Particulate Matter Exposure and Cardiopulmonary Differences in the Multi-Ethnic Study of Atherosclerosis.

BACKGROUND: Particulate matter (PM) exposure may directly affect the pulmonary vasculature. Although the pulmonary vasculature is not easily measurable, differential associations for right ventricular (RV) and left ventricular (LV) mass may provide an indirect assessment of pulmonary vascular damage. OBJECTIVES: We tested whether long-term exposure to PM < 2.5 µm (PM2.5) is associated with greater RV mass and RV mass/end-diastolic volume ratio relative to the LV. METHODS: The Multi-Ethnic Study of Atherosclerosis performed cardiac magnetic resonance (CMR) imaging among participants 45-84 years old without clinical cardiovascular disease in 2000-2002 in six U.S. cities. A fine-scale spatiotemporal model estimated ambient PM2.5 exposure in the year before CMR; individually weighted estimates accounted for indoor exposure to ambient PM2.5. Linear regression models were adjusted for demographics, anthropometrics, smoking status, cardiac risk factors, and LV parameters, with additional adjustment for city. RESULTS: The 4,041 included participants had a mean age of 61.5 years, and 47% were never smokers. The mean ambient PM2.5 was 16.4 µg/m3 and individually weighted PM2.5 was 11.0 µg/m3. PM2.5 exposure was associated with greater RV mass [ambient: 0.11 g per 5 µg/m3 (95% CI: -0.05, 0.27); individually weighted: 0.20 g per 5 µg/m3 (95% CI: 0.04, 0.36)] and a greater RV mass/end-diastolic volume ratio conditional on LV parameters. City-adjusted results for RV mass were of greater magnitude and were statistically significant for both measures of PM2.5, whereas those for RV mass/end-diastolic volume ratio were attenuated. CONCLUSIONS: Long-term PM2.5 exposures were associated with greater RV mass and RV mass/end-diastolic volume ratio conditional on the LV; however, additional adjustment for city attenuated the RV mass/end-diastolic volume findings. These findings suggest that PM2.5 exposure may be associated with subclinical cardiopulmonary differences in this general population sample. CITATION: Aaron CP, Chervona Y, Kawut SM, Diez Roux AV, Shen M, Bluemke DA, Van Hee VC, Kaufman JD, Barr RG. 2016. Particulate matter exposure and cardiopulmonary differences in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 124:1166-1173; http://dx.doi.org/10.1289/ehp.1409451.

Long-Term Air Pollution Exposure and Blood Pressure in the Sister Study.

BACKGROUND: Exposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution. OBJECTIVE: We examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes. METHODS: This analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (≤ 2.5 µm; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding. RESULTS: A 10-µg/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure. CONCLUSIONS: Long-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.

Traffic-related air pollution and the right ventricle. The multi-ethnic study of atherosclerosis.

RATIONALE: Right heart failure is a cause of morbidity and mortality in common and rare heart and lung diseases. Exposure to traffic-related air pollution is linked to left ventricular hypertrophy, heart failure, and death. Relationships between traffic-related air pollution and right ventricular (RV) structure and function have not been studied. OBJECTIVES: To characterize the relationship between traffic-related air pollutants and RV structure and function. METHODS: We included men and women with magnetic resonance imaging assessment of RV structure and function and estimated residential outdoor nitrogen dioxide (NO2) concentrations from the Multi-ethnic Study of Atherosclerosis, a study of individuals free of clinical cardiovascular disease at baseline. Multivariable linear regression estimated associations between NO2 exposure (averaged over the year prior to magnetic resonance imaging) and measures of RV structure and function after adjusting for demographics, anthropometrics, smoking status, diabetes mellitus, and hypertension. Adjustment for corresponding left ventricular parameters, traffic-related noise, markers of inflammation, and lung disease were considered in separate models. Secondary analyses considered oxides of nitrogen (NOx) as the exposure. MEASUREMENTS AND MAIN RESULTS: The study sample included 3,896 participants. In fully adjusted models, higher NO2 was associated with greater RV mass and larger RV end-diastolic volume with or without further adjustment for corresponding left ventricular parameters, traffic-related noise, inflammatory markers, or lung disease (all P < 0.05). There was no association between NO2 and RV ejection fraction. Relationships between NOx and RV morphology were similar. CONCLUSIONS: Higher levels of NO2 exposure were associated with greater RV mass and larger RV end-diastolic volume.

Vascular responses to long- and short-term exposure to fine particulate matter: MESA Air (Multi-Ethnic Study of Atherosclerosis and Air Pollution).

OBJECTIVES: This study evaluated the association of long- and short-term air pollutant exposures with flow-mediated dilation (FMD) and baseline arterial diameter (BAD) of the brachial artery using ultrasound in a large multicity cohort. BACKGROUND: Exposures to ambient air pollution, especially long-term exposure to particulate matter <2.5 µm in aerodynamic diameter (PM(2.5)), are linked with cardiovascular mortality. Short-term exposure to PM(2.5) has been associated with decreased FMD and vasoconstriction, suggesting that adverse effects of PM(2.5) may involve endothelial dysfunction. However, long-term effects of PM(2.5) on endothelial dysfunction have not been investigated. METHODS: FMD and BAD were measured by brachial artery ultrasound at the initial examination of the Multi-Ethnic Study of Atherosclerosis. Long-term PM(2.5) concentrations were estimated for the year 2000 at each participant's residence (n = 3,040) using a spatio-temporal model informed by cohort-specific monitoring. Short-term PM(2.5) concentrations were based on daily central-site monitoring in each of the 6 cities. RESULTS: An interquartile increase in long-term PM(2.5) concentration (3 µg/m(3)) was associated with a 0.3% decrease in FMD (95% confidence interval [CI] of difference: -0.6 to -0.03; p = 0.03), adjusting for demographic characteristics, traditional risk factors, sonographers, and 1/BAD. Women, nonsmokers, younger participants, and those with hypertension seemed to show a greater association of PM(2.5) with FMD. FMD was not significantly associated with short-term variation in PM(2.5) (-0.1% per 12 µg/m(3) daily increase [95% CI: -0.2 to 0.04] on the day before examination). CONCLUSIONS: Long-term PM(2.5) exposure was significantly associated with decreased endothelial function according to brachial ultrasound results. These findings may elucidate an important pathway linking air pollution and cardiovascular mortality.

Association of long-term air pollution with ventricular conduction and repolarization abnormalities.

BACKGROUND: Short-term exposure to air pollution may affect ventricular repolarization, but there is limited information on how long-term exposures might affect the surface ventricular electrocardiographic (ECG) abnormalities associated with cardiovascular events. We carried out a study to determine whether long-term air pollution exposure is associated with abnormalities of ventricular repolarization and conduction in adults without known cardiovascular disease. METHODS: A total of 4783 participants free of clinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis underwent 12-lead ECG examinations, cardiac-computed tomography, and calcium scoring, as well as estimation of air pollution exposure using a finely resolved spatiotemporal model to determine long-term average individual exposure to fine particulate matter (PM(2.5)) and proximity to major roadways. We assessed ventricular electrical abnormalities including presence of QT prolongation (Rautaharju QTrr criteria) and intraventricular conduction delay (QRS duration >120 milliseconds). We used logistic regression to determine the adjusted relationship between air pollution exposures and ECG abnormalities. RESULTS: A 10-µg/m³ increase in estimated residential PM(2.5) was associated with an increased odds of prevalent QT prolongation (adjusted odds ratio [OR] = 1.6 [95% confidence interval (CI) = 1.2-2.2]) and intraventricular conduction delay (1.7 [1.0-2.6]), independent of coronary-artery calcium score. Living near major roadways was not associated with ventricular electrical abnormalities. No evidence of effect modification by traditional risk factors or study site was observed. CONCLUSIONS: This study demonstrates an association between long-term exposure to air pollution and ventricular repolarization and conduction abnormalities in adults without clinical cardiovascular disease, independent of subclinical coronary arterial calcification.

Air pollution and cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis.

Research to date demonstrates a relationship between exposure to ambient air pollutants and cardiovascular disease (CVD). Many studies have shown associations between short-term exposures to elevated levels of air pollutants and CVD events, and several cohort studies suggest effects of long-term exposure on cardiovascular mortality, coronary heart disease events, and stroke. The biologic mechanisms underlying this long-term exposure relationship are not entirely clear but are hypothesized to include systemic inflammation, autonomic nervous system imbalance, changes in vascular compliance, altered cardiac structure, and development of atherosclerosis. The Multi-Ethnic Study of Atherosclerosis provides an especially well-characterized population in which to investigate the relationship between air pollution and CVD and to explore these biologic pathways. This article reviews findings reported to date within this cohort and summarizes the aims and anticipated contributions of a major ancillary study, the Multi-Ethnic Study of Atherosclerosis and Air Pollution.

Common genetic variation, residential proximity to traffic exposure, and left ventricular mass: the multi-ethnic study of atherosclerosis.

BACKGROUND: Elevated left ventricular mass (LVM) is a strong predictor of negative cardiovascular outcomes, including heart failure, stroke, and sudden cardiac death. A relationship between close (< 50 m compared with > 150 m) residential proximity to major roadways and higher LVM has previously been described, but the mechanistic pathways that are involved in this relationship are not known. Understanding genetic factors that influence susceptibility to these effects may provide insight into relevant mechanistic pathways. OBJECTIVE: We set out to determine whether genetic polymorphisms in genes affecting vascular and autonomic function, blood pressure, or inflammation influence the relationship between traffic proximity and LVM. METHODS: This was a cross-sectional study of 1,376 genotyped participants in the Multi-Ethnic Study of Atherosclerosis, with cardiac magnetic resonance imaging performed between 2000 and 2002. The impact of tagged single-nucleotide polymorphisms (tagSNPs) and inferred haplotypes in 12 candidate genes (ACE, ADRB2, AGT, AGTR1, ALOX15, EDN1, GRK4, PTGS1, PTGS2, TLR4, VEGFA, and VEGFB) on the relationship between residential proximity to major roadways and LVM was analyzed using multiple linear regression, adjusting for multiple potential confounders. RESULTS: After accounting for multiple testing and comparing homozygotes, tagSNPs in the type 1 angiotensin II receptor (AGTR1, rs6801836) and arachidonate 15-lipoxygenase (ALOX15, rs2664593) genes were each significantly (q < 0.2) associated with a 9-10% difference in the association between residential proximity to major roadways and LVM. Participants with suboptimal blood pressure control demonstrated stronger interactions between AGTR1 and traffic proximity. CONCLUSIONS: Common polymorphisms in genes responsible for vascular function, inflammation, and oxidative stress appear to modify associations between proximity to major roadways and LVM. Further understanding of how genes modify effects of air pollution on CVD may help guide research efforts into specific mechanistic pathways.

Exposure to traffic and left ventricular mass and function: the Multi-Ethnic Study of Atherosclerosis.

RATIONALE: Ambient air pollution has been associated with heart failure morbidity and mortality. The mechanisms responsible for these associations are unknown but may include the effects of traffic-related pollutants on vascular or autonomic function. OBJECTIVES: We assessed the cross-sectional relation between long-term air pollution, traffic exposures, and important end-organ measures of alterations in cardiac function-left ventricular mass index (LVMI) and ejection fraction-in the Multi-Ethnic Study of Atherosclerosis, a multicenter study of adults without previous clinical cardiovascular disease. METHODS: A total of 3,827 eligible participants (aged 45-84 yr) underwent cardiac magnetic resonance imaging between 2000 and 2002. We estimated air pollution exposures using residential proximity to major roadways and interpolated concentrations of fine particulate matter (less than 2.5 microns in diameter). We examined adjusted associations between these exposures and left ventricular mass and function. MEASUREMENTS AND MAIN RESULTS: Relative to participants living more than 150 m from a major roadway, participants living within 50 m of a major roadway showed an adjusted 1.4 g/m(2) (95% CI, 0.3-2.5) higher LVMI, a difference in mass corresponding to a 5.6 mm Hg greater systolic blood pressure. Ejection fraction was not associated with proximity to major roadways. Limited variability in estimates of fine particulate matter was observed within cities, and no associations with particulate matter were found for either outcome after adjustment for center. CONCLUSIONS: Living in close proximity to major roadways is associated with higher LVMI, suggesting chronic vascular end-organ damage from a traffic-related environmental exposure. Air pollutants or another component of roadway proximity, such as noise, could be responsible.

Pleural plaques related to "take-home" exposure to asbestos: An international case series.

CONTEXT: While a large number of studies indicate the risks of high-level exposures to asbestos in the workplace setting, a relatively small number of studies describe the risk of pleural disease related to "take-home" asbestos brought into the household by workers exposed to asbestos. Consequently, the risk of pleural disease in family members of asbestos-exposed workers is likely underappreciated. CASE PRESENTATIONS: Two families of siblings, one in Israel and one in the US, were evaluated because of their significant exposures to asbestos brought into the home by family members with heavy occupational exposures. Two of the four children of an asbestos cement debagger in Petach Tikvah, Israel and two children of a pipe lagger in a naval shipyard near Seattle, Washington, manifested benign pleural disease without parenchymal disease, despite having no occupational exposure to asbestos. DISCUSSION: These cases illustrate that "take-home" asbestos exposure may lead to pleural disease at higher rates than commonly realized. RELEVANCE TO CLINICAL PRACTICE: Providers should recognize that due to the potential for "take-home" exposures, asbestos-related disease in a patient may be a marker for disease in household contacts. Patients with family members heavily exposed to asbestos should be strongly encouraged to quit smoking in an effort to reduce any further carcinogenic exposures. Additionally, workplace control and regulation of asbestos use should be emphasized to protect both workers and their families.