Ambient air pollution is a major risk factor for CVDs, and a plausible mechanism is speculated to be alteration of autonomic nervous system (ANS) function. Yet, the short-term effects of air pollution on heart rate variability (HRV), a measure of ANS balance are inconsistent. This study aimed to evaluate the short-term effects of ambient PM2.5 and NO2 on cardiovascular autonomic function, and to determine vulnerable subgroups and temporal trends from repeated HRV and HR measurements over 14 years in the KORA cohort. We analyzed data from 4,032 participants in KORA S4 (1999–2001) and 1,912 in KORA FF4 (2013–2014). Air pollution data were from fixed monitoring stations, and HRV indices were derived from 5-minute ECG recordings. Generalized additive models (GAMs) and generalized additive mixed models (GAMMs) were used to assess associations. In S4, each IQR increase in PM2.5 at the 14-day moving average was associated with a 2.32

Climate change may increase the risk of adverse cardiovascular outcomes by causing direct physiologic changes, psychological distress, and disruption of health-related infrastructure. Yet, the association between numerous climate change–related environmental stressors and the incidence of adverse cardiovascular events has not been systematically reviewed. To review the current evidence on the association between climate change–related environmental stressors and adverse cardiovascular outcomes. PubMed, Embase, Web of Science, and Cochrane Library were searched to identify peer-reviewed publications from January 1, 1970, through November 15, 2023, that evaluated associations between environmental exposures and cardiovascular mortality, acute cardiovascular events, and related health care utilization. Studies that examined only nonwildfire-sourced particulate air pollution were excluded. Two investigators independently screened 20 798 articles and selected 2564 for full-text review. Study quality was assessed using the Navigation Guide framework. Findings were qualitatively synthesized as substantial differences in study design precluded quantitative meta-analysis. Of 492 observational studies that met inclusion criteria, 182 examined extreme temperature, 210 ground-level ozone, 45 wildfire smoke, and 63 extreme weather events, such as hurricanes, dust storms, and droughts. These studies presented findings from 30 high-income countries, 17 middle-income countries, and 1 low-income country. The strength of evidence was rated as sufficient for extreme temperature; ground-level ozone; tropical storms, hurricanes, and cyclones; and dust storms. Evidence was limited for wildfire smoke and inadequate for drought and mudslides. Exposure to extreme temperature was associated with increased cardiovascular mortality and morbidity, but the magnitude varied with temperature and duration of exposure. Ground-level ozone amplified the risk associated with higher temperatures and vice versa. Extreme weather events, such as hurricanes, were associated with increased cardiovascular risk that persisted for many months after the initial event. Some studies noted a small increase in cardiovascular mortality, out-of-hospital cardiac arrests, and hospitalizations for ischemic heart disease after exposure to wildfire smoke, while others found no association. Older adults, racial and ethnic minoritized populations, and lower-wealth communities were disproportionately affected. Several environmental stressors that are predicted to increase in frequency and intensity with climate change are associated with increased cardiovascular risk, but data on outcomes in low-income countries are lacking. Urgent action is needed to mitigate climate change–associated cardiovascular risk, particularly in vulnerable populations.

BackgroundSudden death accounts for approximately 10% of deaths among working-age adults and is associated with poor air quality. Objectives: To identify high-risk groups and potential modifiers and mediators of risk, we explored previously established associations between fine particulate matter (PM2.5) and sudden death stratified by potential risk factors.MethodsSudden death victims in Wake County, NC, from 1 March 2013 to 28 February 2015 were identified by screening Emergency Medical Systems reports and adjudicated (n = 399). Daily PM2.5 concentrations for Wake County from the Air Quality Data Mart were linked to event and control periods. Potential modifiers included greenspace metrics, clinical conditions, left ventricular hypertrophy (LVH), and neutrophil-to-lymphocyte ratio (NLR). Using a case-crossover design, conditional logistic regression estimated the OR (95%CI) for sudden death for a 5 μg/m3 increase in PM2.5 with a 1-day lag, adjusted for temperature and humidity, across risk factor strata.ResultsIndividuals having LVH or an NLR above 2.5 had PM2.5 associations of greater magnitude than those without [with LVH OR: 1.90 (1.04, 3.50); NLR > 2.5: 1.25 (0.89, 1.76)]. PM2.5 was generally less impactful for individuals living in areas with higher levels of greenspace.ConclusionLVH and inflammation may be the final step in the causal pathway whereby poor air quality and traditional risk factors trigger arrhythmia or myocardial ischemia and sudden death. The combination of statistical evidence with clinical knowledge can inform medical providers of underlying risks for their patients generally, while our findings here may help guide interventions to mitigate the incidence of sudden death.

Background:Climate change is increasing the frequency of high heat and high humidity days. Whether these conditions can trigger ventricular arrhythmias [ventricular tachycardia/ventricular fibrillation, VT/VF] in susceptible persons is unknown. Objectives:The purpose of this study was to determine the relationship between warm-season weather conditions and risk of VT/VF in individuals with pacemakers and defibrillators. Methods:Baseline clinical and device data from 5,944 patients in North Carolina (2010-2021) were linked to daily weather data geocoded to individuals' residential addresses. Associations between extreme humidity, temperature, and VT/VF overall and by patient, community, and built environment factors were estimated using a case time-series design with distributed lag nonlinear models, adjusting for temporal trends and individual factors. Results:VT/VF events occurred on 4,486 of the 484,988 person-days. Extreme humidity (95th percentile: 90% relative humidity) increased odds of VT/VF in the 7 days following exposure (aOR 1.23 [95% CI: 1.00-1.51]). Humidity-associated VT/VF risk was highest among those who were male (aOR: 1.38 [95% CI: 1.08-1.76]), age 67 to 75 years (aOR: 1.65 [95% CI: 1.16-2.35]) with coronary artery disease (aOR: 1.79 [95% CI: 1.25-2.57]), heart failure (aOR: 1.72 [95% CI: 1.2-2.46]), diabetes (aOR: 3.01 [95% CI: 1.99-4.56]), hypertension (aOR: 2.06 [95% CI: 1.48-2.88]), and prior myocardial infarction (aOR: 1.75 [95% CI: 1.23-2.48]). Communities with high socioeconomic deprivation (aOR: 1.83 [95% CI: 1.28-2.62]), high income inequality (aOR: 1.56 [95% CI: 1.19-2.04]), and urban areas with less greenspace (aOR: 1.29 [95% CI: 0.93-1.78]) also had increased VT/VF risk. High temperatures were not associated with VT/VF. Conclusions:In patients with preexisting cardiovascular disease, exposure to extreme humidity increased VT/VF risk, especially among vulnerable individuals, disadvantaged communities, and urban areas with less green space. These findings emphasize the need for policies that address environmental risks in susceptible individuals and communities.

Background: Global urbanization is leading to increased exposure to traffic-related air pollution (TRAP), which is associated with adverse health events. While individuals with cardiovascular disease (CVD) are known to have elevated susceptibility to air pollution exposure, no studies have evaluated how mortality risks associated with TRAP exposure differ based on the presence of CVD. Methods: We used three electronic health record-based cohorts to examine associations between proximity to major roadways and all-cause mortality. The three cohorts were a random sample of the hospital population, individuals with a prior myocardial infarction, and individuals with diagnosed heart failure (HF). We used Cox proportional hazards models to evaluate associations while adjusting for age, race, sex, and census block group socioeconomic status. Results: Residing <250 m from a major roadway was associated with a hazard ratio (HR) of 1.13 (95% confidence interval = 1.05, 1.23) for individuals with HF, an HR of 1.07 (95% confidence interval = 0.96, 1.20) for those with a prior myocardial infarction, and an HR of 1.03 (95% confidence interval = 0.89, 1.20) for a random sample of hospital patients. This pattern persisted across several sensitivity analyses including alternative definitions of proximity to major roadways and matching the cohorts on demographics. Conclusion: These results highlight the differences in air quality-related health risks based on underlying CVD. Individuals with HF consistently had the highest environmental health risks. These results may better inform risks related to TRAP exposure in populations with differing underlying CVD.

Ozone exposure induces a myriad of adverse cardiopulmonary outcomes in humans. Although advanced age and chronic disease are factors that may exacerbate a person's negative response to ozone exposure, there are no molecular biomarkers of susceptibility. Here, we examine whether epigenetic age acceleration (EAA) is associated with responsiveness to short-term ozone exposure. Using data from a crossover-controlled exposure study (n = 17), we examined whether EAA, as measured in lung epithelial cells collected 24 h after clean air exposure, modifies the observed effect of ozone on autonomic function, cardiac electrophysiology, hemostasis, pulmonary function, and inflammation. EAA was assessed in lung epithelial cells extracted from bronchoalveolar lavage fluids, using the pan-tissue aging clock. We used two analytic approaches: (i) median regression to estimate the association between EAA and the estimated risk difference for subclinical responses to ozone and (ii) a block randomization approach to estimate EAA's effect modification of subclinical responses. For both approaches, we calculated Fisher-exact P-values, allowing us to bypass large sample size assumptions. In median regression analyses, accelerated epigenetic age modified associations between ozone and heart rate-corrected QT interval (QTc) ( ${{\hat \beta }}$ = 0.12, P-value = 0.007) and between ozone and C-reactive protein ( ${{\hat \beta }}$ = -0.18, P = 0.069). During block randomization, the directions of association remained consistent for QTc and C-reactive protein; however, the P-values weakened. Block randomization also revealed that responsiveness of plasminogen activator inhibitor-1 (PAI-1) to ozone exposure was modified by accelerated epigenetic aging (PAI-1 difference between accelerated aging-defined block groups = -0.54, P-value = 0.039). In conclusion, EAA is a potential biomarker for individuals with increased susceptibility to ozone exposure even among young, healthy adults.

Epigenetics holds great promise within the clinical and health fields both for its ability to impact health outcomes and for its ability to be a record of the exposures an individual receives. While the role of epigenetics in environmental health is still being established, it is not too early to consider what might lie at the intersection of epigenetics, therapeutic interventions, and environmental exposures. In this chapter we will explore the evidence for epigenetic markers being modified by the social environment, chemical environment, and climate change. We will also discuss and where epigenetics could inform our growing understanding and consideration of personalized interventions and policy-based public health interventions aimed at combatting a growing tide of legacy and emerging environmental health risks.

FOR RELATED ARTICLE, SEE PAGE 825The causal relationship between short-term and long-term exposure to fine particulate matter (PM2.5) and cardiovascular disease and death are well-established.1US Environmental Protection AgencyIntegrated Science Assessment (ISA) for Particulate Matter (Final Report, Dec 2019). US Environmental Protection Agency, Washington, DC2019Google Scholar,2US Environmental Protection AgencySupplement to the 2019 Integrated Science Assessment for Particulate Matter (Final Report, 2022). US Environmental Protection Agency, Washington, DC2022Google Scholar The US Environmental Protection Agency's National Ambient Air Quality Standards are intended to protect public health with an adequate margin of safety, which includes protection for groups potentially at increased risk for health effects from exposure to criteria air pollutants like PM2.5. Although it is generally accepted that health effects from PM2.5 exposure may be modified as a result of intrinsic factors (eg, preexisting disease, genetics, epigenetics) or extrinsic factors (eg, social determinants of health or behavioral patterns), relatively few epidemiologic studies quantify the potential effect of the measure modification by these factors, and the groups that are most at risk to the effects of air pollution are still uncertain. In this issue of CHEST, Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar estimate the association between short-term PM2.5 exposure and all-cause death among veterans with preexisting COPD using a case-crossover design. In addition, they evaluate the potential for modification of the association by other preexisting diseases (coronary artery disease [CAD], diabetes mellitus, obesity) and sociodemographic factors (race, area deprivation index). Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar report higher ORs for an increase in PM2.5 exposure and all-cause death among veterans with preexisting COPD when the same individuals also have CAD, diabetes mellitus, and/or obesity. We commend these authors for diligent evaluation of each of these factors. Their results provide valuable insights to inform regulatory actions, health protective individual behaviors, and clinical interventions. FOR RELATED ARTICLE, SEE PAGE 825 In particular, Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar investigate a very specific, relatively large, and well-characterized population, veterans with COPD, during the winter months when exposure most likely will exacerbate a health response. The case-crossover approach controls for time-stable confounding factors, which is of importance in a veteran population in which individuals may have experienced a wide variety of detrimental exposures over their lives and service. However, the case-crossover design does not allow for direct comparison of subpopulations. To investigate potential effect modification, the authors used stratification and estimate ORs for each subpopulation independently and then compared the ORs for the subpopulation to the OR for the overall population. This method allows for identification of potentially at-risk populations while benefiting from the strengths of the case-crossover design, but full assessment of interaction is not possible. In the 2019 Particulate Matter Integrated Science Assessment,1US Environmental Protection AgencyIntegrated Science Assessment (ISA) for Particulate Matter (Final Report, Dec 2019). US Environmental Protection Agency, Washington, DC2019Google Scholar,2US Environmental Protection AgencySupplement to the 2019 Integrated Science Assessment for Particulate Matter (Final Report, 2022). US Environmental Protection Agency, Washington, DC2022Google Scholar there was "suggestive evidence" that populations with preexisting cardiovascular or respiratory disease, those who are overweight or obese, and those with low socioeconomic status were at increased risk for PM2.5-related health effects. The results reported by Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar will contribute to the overall body of evidence that supports this conclusion and may aid in the reduction of uncertainties that are associated with the existing evidence. One uncertainty Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar do not address is what effect (if any) that preexisting COPD has on the association between short-term PM2.5 exposure and all-cause death. If the relationship between PM2.5 and all-cause death was evaluated previously in the veterans cohort, those results could provide context and aid in interpreting the results in a COPD population. For example, it is unclear whether the modification of the effect by CAD (in addition to COPD) would be different among individuals with CAD (or diabetes mellitus or obesity) but without COPD. In the report by Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar there is always one (potential) modifier–COPD–and then more are added. Although pairing other potential modifiers with COPD provides important information, it does not help reduce uncertainties related with COPD alone. Still, this study provides important evidence to further highlight populations at increased risk from air pollution exposures, and we hope that it will influence others to conduct similar analyses. Evidence from such studies is vital to examine interactions, effect measure modification, and joint effects that are associated with preexisting disease, social determinants of health, and air pollution exposure as we work to increase awareness to and demonstrate the feasibility of conducting cumulative impact studies. In addition, the evaluation of effect measure modification by preexisting disease or sociodemographic characteristics provides important information to clinicians as they counsel their patients and discuss the health implications that are associated with exposure to air pollution. The evidence provided in studies like the one by Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar helps to improve clinical awareness of environmental risk factors for cardiovascular disease, respiratory disease, and death. By providing health care professionals with information about the detrimental health effects of air pollution and the disparities in these effects by underlying health status or demographic characteristics, clinicians can make informed decisions about recommended changes to personal behavior or potential interventions or treatments for individuals most at risk. This allows individuals to optimize healthy behaviors and clinical management of health conditions for those most at risk of the effects of air pollution. For example, individuals may choose to reduce air pollutant exposures by adjusting the type of outdoor activities or the time spent outdoors, using in-home HEPA filtration, or wearing a high-efficiency respirators (eg, N95 masks) outdoors when air pollution concentrations are high.4Rajagopalan S. Brauer M. Bhatnagar A. et al.Personal-level protective actions against particulate matter air pollution exposure: a scientific statement from the American Heart Association.Circulation. 2020; 142: e411-e431Crossref PubMed Scopus (108) Google Scholar Recent studies have demonstrated the utility of in-home air cleaners for PM2.5 reduction from wildfires5Belz D.C. Myers L.C. Hansel N.N. Cardiopulmonary health burden of wildfire particulate exposure urges us to consider interventions.Am J Respir Crit Care Med. 2023; 207: 807-809Crossref Scopus (0) Google Scholar and for improved respiratory symptoms for patients with COPD as a direct result of ambient PM2.5 reduction.6Woo H. Koehler K. Putcha N. et al.Principal stratification analysis to determine health benefit of indoor air pollution reduction in a randomized environmental intervention in COPD: results from the CLEAN AIR study.Sci Total Environ. 2023; 868161573Crossref Scopus (1) Google Scholar Potential benefits from antiinflammatory treatments and nutritional supplements that could reduce the impacts of air pollutant exposures7Sherratt S.C. Libby P. Dawoud H. Bhatt D.L. Malinski T. Mason R.P. Eicosapentaenoic acid (EPA) reduces pulmonary endothelial dysfunction and inflammation due to changes in protein expression during exposure to particulate matter air pollution.Biomed Pharmacother. 2023; 162114629Crossref Scopus (3) Google Scholar, 8Tong H. Rappold A.G. Diaz-Sanchez D. et al.Omega-3 fatty acid supplementation appears to attenuate particulate air pollution-induced cardiac effects and lipid changes in healthy middle-aged adults.Environ Health Perspect. 2012; 120: 952-957Crossref Scopus (83) Google Scholar, 9Tong H. Zhang S. Shen W. et al.Lung function and short-term ambient air pollution exposure: differential impacts of omega-3 and omega-6 fatty acids.Ann Am Thorac Soc. 2022; 19: 583-593Crossref PubMed Scopus (13) Google Scholar are being explored, though general evidence for dietary changes and pharmacotherapy is mixed.4Rajagopalan S. Brauer M. Bhatnagar A. et al.Personal-level protective actions against particulate matter air pollution exposure: a scientific statement from the American Heart Association.Circulation. 2020; 142: e411-e431Crossref PubMed Scopus (108) Google Scholar Overall, the analyses by Aron et al3Aron J. Baldomero A.K. Rau A. Fiecas M.B. Wendt C.H. Berman J.D. Individual risk factors of PM2.5 associated with wintertime mortality in urban patients with COPD.Chest. 2024; 165: 825-835Google Scholar in this issue of CHEST will aid in the identification of potential intervention points at the individual (eg, clinical and behavioral) and policy (eg, government actions, regulations) levels. We encourage others in the scientific community to consider the feasibility and appropriateness of including these types of analyses in future air pollution and health research. Results from such studies will be useful in the characterization of the role of air pollution as part of the greater cumulative impact of ubiquitous environmental and social stressors. None declared. Disclaimer: The views expressed in this article are those of the author(s) and do not necessarily represent the views or policies of the US Environmental Protection Agency. Individual Risk Factors of PM2.5 Associated With Wintertime Mortality in Urban Patients With COPDCHESTVol. 165Issue 4PreviewWintertime PM2.5 exposure was associated with elevated mortality risk in people with COPD, but individuals with multiple comorbidities, notably obesity, had high vulnerability. Our study suggests that obesity, CAD, and diabetes are understudied modifiers of air pollution-related risks for people with existing COPD. Full-Text PDF

Dr. Wayne Cascio, M.D., serves as the director of the Center for Public Health and Environmental Assessment at the US Environmental Protection Agency (EPA). Prior to his current position, Dr. Cascio worked as a physician and scientist focusing on the impacts of air pollutants on heart health. At the EPA, he has spearheaded efforts to help reduce the public health risks of wildfire smoke. The views of Dr. Cascio are his only and do not necessarily reflect those of the EPA.

Exposure science plays an essential role in the U.S. Environmental Protection Agency's (U.S. EPA) mission to protect human health and the environment. The U.S. EPA's Center for Public Health and Environmental Assessment (CPHEA) within the Office of Research and Development (ORD) provides the exposure science needed to characterize the multifaceted relationships between people and their surroundings in support of national, regional, local and individual-level actions. Furthermore, exposure science research must position its enterprise to tackle the most pressing public health challenges in an ever-changing environment. These challenges include understanding and confronting complex human disease etiologies, disparities in the social environment, and system-level changes in the physical environment. Solutions will sustainably balance and optimize the health of people, animals, and ecosystems. Our objectives for this paper are to review the role of CPHEA exposure science research in various recent decision-making contexts, to present current challenges facing U.S. EPA and the larger exposure science field, and to provide illustrative case examples where CPHEA exposure science is demonstrating the latest methodologies at the intersection of these two motivations. This blueprint provides a foundation for applying exposomic tools and approaches to holistically understand real-world exposures so optimal environmental public health protective actions can be realized within the broader context of a One Health framework. IMPACT STATEMENT: The U.S. EPA's Center for Public Health and Environmental Assessment exposure research priorities reside at the intersection of environmental decision contexts and broad public health challenges. The blueprint provides a foundation for advancing the tools and approaches to holistically understand real-world exposures so optimal environmental protection actions can be realized. A One Health lens can help shape exposure research for maximum impact to support solutions that are transdisciplinary and must engage multiple sectors.

Importance:Climate change may increase the risk of adverse cardiovascular outcomes by causing direct physiologic changes, psychological distress, and disruption of health-related infrastructure. Yet, the association between numerous climate change-related environmental stressors and the incidence of adverse cardiovascular events has not been systematically reviewed. Objective:To review the current evidence on the association between climate change-related environmental stressors and adverse cardiovascular outcomes. Evidence Review:PubMed, Embase, Web of Science, and Cochrane Library were searched to identify peer-reviewed publications from January 1, 1970, through November 15, 2023, that evaluated associations between environmental exposures and cardiovascular mortality, acute cardiovascular events, and related health care utilization. Studies that examined only nonwildfire-sourced particulate air pollution were excluded. Two investigators independently screened 20 798 articles and selected 2564 for full-text review. Study quality was assessed using the Navigation Guide framework. Findings were qualitatively synthesized as substantial differences in study design precluded quantitative meta-analysis. Findings:Of 492 observational studies that met inclusion criteria, 182 examined extreme temperature, 210 ground-level ozone, 45 wildfire smoke, and 63 extreme weather events, such as hurricanes, dust storms, and droughts. These studies presented findings from 30 high-income countries, 17 middle-income countries, and 1 low-income country. The strength of evidence was rated as sufficient for extreme temperature; ground-level ozone; tropical storms, hurricanes, and cyclones; and dust storms. Evidence was limited for wildfire smoke and inadequate for drought and mudslides. Exposure to extreme temperature was associated with increased cardiovascular mortality and morbidity, but the magnitude varied with temperature and duration of exposure. Ground-level ozone amplified the risk associated with higher temperatures and vice versa. Extreme weather events, such as hurricanes, were associated with increased cardiovascular risk that persisted for many months after the initial event. Some studies noted a small increase in cardiovascular mortality, out-of-hospital cardiac arrests, and hospitalizations for ischemic heart disease after exposure to wildfire smoke, while others found no association. Older adults, racial and ethnic minoritized populations, and lower-wealth communities were disproportionately affected. Conclusions and Relevance:Several environmental stressors that are predicted to increase in frequency and intensity with climate change are associated with increased cardiovascular risk, but data on outcomes in low-income countries are lacking. Urgent action is needed to mitigate climate change-associated cardiovascular risk, particularly in vulnerable populations.

Air pollution is a risk factor for many cardiovascular diseases, including heart failure (HF). Although the links between air pollution and HF have been explored, the results are scattered and difficult to piece together into a cohesive story. Therefore, we undertook a narrative review of all aspects of the relationship between HF and air pollution exposure, including risks of developing HF when exposed to air pollution, the exacerbation of HF symptoms by air pollution exposure, and the increased susceptibility that individuals with HF have for air pollution–related health risks. We also examined the literature on environmental justice as well as air pollution interventions for HF. We found substantial evidence linking air pollution exposure to HF incidence. There were a limited number of studies that examined air pollution exposure in clearly defined populations with HF to explore exacerbation of HF or the susceptibility of individuals with HF to air pollution health risks. However, there is substantial evidence that HF-related hospitalisations are increased under air pollution exposure and that the air pollution associated increase in HF-related hospitalisations is greater than hospitalisations for other chronic diseases, supporting links between air pollution and both exacerbation of HF and susceptibility of individuals with HF. There is emerging evidence for interventions that can decrease air pollution health risks for individuals with HF, and more studies are needed, particularly randomised controlled trials. Thus, although the air pollution-related health risks for HF incidence and hospitalisations are clear, further studies specifically targeted at identified data gaps will greatly improve our knowledge of the susceptibility of individuals with HF and interventions to reduce risks.

OBJECTIVE:Short-term ambient fine particulate matter (PM2.5) is associated with adverse cardiovascular events including myocardial infarction (MI). However, few studies have examined associations between PM2.5 and subclinical cardiomyocyte damage outside of overt cardiovascular events. Here we evaluate the impact of daily PM2.5 on cardiac troponin I, a cardiomyocyte specific biomarker of cellular damage.METHODS:We conducted a retrospective cohort study of 2924 patients identified using electronic health records from the University of North Carolina Healthcare System who had a recorded MI between 2004 and 2016. Troponin I measurements were available from 2014 to 2016, and were required to be at least 1 week away from a clinically diagnosed MI. Daily ambient PM2.5 concentrations were estimated at 1 km resolution and assigned to patient residence. Associations between log-transformed troponin I and daily PM2.5 were evaluated using distributed lag linear mixed effects models adjusted for patient demographics, socioeconomic status and meteorology.RESULTS:A 10 µg/m3 elevation in PM2.5 3 days before troponin I measurement was associated with 0.06 ng/mL higher troponin I (95% CI=0.004 to 0.12). In stratified models, this association was strongest in patients that were men, white and living in less urban areas. Similar associations were observed when using 2-day rolling averages and were consistently strongest when using the average exposure over the 5 days prior to troponin I measurement.CONCLUSIONS:Daily elevations in PM2.5 were associated with damage to cardiomyocytes, outside of the occurrence of an MI. Poor air quality may cause persistent damage to the cardiovascular system leading to increased risk of cardiovascular disease and adverse cardiovascular events.

BACKGROUND:Neighborhood-level socioeconomic status (SES) is associated with health outcomes, including cardiovascular disease and diabetes, but these associations are rarely studied across large, diverse populations. METHODS:We used Ward's Hierarchical clustering to define eight neighborhood clusters across North Carolina using 11 census-based indicators of SES, race, housing, and urbanicity and assigned 6992 cardiac catheterization patients at Duke University Hospital from 2001 to 2010 to clusters. We examined associations between clusters and coronary artery disease index > 23 (CAD), history of myocardial infarction, hypertension, and diabetes using logistic regression adjusted for age, race, sex, body mass index, region of North Carolina, distance to Duke University Hospital, and smoking status. RESULTS:Four clusters were urban, three rural, and one suburban higher-middle-SES (referent). We observed greater odds of myocardial infarction in all six clusters with lower or middle-SES. Odds of CAD were elevated in the rural cluster that was low-SES and plurality Black (OR 1.16, 95% CI 0.94-1.43) and in the rural cluster that was majority American Indian (OR 1.31, 95% CI 0.91-1.90). Odds of diabetes and hypertension were elevated in two urban and one rural low- and lower-middle SES clusters with large Black populations. CONCLUSIONS:We observed higher prevalence of cardiovascular disease and diabetes in neighborhoods that were predominantly rural, low-SES, and non-White, highlighting the importance of public health and healthcare system outreach into these communities to promote cardiometabolic health and prevent and manage hypertension, diabetes and coronary artery disease.