Urban heat island impacts on heat-related cardiovascular morbidity: A time series analysis of older adults in US metropolitan areas.

Many United States (US) cities are experiencing urban heat islands (UHIs) and climate change-driven temperature increases. Extreme heat increases cardiovascular disease (CVD) risk, yet little is known about how this association varies with UHI intensity (UHII) within and between cities. We aimed to identify the urban populations most at-risk of and burdened by heat-related CVD morbidity in UHI-affected areas compared to unaffected areas. ZIP code-level daily counts of CVD hospitalizations among Medicare enrollees, aged 65-114, were obtained for 120 US metropolitan statistical areas (MSAs) between 2000 and 2017. Mean ambient temperature exposure was estimated by interpolating daily weather station observations. ZIP codes were classified as low and high UHII using the first and fourth quartiles of an existing surface UHII metric, weighted to each have 25% of all CVD hospitalizations. MSA-specific associations between ambient temperature and CVD hospitalization were estimated using quasi-Poisson regression with distributed lag non-linear models and pooled via multivariate meta-analyses. Across the US, extreme heat (MSA-specific 99th percentile, on average 28.6 °C) increased the risk of CVD hospitalization by 1.5% (95% CI: 0.4%, 2.6%), with considerable variation among MSAs. Extreme heat-related CVD hospitalization risk in high UHII areas (2.4% [95% CI: 0.4%, 4.3%]) exceeded that in low UHII areas (1.0% [95% CI: -0.8%, 2.8%]), with upwards of a 10% difference in some MSAs. During the 18-year study period, there were an estimated 37,028 (95% CI: 35,741, 37,988) heat-attributable CVD admissions. High UHII areas accounted for 35% of the total heat-related CVD burden, while low UHII areas accounted for 4%. High UHII disproportionately impacted already heat-vulnerable populations; females, individuals aged 75-114, and those with chronic conditions living in high UHII areas experienced the largest heat-related CVD impacts. Overall, extreme heat increased cardiovascular morbidity risk and burden in older urban populations, with UHIs exacerbating these impacts among those with existing vulnerabilities.

Exposures to low-levels of fine particulate matter are associated with acute changes in heart rate variability, cardiac repolarization, and circulating blood lipids in coronary artery disease patients.

Exposure to air pollution is a major risk factor for cardiovascular disease, disease risk factors, and mortality. Specifically, particulate matter (PM), and to some extent ozone, are contributors to these effects. In addition, exposures to these pollutants may be especially dangerous for susceptible populations. In this repeated-visit panel study, cardiovascular markers were collected from thirteen male participants with stable coronary artery disease. For 0-4 days prior to the health measurement collections, daily concentrations of fine PM (PM2.5) and ozone were obtained from local central monitoring stations located near the participant's homes. Then, single (PM2.5) and two-pollutant (PM2.5 and ozone) models were used to assess whether there were short-term changes in cardiovascular health markers. Per interquartile range increase in PM2.5, there were decrements in several heart rate variability metrics, including the standard deviation of the normal-to-normal intervals (lag 3, -5.8%, 95% confidence interval (CI) = -11.5, 0.3) and root-mean squared of successive differences (five day moving average, -8.1%, 95% CI = -15.0, -0.7). In addition, increases in PM2.5 were also associated with changes in P complexity (lag 1, 4.4%, 95% CI = 0.5, 8.5), QRS complexity (lag 1, 4.9%, 95% CI = 1.4, 8.5), total cholesterol (five day moving average, -2.1%, 95% CI = -4.1, -0.1), and high-density lipoprotein cholesterol (lag 2, -1.6%, 95% CI = -3.1, -0.1). Comparisons to our previously published work on ozone were conducted. We found that ozone affected inflammation and endothelial function, whereas PM2.5 influenced heart rate variability, repolarization, and lipids. All the health changes from these two studies were found at concentrations below the United States Environmental Protection Agency's National Ambient Air Quality Standards. Our results imply clear differences in the cardiovascular outcomes observed with exposure to the two ubiquitous air pollutants PM2.5 and ozone; this observation suggests different mechanisms of toxicity for these exposures.

Household air pollution from wood-burning cookstoves and C-reactive protein among women in rural Honduras.

Household air pollution from solid fuel combustion was estimated to cause 2.31 million deaths worldwide in 2019; cardiovascular disease is a substantial contributor to the global burden. We evaluated the cross-sectional association between household air pollution (24-h gravimetric kitchen and personal particulate matter (PM2.5) and black carbon (BC)) and C-reactive protein (CRP) measured in dried blood spots among 107 women in rural Honduras using wood-burning traditional or Justa (an engineered combustion chamber) stoves. A suite of 6 additional markers of systemic injury and inflammation were considered in secondary analyses. We adjusted for potential confounders and assessed effect modification of several cardiovascular-disease risk factors. The median (25th, 75th percentiles) 24-h-average personal PM2.5 concentration was 115 µg/m3 (65,154 µg/m3) for traditional stove users and 52 µg/m3 (39, 81 µg/m3) for Justa stove users; kitchen PM2.5 and BC had similar patterns. Higher concentrations of PM2.5 and BC were associated with higher levels of CRP (e.g., a 25% increase in personal PM2.5 was associated with a 10.5% increase in CRP [95% CI: 1.2-20.6]). In secondary analyses, results were generally consistent with a null association. Evidence for effect modification between pollutant measures and four different cardiovascular risk factors (e.g., high blood pressure) was inconsistent. These results support the growing evidence linking household air pollution and cardiovascular disease.

Associations between neighborhood socioeconomic cluster and hypertension, diabetes, myocardial infarction, and coronary artery disease within a cohort of cardiac catheterization patients.

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.

Evaluation of PM2.5 air pollution sources and cardiovascular health.

Long-term air pollution exposure, notably fine particulate matter, is a global contributor to morbidity and mortality and a known risk factor for coronary artery disease (CAD) and myocardial infarctions (MI). Knowledge of impacts related to source-apportioned PM2.5 is limited. New modeling methods allow researchers to estimate source-specific long-term impacts on the prevalence of CAD and MI. The Catheterization Genetics (CATHGEN) cohort consists of patients who underwent a cardiac catheterization at Duke University Medical Center between 2002 and 2010. Severity of coronary blockage was determined by coronary angiography and converted into a binary indicator of clinical CAD. History of MI was extracted from medical records. Annual averages of source specific PM2.5 were estimated using an improved gas-constrained source apportionment model for North Carolina from 2002 to 2010. We tested six sources of PM2.5 mass for associations with CAD and MI using mixed effects multivariable logistic regression with a random intercept for county and multiple adjustments. PM2.5 fractions of ammonium bisulfate and ammonium nitrate were associated with increased prevalence of CAD (odds ratio [OR] 1.20; 95% CI = 1.11, 1.22 and OR 1.18; 95% CI = 1.05, 1.32, respectively). PM2.5 from ammonium bisulfate and ammonium nitrate were also associated with increased prevalence of MI (OR 1.20; 95% CI = 1.10, 1.29 and OR 1.35; 95% CI = 1.20, 1.53, respectively). Greater PM2.5 concentrations of ammonium bisulfate and ammonium nitrate are associated with greater MI and CAD prevalence. The association with bisulfate suggests aerosol acidity may play a role. Our findings suggest analyses of source specific PM2.5 mass can reveal novel associations.

Association between short-term exposure to ambient fine particulate matter and myocardial injury in the CATHGEN cohort.

Exposure to fine particulate matter (PM2.5) has been associated with a higher risk for coronary events. Elevated circulating cardiac troponins (cTn) are suggestive of myocardial injury in both ischemic and non-ischemic conditions. However, little is known about the association between PM2.5 and cTn. In this study, we investigated short-term PM2.5 effects on cardiac troponin T (cTnT), as well as N-terminal-pro brain natriuretic peptide (NT-pro BNP) and inflammatory biomarkers among cardiac catheterized participants. We analyzed 7444 plasma cTnT measurements in 2732 participants who presented to Duke University Hospital with myocardial infarction symptoms between 2001 and 2012, partly along with measurements of NT-pro BNP and inflammatory biomarkers. Daily PM2.5 concentrations were predicted by a neural network-based hybrid model and were assigned to participants' residential addresses. We applied generalized estimating equations to assess associations of PM2.5 with biomarker levels and the risk of a positive cTnT test (cTnT > 0.1 ng/mL). The median plasma cTnT concentration at presentation was 0.05 ng/mL and the prevalence of a positive cTnT test was 35.4%. For an interquartile range (7.6 µg/m3) increase in PM2.5 on the previous day, cTnT concentrations increased by 7.7% (95% CI: 3.4-12.3) and the odds ratio of a positive cTnT test was 1.08 (1.01-1.16). Participants under 60 years (effect estimate: 15.2%; 95% CI: 7.4-23.5) or living in rural areas (12.3%; 95% CI: 4.8-20.3) were more susceptible. There was evidence for increases in fibrinogen and NT-pro BNP associated with elevated PM2.5 on the concurrent and previous two days. Our study suggests that acute PM2.5 exposure may elevate indicators of myocardial tissue damage. This finding substantiates the association of air pollution exposure with adverse cardiovascular events.

Exploration of PM mass, source, and component-related factors that might explain heterogeneity in daily PM2.5-mortality associations across the United States.

Multi-city epidemiologic studies examining short-term (daily) differences in fine particulate matter (PM2.5) provide evidence of substantial spatial heterogeneity in city-specific mortality risk estimates across the United States. Because PM2.5 is a mixture of particles, both directly emitted from sources or formed through atmospheric reactions, some of this heterogeneity may be due to regional variations in PM2.5 toxicity. Using inverse variance weighted linear regression, we examined change in percent change in mortality in association with 24 "exposure" determinants representing three basic groupings based on potential explanations for differences in PM toxicity - size, source, and composition. Percent changes in mortality for the PM2.5-mortality association for 313 core-based statistical areas and their metropolitan divisions over 1999-2005 were used as the outcome. Several determinants were identified as potential contributors to heterogeneity: all mass fraction determinants, vehicle miles traveled (VMT) for diesel total, VMT gas per capita, PM2.5 ammonium, PM2.5 nitrate, and PM2.5 sulfate. In multivariable models, only daily correlation of PM2.5 with PM10 and long-term average PM2.5 mass concentration were retained, explaining approximately 10% of total variability. The results of this analysis contribute to the growing body of literature specifically focusing on assessing the underlying basis of the observed spatial heterogeneity in PM2.5-mortality effect estimates, continuing to demonstrate that this heterogeneity is multifactorial and not attributable to a single aspect of PM.

Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.

BACKGROUND: Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures. METHODS: Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status. RESULTS: We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5. CONCLUSION: Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.

Annual PM2.5 and cardiovascular mortality rate data: Trends modified by county socioeconomic status in 2,132 US counties.

This article contains data on county-level socioeconomic status for 2132 US counties and each county's average annual cardiovascular mortality rate (CMR) and fine particulate matter (PM2.5) concentration for 21 years (1990-2010). County CMR, PM2.5, and socioeconomic data were obtained from the US National Center for Health Statistics, US Environmental Protection Agency's Community Multiscale Air Quality modeling system, and the US Census, respectively. Annual socioeconomic indices were created using seven county-level measures from the 1990, 2000, and 2010 US Census using factor analysis. Quintiles of this index were used to generate categories of county socioeconomic status. This national data set contains data for annual PM2.5 and CMR changes over a time-period when there was a significant reduction in US air pollutants (following the enactment of the 1970 Clean Air Act). These data are associated with the article "The contribution of improved air quality to reduced cardiovascular mortality: Declines in socioeconomic differences over time" [1]. Data are stored in a comma separated value format and can be downloaded from the USEPA ScienceHub data repository (https://doi.org/10.23719/1506014).

Associations Between Long-Term Fine Particulate Matter Exposure and Mortality in Heart Failure Patients.

Background Environmental health risks for individuals with heart failure (HF) have been inadequately studied, as these individuals are not well represented in traditional cohort studies. To address this we studied associations between long-term air pollution exposure and mortality in HF patients. Methods and Results The study population was a hospital-based cohort of individuals diagnosed with HF between July 1, 2004 and December 31, 2016 compiled using electronic health records. Individuals were followed from 1 year after initial diagnosis until death or the end of the observation period (December 31, 2016). We used Cox proportional hazards models to evaluate the association of annual average fine particulate matter (PM2.5) exposure at the time of initial HF diagnosis with all-cause mortality, adjusted for age, race, sex, distance to the nearest air pollution monitor, and socioeconomic status indicators. Among 23 302 HF patients, a 1 µg/m3 increase in annual average PM2.5 was associated with an elevated risk of all-cause mortality (hazard ratio 1.13; 95% CI, 1.10-1.15). As compared with people with exposures below the current national PM2.5 exposure standard (12 µg/m3), those with elevated exposures experienced 0.84 (95% CI, 0.73-0.95) years of life lost over a 5-year period, an observation that persisted even for those residing in areas with PM2.5 concentrations below current standards. Conclusions Residential exposure to elevated concentrations of PM2.5 is a significant mortality risk factor for HF patients. Elevated PM2.5 exposures result in substantial years of life lost even at concentrations below current national standards.

Impact of Reductions in Emissions from Major Source Sectors on Fine Particulate Matter-Related Cardiovascular Mortality.

BACKGROUND: Reductions in ambient concentrations of fine particulate matter (PM2.5) have contributed to reductions in cardiovascular (CV) mortality. OBJECTIVES: We examined changes in CV mortality attributed to reductions in emissions from mobile, point, areal, and nonroad sources through changes in concentrations of PM2.5 and its major components [nitrates, sulfates, elemental carbon (EC), and organic carbon (OC)] in 2,132 U.S. counties between 1990 and 2010. METHODS: Using Community Multiscale Air Quality model estimated PM2.5 total and component concentrations, we calculated population-weighted annual averages for each county. We estimated PM2.5 total- and component-related CV mortality, adjusted for county-level population characteristics and baseline PM2.5 concentrations. Using the index of Emission Mitigation Efficiency for primary emission-to-particle pathways, we expressed changes in particle-related mortality in terms of precursor emissions by each sector. RESULTS: PM2.5 reductions represented 5.7% of the overall decline in CV mortality. Large point source emissions of sulfur dioxide accounted for 6.685 [95% confidence interval (CI): 5.703, 7.667] fewer sulfate-related CV deaths per 100,000 people. Mobile source emissions of primary EC and nitrous oxides accounted for 3.396 (95% CI: 2.772, 4.020) and 3.984 (95% CI: 2.472, 5.496) fewer CV deaths per 100,000 people respectively. Increased EC and OC emissions from areal sources increased carbon-related CV mortality by 0.788 (95% CI: -0.540, 2.116) and 0.245 (95% CI: -0.697, 1.187) CV deaths per 100,000 people. DISCUSSION: In a nationwide epidemiological study of emission sector contribution to PM2.5-related mortality, we found that reductions in sulfur-dioxide emissions from large point sources and nitrates and EC emissions from mobile sources contributed the largest reduction in particle-related mortality rates respectively. https://doi.org/10.1289/EHP5692.

Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Findings from a Multisite Case-Control Study.

BACKGROUND: Epidemiologic studies have reported associations between prenatal and early postnatal air pollution exposure and autism spectrum disorder (ASD); however, findings differ by pollutant and developmental window. OBJECTIVES: We examined associations between early life exposure to particulate matter ≤2.5 µm in diameter (PM2.5) and ozone in association with ASD across multiple US regions. METHODS: Our study participants included 674 children with confirmed ASD and 855 population controls from the Study to Explore Early Development, a multi-site case-control study of children born from 2003 to 2006 in the United States. We used a satellite-based model to assign air pollutant exposure averages during several critical periods of neurodevelopment: 3 months before pregnancy; each trimester of pregnancy; the entire pregnancy; and the first year of life. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for study site, maternal age, maternal education, maternal race/ethnicity, maternal smoking, and month and year of birth. RESULTS: The air pollution-ASD associations appeared to vary by exposure time period. Ozone exposure during the third trimester was associated with ASD, with an OR of 1.2 (95% CI: 1.1, 1.4) per 6.6 ppb increase in ozone. We additionally observed a positive association with PM2.5 exposure during the first year of life (OR = 1.3 [95% CI: 1.0, 1.6] per 1.6 µg/m increase in PM2.5). CONCLUSIONS: Our study corroborates previous findings of a positive association between early life air pollution exposure and ASD, and identifies a potential critical window of exposure during the late prenatal and early postnatal periods.

C-reactive protein from dried blood spots: Application to household air pollution field studies.

Household air pollution (HAP) is estimated to be an important risk factor for cardiovascular disease, but little clinical evidence exists and collecting biomarkers of disease risk is difficult in low-resource settings. Among 54 Nicaraguan women with woodburning cookstoves, we evaluated cross-sectional associations between 48-hour measures of HAP (eg, fine particulate matter, PM2.5 ) and C-reactive protein (CRP) via dried blood spots; secondary analyses included seven additional biomarkers of systemic injury and inflammation. We conducted sub-studies to calculate the intraclass correlation coefficient (ICC) in biomarkers collected over four consecutive days in Nicaragua and to assess the validity of measuring biomarkers in dried blood by calculating the correlation with paired venous-drawn samples in Colorado. Measures of HAP were associated with CRP (eg, a 25% increase in indoor PM2.5 was associated with a 7.4% increase in CRP [95% confidence interval: 0.7, 14.5]). Most of the variability in CRP concentrations over the 4-day period was between-person (ICC: 0.88), and CRP concentrations were highly correlated between paired dried blood and venous-drawn serum (Spearman ρ = .96). Results for secondary biomarkers were primarily consistent with null associations, and the sub-study ICCs and correlations were lower. Assessing CRP via dried blood spots provides a feasible approach to elucidate the association between HAP and cardiovascular disease risk.

The contribution of improved air quality to reduced cardiovascular mortality: Declines in socioeconomic differences over time.

Major improvements in air quality since 1990, observed through reductions in fine particulate matter (PM2.5), have been associated with reduced cardiovascular mortality rates (CMR). However, it is not well understood whether the health benefit attributed to PM2.5 reductions has been similar across strata of socioeconomic deprivation (SED). Using mixed effect regression models, we estimated the PM2.5-related change in the CMR across 2,132 US counties in five SED strata between 1990 and 2010. The analysis included annual county CMR (deaths/100,000 person-year), annual county PM2.5 (µg/m3), and an index of county SED based on socioeconomic factors from the 1990 US Census. The contribution of PM2.5 reductions to decreased CMR varied by SED strata and over time. Yearly differences resulted from varying rates of PM2.5 reduction and because of the non-linear relationship between CMR and PM2.5 concentration. In early years, PM2.5-related CMR reductions were smallest in the most deprived counties compared to all other counties (range: 0.4-0.6 vs 0.7-1.6 fewer deaths/100,000 person-year), due to slower rates of PM2.5 reduction in these counties. However, in later years, PM2.5-related CMR reductions were highest counties with moderate to high deprivation, compared to counties with the least deprivation (range: 1.0-2.2 vs 0.5-0.9 fewer deaths/100,000 person-year) due to larger CMR reductions per decrease in PM2.5. We identified that CMR reductions related to air quality improvements have become more similar over time between socioeconomic strata.

Divergent trends in life expectancy across the rural-urban gradient and association with specific racial proportions in the contiguous USA 2000-2005.

OBJECTIVES: To estimate county-level adult life expectancy for Whites, Black/African Americans (Black), American Indian/Alaska Native (AIAN) and Asian/Pacific Islander (Asian) populations and assess the difference across racial groups in the relationship among life expectancy, rurality and specific race proportion. METHODS: We used individual-level death data to estimate county-level life expectancy at age 25 (e25) for Whites, Black, AIAN and Asian in the contiguous USA for 2000-2005. Race-sex-stratified models were used to examine the associations among e25, rurality and specific race proportion, adjusted for socioeconomic variables. RESULTS: Lower e25 was found in the central USA for AIANs and in the west coast for Asians. We found higher e25 in the most rural areas for Whites but in the most urban areas for AIAN and Asians. The associations between specific race proportion and e25 were positive or null for Whites but were negative for Blacks, AIAN, and Asians. The relationship between specific race proportion and e25 varied across rurality. CONCLUSIONS: Identifying differences in adult life expectancy, both across and within racial groups, provides new insights into the geographic determinants of life expectancy disparities.

Neighborhood sociodemographic effects on the associations between long-term PM2.5 exposure and cardiovascular outcomes and diabetes.

Introduction: Exposure to PM2.5 air pollution and neighborhood-level sociodemographic characteristics are associated with cardiovascular disease and possibly diabetes. However, the joint effect of sociodemographics and PM2.5 on these outcomes is uncertain. Methods: We examined whether clusters of sociodemographic characteristics modified effects of long-term PM2.5 exposure on coronary artery disease (CAD), myocardial infarction (MI), hypertension, and diabetes. We used medical records data from 2192 cardiac catheterization patients residing in North Carolina and assigned to one of six previously-determined clusters. For each participant, we estimated annual PM2.5 exposure at their primary residence using a hybrid model with a 1 km2 resolution. We used logistic regression models adjusted for age, sex, body mass index, and smoking status, to assess cluster-specific associations with PM2.5 and to determine if there were interactions between cluster and PM2.5 on outcomes. Results: Compared to cluster 3 (OR 0.93, 95% CI 0.82-1.07; urban, low proportion of black individuals and high socioeconomic status), we observed greater associations between PM2.5 and hypertension in clusters 1 (OR 1.22, 95% CI 0.99-1.50, pint 0.03) and 2 (OR 1.64, 95% CI 1.16-2.32, pint 0.003), which were urban, high proportion of black individuals, and low socioeconomic status. PM2.5 was associated with MI (OR 1.29, 95% CI 1.16-1.42) but not diabetes, regardless of cluster and was associated with CAD in cluster 3 (OR 1.15, 95% CI 1.00, 1.31) and overall (OR 1.07, 95% CI 0.98, 1.17). Discussion: Areas of relative disadvantage have a stronger association between PM2.5 and hypertension compared to areas of relative advantage.

Association of long-term PM2.5 exposure with traditional and novel lipid measures related to cardiovascular disease risk.

BACKGROUND: Fine particulate matter (PM2.5) exposure is associated with increased morbidity and mortality, particularly for cardiovascular disease. The association between long-term exposure to PM2.5 and measures of lipoprotein subfractions remains unclear. Therefore, we examined associations between long-term PM2.5 exposure and traditional and novel lipoprotein measures in a cardiac catheterization cohort in North Carolina. METHODS: This cross-sectional study included 6587 patients who had visited Duke University for a cardiac catheterization between 2001 and 2010 and resided in North Carolina. We used estimates of daily PM2.5 concentrations on a 1 km-grid based on satellite measurements. PM2.5 predictions were matched to the address of each patient and averaged for the year prior to catheterization date. Serum lipids included HDL, LDL, and triglyceride-rich particle, and apolipoprotein B concentrations (HDL-P, LDL-P, TRL-P, and apoB, respectively). Linear and quantile regression models were used to estimate change in lipoprotein levels with each µg/m3 increase in annual average PM2.5. Models were adjusted for age, sex, race/ethnicity, history of smoking, area-level education, urban/rural status, body mass index, and diabetes. RESULTS: For a 1-µg/m3 increment in PM2.5 exposure, we observed increases in total and small LDL-P, LDL-C, TRL-P, apoB, total cholesterol, and triglycerides. The percent change from the mean outcome level was 2.00% (95% CI: 1.38%, 2.64%) for total LDL-P and 2.25% (95% CI: 1.43%, 3.06%) for small LDL-P. CONCLUSION: Among this sample of cardiac catheterization patients residing in North Carolina, long-term PM2.5 exposure was associated with increases in several lipoprotein concentrations. This abstract does not necessarily reflect U.S. EPA policy.

Human exposure factors as potential determinants of the heterogeneity in city-specific associations between PM2.5 and mortality.

Multi-city population-based epidemiological studies of short-term fine particulate matter (PM2.5) exposures and mortality have observed heterogeneity in risk estimates between cities. Factors affecting exposures, such as pollutant infiltration, which are not captured by central-site monitoring data, can differ between communities potentially explaining some of this heterogeneity. This analysis evaluates exposure factors as potential determinants of the heterogeneity in 312 core-based statistical areas (CBSA)-specific associations between PM2.5 and mortality using inverse variance weighted linear regression. Exposure factor variables were created based on data on housing characteristics, commuting patterns, heating fuel usage, and climatic factors from national surveys. When survey data were not available, air conditioning (AC) prevalence was predicted utilizing machine learning techniques. Across all CBSAs, there was a 0.95% (Interquartile range (IQR) of 2.25) increase in non-accidental mortality per 10 µg/m3 increase in PM2.5 and significant heterogeneity between CBSAs. CBSAs with larger homes, more heating degree days, a higher percentage of home heating with oil had significantly (p < 0.05) higher health effect estimates, while cities with more gas heating had significantly lower health effect estimates. While univariate models did not explain much of heterogeneity in health effect estimates (R2 < 1%), multivariate models began to explain some of the observed heterogeneity (R2 = 13%).

Air pollution, neighborhood deprivation, and autism spectrum disorder in the Study to Explore Early Development.

BACKGROUND: To examine whether neighborhood deprivation modifies the association between early life air pollution exposure and autism spectrum disorder (ASD), we used resources from a multisite case-control study, the Study to Explore Early Development. METHODS: Cases were 674 children with confirmed ASD born in 2003-2006; controls were 855 randomly sampled children born during the same time period and residents of the same geographic areas as cases. Air pollution was assessed by roadway proximity and particulate matter <2.5 µm (PM2.5) exposure during pregnancy and first year of life. To characterize neighborhood deprivation, an index was created based on eight census tract-level socioeconomic status-related parameters. The continuous index was categorized into tertiles, representing low, moderate, and high deprivation. Logistic regression was used to estimate odds ratios (ORs) and corresponding 95% confidence intervals (CIs). RESULTS: Neighborhood deprivation modified (P for interaction = 0.08) the association between PM2.5 exposure during the first year of life and ASD, with a stronger association for those living in high (OR = 2.42, 95% CI = 1.20, 4.86) rather than moderate (OR=1.21, 95% CI = 0.67, 2.17) or low (OR=1.46, 95% CI = 0.80, 2.65) deprivation neighborhoods. Departure from additivity or multiplicativity was not observed for roadway proximity or exposures during pregnancy. CONCLUSION: These results provide suggestive evidence of interaction between neighborhood deprivation and PM2.5 exposure during the first year of life in association with ASD.

Short-term effects of fine particulate matter and ozone on the cardiac conduction system in patients undergoing cardiac catheterization.

BACKGROUND: Air pollution-induced changes in cardiac electrophysiological properties could be a pathway linking air pollution and cardiovascular events. The evidence of air pollution effects on the cardiac conduction system is incomplete yet. We investigated short-term effects of particulate matter ≤ 2.5 µm in aerodynamic diameter (PM2.5) and ozone (O3) on cardiac electrical impulse propagation and repolarization as recorded in surface electrocardiograms (ECG). METHODS: We analyzed repeated 12-lead ECG measurements performed on 5,332 patients between 2001 and 2012. The participants came from the Duke CATHGEN Study who underwent cardiac catheterization and resided in North Carolina, United States (NC, U.S.). Daily concentrations of PM2.5 and O3 at each participant's home address were predicted with a hybrid air quality exposure model. We used generalized additive mixed models to investigate the associations of PM2.5 and O3 with the PR interval, QRS interval, heart rate-corrected QT interval (QTc), and heart rate (HR). The temporal lag structures of the associations were examined using distributed-lag models. RESULTS: Elevated PM2.5 and O3 were associated with four-day lagged lengthening of the PR and QRS intervals, and with one-day lagged increases in HR. We observed immediate effects on the lengthening of the QTc interval for both PM2.5 and O3, as well as delayed effects for PM2.5 (lagged by 3 - 4 days). The associations of PM2.5 and O3 with the PR interval and the association of O3 with the QRS interval persisted until up to seven days after exposure. CONCLUSIONS: In patients undergoing cardiac catheterization, short-term exposure to air pollution was associated with increased HR and delays in atrioventricular conduction, ventricular depolarization and repolarization.