed the study protocol. Specifically, 2-h fine particulate matter (PM2.5) exposure during the outdoor walk was significantly associated with hypomethylation in mt12sRNA; 24-h PM2.5 and black carbon (BC) exposures from the start of the walk till next morning were both significantly associated with hypomethylation in the D-loop region; 24-h BC exposure was also significantly associated with hypomethylation in ATP8_P1. Supplementation with L-Arg could mitigate the air pollution effects on platelet mtDNA methylation, especially the D-loop region. These findings suggest that platelet mtDNA methylation may be sensitive effect biomarker for short-term exposure to air pollution and may help deepen the understanding of the epigenetic mechanisms of adverse cardiovascular effects of air pollution.

Cardiovascular effects of air pollution: current evidence from animal and human studies.

Air pollution is a global health concern. Particulate matter (PM)2.5, a component of ambient air pollution, has been identified by the World Health Organization as one of the pollutants that poses the greatest threat to public health. Cardiovascular health effects have been extensively documented, and these effects are still being researched to provide an overview of recent literature regarding air pollution-associated cardiovascular morbidity and mortality in humans. Additionally, potential mechanisms through which air pollutants affect the cardiovascular system are discussed based on human and additional animal studies. We used the strategy of a narrative review to summarize the scientific literature of studies that were published in the past 7 yr. Searches were carried out on PubMed and Web of Science using predefined search queries. We obtained an initial set of 800 publications that were filtered to 78 publications that were relevant to include in this review. Analysis of the literature showed significant associations between air pollution, especially PM2.5, and the risk of elevated blood pressure (BP), acute coronary syndrome, myocardial infarction (MI), cardiac arrhythmia, and heart failure (HF). Prominent mechanisms that underlie the adverse effects of air pollution include oxidative stress, systemic inflammation, endothelial dysfunction, autonomic imbalance, and thrombogenicity. The current review underscores the relevance of air pollution as a global health concern that affects cardiovascular health. More rigorous standards are needed to reduce the cardiovascular disease burden imposed by air pollution. Continued research on the health impact of air pollution is needed to provide further insight.

Residential proximity to greenness mitigates the hemodynamic effects of ambient air pollution.

Residential proximity to greenness is associated with a lower risk of cardiovascular disease (CVD) and all-cause mortality. However, it is unclear whether the beneficial effects of greenness are linked to a reduction in the effects of ambient air pollutants. We measured arterial stiffness in 73 participants with moderate to high CVD risk. Average levels of ambient PM2.5 and ozone were calculated from local monitoring stations. Residential greenness was estimated using satellite-derived normalized difference vegetation index (NDVI) for a 200-m and 1-km radius around each participant's home. Participants were 51% female, average age of 52 yr, and 79% had diagnosed hypertension. In multiple linear regression models, residential NDVI was negatively associated with augmentation index (-3.8% per 0.1 NDVI). Ambient levels of PM2.5 [per interquartile range (IQR) of 6.9 μg/m3] were positively associated with augmentation pressure (3.1 mmHg), pulse pressure (5.9 mmHg), and aortic systolic pressure (8.1 mmHg). Ozone (per IQR of 0.03 ppm) was positively associated with augmentation index (5.5%), augmentation pressure (3.1 mmHg), and aortic systolic pressure (10 mmHg). In areas of low greenness, both PM2.5 and ozone were positively associated with pulse pressure. Additionally, ozone was positively associated with augmentation pressure and systolic blood pressure. However, in areas of high greenness, there was no significant association between indices of arterial stiffness with either PM2.5 or ozone. Residential proximity to greenness is associated with lower values of arterial stiffness. Residential greenness may mitigate the adverse effects of PM2.5 and ozone on arterial stiffness.NEW & NOTEWORTHY Previous studies have linked proximity to green spaces with lower cardiovascular disease risk. However, the mechanisms underlying the salutary effects of green areas are not known. In our study of participants at risk of cardiovascular disease, we found that arterial stiffness was positively associated with short-term exposure to PM2.5, PM10, and ozone and inversely associated with greenness. The association between pollution and arterial stiffness was attenuated in areas of high greenness, suggesting that living green neighborhoods can lessen the adverse cardiovascular effects of air pollution.

Cardiovascular effects of air pollution: A review

Cardiovascular effects of air pollution: A review

Association of ambient air pollution with cardiovascular disease risks in people with type 2 diabetes: a Bayesian spatial survival analysis

BackgroundEvidence is limited on excess risks of cardiovascular diseases (CVDs) associated with ambient air pollution in diabetic populations. Survival analyses without considering the spatial structure and possible spatial correlations in health and environmental data may affect the precision of estimation of adverse environmental pollution effects. We assessed the association between air pollution and CVDs in type 2 diabetes through a Bayesian spatial survival approach.MethodsTaiwan’s national-level health claims and air pollution databases were utilized. Fine individual-level latitude and longitude were used to determine pollution exposure. The exponential spatial correlation between air pollution and CVDs was analyzed in our Bayesian model compared to traditional Weibull and Cox models.ResultsThere were 2072 diabetic patients included in analyses. PM2.5 and SO2 were significant CVD risk factors in our Bayesian model, but such associations were attenuated or underestimated in traditional models; adjusted hazard ratio (HR) and 95% credible interval (CrI) or confidence interval (CI) of CVDs for a 1 μg/m3 increase in the monthly PM2.5 concentration for our model, the Weibull and Cox models was 1.040 (1.004–1.073), 0.994 (0.984–1.004), and 0.994 (0.984–1.004), respectively. With a 1 ppb increase in the monthly SO2 concentration, adjusted HR (95% CrI or CI) was 1.886 (1.642–2.113), 1.092 (1.022–1.168), and 1.091 (1.021–1.166) for these models, respectively.ConclusionsAgainst traditional non-spatial analyses, our Bayesian spatial survival model enhances the assessment precision for environmental research with spatial survival data to reveal significant adverse cardiovascular effects of air pollution among vulnerable diabetic patients.Graphical abstract

Mind over matter

Keynote Lectures Wednesday, Beatrix Theater, August 28, 2019, 9:00 AM - 10:00 AM Following decades of research into respiratory and cardiovascular effects of air pollution, the past decade has seen exploding interest in the effects of air pollution on the brain. Epidemiological evidence has been growing for effects on outcomes across the lifespan such as neurodevelopment, mental health, and cognitive aging, and experimental evidence has demonstrated biological effects of air pollutants on the brain. Understanding how these effects interact with the biology of the brain can help us better understand the nature of the relation between air pollutants and neuropsychological function and help inform the epidemiological study of these relations.

Association of Long-term Exposure to Ambient Air Pollutants With Risk Factors for Cardiovascular Disease in China

Which cardiometabolic risk factors (eg, hypertension, type 2 diabetes, overweight or obesity, and dyslipidemia) are more sensitive to long-term exposure to ambient air pollution and whether participants with these conditions are more susceptible to the cardiovascular effects of air pollution remain unclear. To evaluate the associations among long-term exposure to air pollutants, cardiometabolic risk factors, and cardiovascular disease (CVD) prevalence. This population-based cross-sectional study was conducted from April 1 through December 31, 2009, in 3 cities in Northeastern China. Participants were adults aged 18 to 74 years who had lived in study area for 5 years or longer. Data analysis was performed from May 1 through December 31, 2018. Long-term (2006-2008) exposure to air pollutants was measured using a spatiotemporal statistical model (particulate matter with an aerodynamic diameter of ≤2.5 μm [PM2.5] and ≤1.0 μm [PM1.0]) and data from air monitoring stations (particulate matter with an aerodynamic diameter of ≤10.0 μm [PM10.0], sulfur dioxide [SO2], nitrogen dioxide [NO2], and ozone [O3]). Cardiovascular disease was determined by self-report of physician-diagnosed CVD. Blood pressure, body mass index, and levels of triglycerides and low-density lipoprotein cholesterol were measured using standard methods. Participants included 15 477 adults (47.3% women) with a mean (SD) age of 45.0 (13.5) years. The prevalence of CVD was 4.8%, and the prevalence of cardiometabolic risk factors ranged from 8.6% (hyperbetalipoproteinemia) to 40.5% (overweight or obesity). Mean (SD) air pollutant concentrations ranged from 35.3 (5.5) μg/m3 (for NO2) to 123.1 (14.6) μg/m3 (for PM10.0). Associations with air pollutants were identified for individuals with hyperbetalipoproteinemia (eg, odds ratio [OR], 1.36 [95% CI, 1.03-1.78] for a 10-μg/m3 increase in PM1.0) and the weakest association for those with for overweight or obesity (eg, OR, 1.06 [95% CI, 1.02-1.09] for a 10-μg/m3 increase in PM1.0). Cardiometabolic risk factors only partially mediated associations between air pollution and CVD. However, they modified the associations such that greater associations were found in participants with these cardiometabolic conditions (eg, ORs for CVD and per 10-μg/m3 increase in PM1.0, 1.22 [95% CI, 1.12-1.33] in participants with hyperbetalipoproteinemia and 1.07 [95% CI, 0.98-1.16] in participants without hyperbetalipoproteinemia). In this population-based study of Chinese adults with CVD, long-term exposure to air pollution was associated with a higher prevalence of cardiometabolic risk factors, and the strongest associations were observed for hyperbetalipoproteinemia. In addition, participants with cardiometabolic risk factors may have been more vulnerable to the effects of air pollution on CVD.

Are Ambient Volatile Organic Compounds Environmental Stressors for Heart Failure?

Abstract Background Numerous epidemiological studies have indicated the adverse cardiovascular effects of air pollution on heart failure (HF) risk. However, little data are available directly evaluating the association of ambient volatile organic compounds (VOCs) with HF risk. We aimed to estimate the short-term effects of ambient VOCs on HF emergency hospitalizations in Hong Kong and to evaluate whether the associations were modified by sex and age. Methods We collected the daily VOCs concentrations from the Hong Kong Environmental Protection Department between April 2011 to December 2014. HF emergency hospital admission data were obtained from the Hospital Authority of Hong Kong. Generalized additive model (GAM) integrated with the distributed lag model (DLM) was used to estimate the excess risks of HF emergency hospitalizations with ambient concentrations of each VOCs groups – alkane, alkene, alkyne, benzene and substituted benzene. Results We observed short-term effects of alkyne and benzene on an increased risk of HF emergency hospitalizations. The cumulative effect over 0–6 lag days (dlm0-6) for an IQR increment of alkyne (1.17 ppb) was associated with 4.2% (95% CI: 1.18%–7.26%) increases of HF emergency hospitalizations, while the corresponding effect estimate over dlm0-2 for benzene per IQR (0.43 ppb) was 2.7% (95% CI: 0.39%–5.04%). Each VOCs groups was significantly associated with HF emergency hospitalizations in men. Conclusions Ambient volatile organic compounds, particularly alkyne and benzene, were associated with increased risks of heart failure in the Hong Kong population.

Ambient Air Quality and Cardiovascular Health

Air pollution is intuitively associated with respiratory effects, but evidence has emerged over the past few decades that the cardiovascular effects of air pollution can be much more adverse and represent a greater public health burden. In this article, we present background on the sources, exposures, and health effects of air pollution and discuss the potential for intervention strategies in the health care system to help reduce individual and population exposure and the attendant risk from the cardiovascular effects of air pollution.

Are ambient volatile organic compounds environmental stressors for heart failure?

BackgroundNumerous epidemiological studies have indicated the adverse cardiovascular effects of air pollution on heart failure (HF) risk. However, little data are available directly evaluating the association of ambient volatile organic compounds (VOCs) with HF risk. We aimed to estimate the short-term effects of ambient VOCs on HF emergency hospitalizations in Hong Kong and to evaluate whether the associations were modified by sex and age. MethodsWe collected the daily VOCs concentrations from the Hong Kong Environmental Protection Department between April 2011 to December 2014. HF emergency hospital admission data were obtained from the Hospital Authority of Hong Kong. Generalized additive model (GAM) integrated with the distributed lag model (DLM) was used to estimate the excess risks of HF emergency hospitalizations with ambient concentrations of each VOCs groups – alkane, alkene, alkyne, benzene and substituted benzene. ResultsWe observed short-term effects of alkyne and benzene on an increased risk of HF emergency hospitalizations. The cumulative effect over 0–6 lag days (dlm0-6) for an IQR increment of alkyne (1.17 ppb) was associated with 4.2% (95% CI: 1.18%–7.26%) increases of HF emergency hospitalizations, while the corresponding effect estimate over dlm0-2 for benzene per IQR (0.43 ppb) was 2.7% (95% CI: 0.39%–5.04%). Each VOCs groups was significantly associated with HF emergency hospitalizations in men. ConclusionsAmbient volatile organic compounds, particularly alkyne and benzene, were associated with increased risks of heart failure in the Hong Kong population.

Air Pollution and Stroke.

The adverse health effects of air pollution have long been recognised; however, there is less awareness that the majority of the morbidity and mortality caused by air pollution is due to its effects on the cardiovascular system. Evidence from epidemiological studies have demonstrated a strong association between air pollution and cardiovascular diseases including stroke. Although the relative risk is small at an individual level, the ubiquitous nature of exposure to air pollution means that the absolute risk at a population level is on a par with “traditional” risk factors for cardiovascular disease. Of particular concern are findings that the strength of this association is stronger in low and middle income countries where air pollution is projected to rise as a result of rapid industrialisation. The underlying biological mechanisms through which air pollutants exert their effect on the vasculature are still an area of intense discussion. A greater understanding of the effect size and mechanisms is necessary to develop effective strategies at individual and policy levels to mitigate the adverse cardiovascular effects of air pollution.

Walking to a pathway for cardiovascular effects of air pollution

Walking to a pathway for cardiovascular effects of air pollution

Is physical activity a modifier of the association between air pollution and arterial stiffness in older adults: The SAPALDIA cohort study.

Air pollution and insufficient physical activity have been associated with inflammation and oxidative stress, molecular mechanisms linked to arterial stiffness and cardiovascular disease. There are no studies on how physical activity modifies the association between air pollution and arterial stiffness. We examined whether the adverse cardiovascular effects of air pollution were modified by individual physical activity levels in 2823 adults aged 50-81 years from the well-characterized Swiss Cohort Study on Air Pollution and Lung and Heart Diseases (SAPALDIA). We assessed arterial stiffness as the brachial-ankle pulse wave velocity (baPWV [m/s]) with an oscillometric device. We administered a self-reported physical activity questionnaire to classify each subject's physical activity level. Air pollution exposure was estimated by the annual average individual home outdoor PM10 and PM2.5 (particulate matter <10μm and <2.5μm in diameter, respectively) and NO2 (nitrogen dioxide) exposure estimated for the year preceding the survey. Exposure estimates for ultrafine particles calculated as particle number concentration (PNC) and lung deposited surface area (LDSA) were available for a subsample (N=1353). We used mixed effects logistic regression models to regress increased arterial stiffness (baPWV≥14.4m/s) on air pollution exposure and physical activity while adjusting for relevant confounders. We found evidence that the association of air pollution exposure with baPWV was different between inactive and active participants. The probability of having increased baPWV was significantly higher with higher PM10, PM2.5, NO2, PNC and LDSA exposure in inactive, but not in physically active participants. We found some evidence of an interaction between physical activity and ambient air pollution exposure for PM10, PM2.5 and NO2 (pinteraction=0.06, 0.09, and 0.04, respectively), but not PNC and LDSA (pinteraction=0.32 and 0.35). Our study provides some indication that physical activity may protect against the adverse vascular effects of air pollution in low pollution settings. Additional research in large prospective cohorts is needed to assess whether the observed effect modification translates to high pollution settings in mega-cities of middle and low-income countries.

125 - Cardiovascular effects of air pollution: a review

125 - Cardiovascular effects of air pollution: a review

How Can We Protect Susceptible Individuals from the Adverse Cardiovascular Effects of Air Pollution?

The authors are supported by grants (FS/16/14/32023, SP/15/8/31575) from the British Heart Foundation. Author disclosures are available with the text of this article at www.atsjournals.org.