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Dive into the research topics where Sara D. Adar is active.

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Featured researches published by Sara D. Adar.


PLOS Medicine | 2013

Fine Particulate Air Pollution and the Progression of Carotid Intima-Medial Thickness: A Prospective Cohort Study from the Multi-Ethnic Study of Atherosclerosis and Air Pollution

Sara D. Adar; Lianne Sheppard; Sverre Vedal; Joseph F. Polak; Paul D. Sampson; Ana V. Diez Roux; Matthew J. Budoff; David R. Jacobs; R. Graham Barr; Karol E. Watson; Joel D. Kaufman

In a prospective cohort study, Sara Adar and colleagues find that decreasing levels of fine particulate matter in multiple US urban areas are associated with slowed progression of intima-medial thickness, a surrogate measure of atherosclerosis.


Epidemiology | 2007

Focused exposures to airborne traffic particles and heart rate variability in the elderly.

Sara D. Adar; Diane R. Gold; Brent A. Coull; Joel Schwartz; Peter H. Stone; Helen Suh

Background: Exposure to airborne particles may increase cardiac risk by altering autonomic balance. Because these risks may be particularly great for traffic-related particles, we examined associations between particles and heart rate variability as 44 subjects participated in 4 repeated trips aboard a diesel bus. Methods: Twenty-four hour electrocardiograms were correlated with continuous particle concentrations using generalized additive models controlling for subject, weekday, time, apparent temperature, trip type, activity, medications, and autoregressive terms. Associations were assessed for short- and medium-term moving averages of measured concentrations. Results: Heart rate variability was negatively associated with fine particulate matter. Positive associations were demonstrated with heart rate and the low-to-high frequency power ratio. Associations were strongest with 24-hour mean concentrations, although strong short-term associations also were found during bus periods, independent of daily exposures. Overall, associations were greatest for high-frequency power with the following effects per interquartile change in the 24-hour mean concentrations: –15% (95% confidence interval = –17% to –14%) for PM2.5 (4.6 &mgr;g/m3); –19% (–21% to –17%) for black carbon (459 ng/m3); and –14% (–15% to –12%) for fine particle counts (39 pt/cm3). For each interquartile change in the 5-minute PM2.5 concentration (10 &mgr;g/m3) aboard the bus, an 11% (95% confidence interval = –14% to –8%) decrease in high-frequency power was observed. Conclusions: This investigation indicates that fine particles are negatively associated with heart rate variability, with an overall trend towards reduced parasympathetic tone. Although daily associations were evident for all particles, short-term associations were predominantly limited to traffic-related particles.


The Lancet | 2016

Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study

Joel D. Kaufman; Sara D. Adar; R. Graham Barr; Matthew J. Budoff; Gregory L. Burke; Cynthia L. Curl; Martha L. Daviglus; Ana V. Diez Roux; Amanda J. Gassett; David R. Jacobs; Richard A. Kronmal; Timothy V. Larson; Ana Navas-Acien; Casey Olives; Paul D. Sampson; Lianne Sheppard; David S. Siscovick; James H. Stein; Adam A. Szpiro; Karol E. Watson

BACKGROUND Long-term exposure to fine particulate matter less than 2.5 μm in diameter (PM2.5) and traffic-related air pollutant concentrations are associated with cardiovascular risk. The disease process underlying these associations remains uncertain. We aim to assess association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness. METHODS In this prospective 10-year cohort study, we repeatedly measured coronary artery calcium by CT in 6795 participants aged 45-84 years enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) in six metropolitan areas in the USA. Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. Common carotid artery intima-media thickness was measured by ultrasound in all participants at baseline and in 2010-12 for 3459 participants. Residence-specific spatio-temporal pollution concentration models, incorporating community-specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PM2.5 and nitrogen oxides (NOX) between 1999 and 2012. The primary aim was to examine the association between both progression of coronary artery calcium and mean carotid artery intima-media thickness and long-term exposure to ambient air pollutant concentrations (PM2.5, NOX, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular risk factors, site, and CT scanner technology. FINDINGS In this population, coronary calcium increased on average by 24 Agatston units per year (SD 58), and intima-media thickness by 12 μm per year (10), before adjusting for risk factors or air pollutant exposures. Participant-specific pollutant concentrations averaged over the years 2000-10 ranged from 9.2-22.6 μg PM2.5/m(3) and 7.2-139.2 parts per billion (ppb) NOX. For each 5 μg PM2.5/m(3) increase, coronary calcium progressed by 4.1 Agatston units per year (95% CI 1.4-6.8) and for each 40 ppb NOX coronary calcium progressed by 4.8 Agatston units per year (0.9-8.7). Pollutant exposures were not associated with intima-media thickness change. The estimate for the effect of a 5 μg/m(3) higher long-term exposure to PM2.5 in intima-media thickness was -0.9 μm per year (95% CI -3.0 to 1.3). For 40 ppb higher NOX, the estimate was 0.2 μm per year (-1.9 to 2.4). INTERPRETATION Increased concentrations of PM2.5 and traffic-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases. FUNDING US Environmental Protection Agency and US National Institutes of Health.


Inhalation Toxicology | 2007

Cardiovascular Disease and Air Pollutants: Evaluating and Improving Epidemiological Data Implicating Traffic Exposure

Sara D. Adar; Joel D. Kaufman

Evidence suggests that traffic-related pollutants play a role in the observed associations between air pollution and adverse cardiovascular health effects. The contribution of traffic to individual exposures is difficult to quantify in traditional epidemiological studies, however, and researchers have employed various approaches in attempt to isolate its effects. Many investigators have employed ambient measurements such as nitrogen oxides, carbon monoxide, or black carbon as surrogates for traffic in studying associations with health outcomes. Source-apportionment techniques also have been used in a few studies to identify associations with the mixture of pollutants from specific origins, including traffic. In other studies, estimates of traffic near a persons home have predicted cardiovascular endpoints, and local traffic levels have modified the effect of regional air pollution. More recently, studies have linked changes in cardiovascular health to time spent in traffic. In this article, we review the epidemiological evidence regarding the impact of traffic-related pollution on cardiovascular diseases and examine the different techniques used to examine this important research question. We conclude with a discussion of the future directions being used in ongoing epidemiological studies to identify the cardiovascular health impacts of traffic.


JAMA Internal Medicine | 2015

Longitudinal Associations Between Neighborhood Physical and Social Environments and Incident Type 2 Diabetes Mellitus: The Multi-Ethnic Study of Atherosclerosis (MESA)

Paul J. Christine; Amy H. Auchincloss; Alain G. Bertoni; Mercedes R. Carnethon; Brisa N. Sánchez; Kari Moore; Sara D. Adar; Tamara B. Horwich; Karol E. Watson; Ana V. Diez Roux

IMPORTANCE Neighborhood environments may influence the risk for developing type 2 diabetes mellitus (T2DM), but, to our knowledge, no longitudinal study has evaluated specific neighborhood exposures. OBJECTIVE To determine whether long-term exposures to neighborhood physical and social environments, including the availability of healthy food and physical activity resources and levels of social cohesion and safety, are associated with incident T2DM during a 10-year period. DESIGN, SETTING, AND PARTICIPANTS We used data from the Multi-Ethnic Study of Atherosclerosis, a population-based cohort study of adults aged 45 to 84 years at baseline (July 17, 2000, through August 29, 2002). A total of 5124 participants free of T2DM at baseline underwent 5 clinical follow-up examinations from July 17, 2000, through February 4, 2012. Time-varying measurements of neighborhood healthy food and physical activity resources and social environments were linked to individual participant addresses. Neighborhood environments were measured using geographic information system (GIS)- and survey-based methods and combined into a summary score. We estimated hazard ratios (HRs) of incident T2DM associated with cumulative exposure to neighborhood resources using Cox proportional hazards regression models adjusted for age, sex, income, educational level, race/ethnicity, alcohol use, and cigarette smoking. Data were analyzed from December 15, 2013, through September 22, 2014. MAIN OUTCOMES AND MEASURES Incident T2DM defined as a fasting glucose level of at least 126 mg/dL or use of insulin or oral antihyperglycemics. RESULTS During a median follow-up of 8.9 years (37,394 person-years), 616 of 5124 participants (12.0%) developed T2DM (crude incidence rate, 16.47 [95% CI, 15.22-17.83] per 1000 person-years). In adjusted models, a lower risk for developing T2DM was associated with greater cumulative exposure to indicators of neighborhood healthy food (12%; HR per interquartile range [IQR] increase in summary score, 0.88 [95% CI, 0.79-0.98]) and physical activity resources (21%; HR per IQR increase in summary score, 0.79 [95% CI, 0.71-0.88]), with associations driven primarily by the survey exposure measures. Neighborhood social environment was not associated with incident T2DM (HR per IQR increase in summary score, 0.96 [95% CI, 0.88-1.07]). CONCLUSIONS AND RELEVANCE Long-term exposure to residential environments with greater resources to support physical activity and, to a lesser extent, healthy diets was associated with a lower incidence of T2DM, although results varied by measurement method. Modifying neighborhood environments may represent a complementary, population-based approach to prevention of T2DM, although further intervention studies are needed.


Environmental Health Perspectives | 2013

Air pollution and individual and neighborhood socioeconomic status: evidence from the Multi-Ethnic Study of Atherosclerosis (MESA).

Anjum Hajat; Ana V. Diez-Roux; Sara D. Adar; Amy H. Auchincloss; Gina S. Lovasi; Marie S. O'Neill; Lianne Sheppard; Joel D. Kaufman

Background: Although research has shown that low socioeconomic status (SES) and minority communities have higher exposure to air pollution, few studies have simultaneously investigated the associations of individual and neighborhood SES with pollutants across multiple sites. Objectives: We characterized the distribution of ambient air pollution by both individual and neighborhood SES using spatial regression methods. Methods: The study population comprised 6,140 participants from the Multi-Ethnic Study of Atherosclerosis (MESA). Year 2000 annual average ambient PM2.5 and NOx concentrations were calculated for each study participant’s home address at baseline examination. We investigated individual and neighborhood (2000 U.S. Census tract level) SES measures corresponding to the domains of income, wealth, education, and occupation. We used a spatial intrinsic conditional autoregressive model for multivariable analysis and examined pooled and metropolitan area–specific models. Results: A 1-unit increase in the z-score for family income was associated with 0.03-μg/m3 lower PM2.5 (95% CI: –0.05, –0.01) and 0.93% lower NOx (95% CI: –1.33, –0.53) after adjustment for covariates. A 1-SD–unit increase in the neighborhood’s percentage of persons with at least a high school degree was associated with 0.47-μg/m3 lower mean PM2.5 (95% CI: –0.55, –0.40) and 9.61% lower NOx (95% CI: –10.85, –8.37). Metropolitan area–specific results exhibited considerable heterogeneity. For example, in New York, high-SES neighborhoods were associated with higher concentrations of pollution. Conclusions: We found statistically significant associations of SES measures with predicted air pollutant concentrations, demonstrating the importance of accounting for neighborhood- and individual-level SES in air pollution health effects research. Citation: Hajat A, Diez-Roux AV, Adar SD, Auchincloss AH, Lovasi GS, O’Neill MS, Sheppard L, Kaufman JD. 2013. Air pollution and individual and neighborhood socioeconomic status: evidence from the Multi-Ethnic Study of Atherosclerosis (MESA). Environ Health Perspect 121:1325–1333; http://dx.doi.org/10.1289/ehp.1206337


American Journal of Epidemiology | 2012

Prospective study of particulate air pollution exposures, subclinical atherosclerosis, and clinical cardiovascular disease: The Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

Joel D. Kaufman; Sara D. Adar; Ryan W. Allen; R. Graham Barr; Matthew J. Budoff; Gregory L. Burke; Adrian M. Casillas; Martin Cohen; Cynthia L. Curl; Martha L. Daviglus; Ana V. Diez Roux; David R. Jacobs; Richard A. Kronmal; Timothy V. Larson; Sally Liu; Thomas Lumley; Ana Navas-Acien; Daniel H. O'Leary; Jerome I. Rotter; Paul D. Sampson; Lianne Sheppard; David S. Siscovick; James H. Stein; Adam A. Szpiro; Russell P. Tracy

The Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) was initiated in 2004 to investigate the relation between individual-level estimates of long-term air pollution exposure and the progression of subclinical atherosclerosis and the incidence of cardiovascular disease (CVD). MESA Air builds on a multicenter, community-based US study of CVD, supplementing that study with additional participants, outcome measurements, and state-of-the-art air pollution exposure assessments of fine particulate matter, oxides of nitrogen, and black carbon. More than 7,000 participants aged 45-84 years are being followed for over 10 years for the identification and characterization of CVD events, including acute myocardial infarction and other coronary artery disease, stroke, peripheral artery disease, and congestive heart failure; cardiac procedures; and mortality. Subcohorts undergo baseline and follow-up measurements of coronary artery calcium using computed tomography and carotid artery intima-medial wall thickness using ultrasonography. This cohort provides vast exposure heterogeneity in ranges currently experienced and permitted in most developed nations, and the air monitoring and modeling methods employed will provide individual estimates of exposure that incorporate residence-specific infiltration characteristics and participant-specific time-activity patterns. The overarching study aim is to understand and reduce uncertainty in health effect estimation regarding long-term exposure to air pollution and CVD.


American Journal of Respiratory and Critical Care Medicine | 2009

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

Victor C. Van Hee; Sara D. Adar; Adam A. Szpiro; R. Graham Barr; David A. Bluemke; Ana V. Diez Roux; Edward A. Gill; Lianne Sheppard; Joel D. Kaufman

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.


Environmental Health Perspectives | 2012

Modeling the residential infiltration of outdoor PM2.5 in the multi-ethnic study of atherosclerosis and air pollution (MESA Air)

Ryan W. Allen; Sara D. Adar; Edward L. Avol; Martin Cohen; Cynthia L. Curl; Timothy V. Larson; L.-J. Sally Liu; Lianne Sheppard; Joel D. Kaufman

Background: Epidemiologic studies of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] typically use outdoor concentrations as exposure surrogates. Failure to account for variation in residential infiltration efficiencies (Finf) will affect epidemiologic study results. Objective: We aimed to develop models to predict Finf for > 6,000 homes in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a prospective cohort study of PM2.5 exposure, subclinical cardiovascular disease, and clinical outcomes. Methods: We collected 526 two-week, paired indoor–outdoor PM2.5 filter samples from a subset of study homes. PM2.5 elemental composition was measured by X-ray fluorescence, and Finf was estimated as the indoor/outdoor sulfur ratio. We regressed Finf on meteorologic variables and questionnaire-based predictors in season-specific models. Models were evaluated using the R2 and root mean square error (RMSE) from a 10-fold cross-validation. Results: The mean ± SD Finf across all communities and seasons was 0.62 ± 0.21, and community-specific means ranged from 0.47 ± 0.15 in Winston-Salem, North Carolina, to 0.82 ± 0.14 in New York, New York. Finf was generally greater during the warm (> 18°C) season. Central air conditioning (AC) use, frequency of AC use, and window opening frequency were the most important predictors during the warm season; outdoor temperature and forced-air heat were the best cold-season predictors. The models predicted 60% of the variance in 2-week Finf, with an RMSE of 0.13. Conclusions: We developed intuitive models that can predict Finf using easily obtained variables. Using these models, MESA Air will be the first large epidemiologic study to incorporate variation in residential Finf into an exposure assessment.


Environmental Research | 2008

Effects of diesel exhaust inhalation on heart rate variability in human volunteers.

Alon Peretz; Joel D. Kaufman; Carol A. Trenga; Jason Allen; Chris Carlsten; Mary R. Aulet; Sara D. Adar; Jeffrey H. Sullivan

OBJECTIVES Particulate matter (PM) air pollution is associated with alterations in cardiac conductance and sudden cardiac death in epidemiological studies. Traffic-related air pollutants, including diesel exhaust (DE) may be at least partly responsible for these effects. In this experimental study we assessed whether short-term exposure to DE would result in alterations in heart rate variability (HRV), a non-invasive measure of autonomic control of the heart. METHODS In a double-blind, crossover, controlled-exposure study, 16 adult volunteers were exposed (at rest) in randomized order to filtered air (FA) and two levels of diluted DE (100 or 200 microg/m(3) of fine particulate matter) in 2-h sessions. Before, and at four time points after each exposure we assessed HRV. HRV parameters assessed included both time domain statistics (standard deviation of N-N intervals (SDNN), and the square root of the mean of the sum of squared differences between successive N-N intervals (RMSSD)) and frequency domain statistics (high-frequency (HF) power, low-frequency (LF) power, and the LF/HF ratio). RESULTS We observed an effect at 3-h after initiation of DE inhalation on the frequency domain statistics of HRV. DE at 200 microg/m(3) elicited an increase in HF power compared to FA (Delta=0.33; 95% CI: 0.01-0.7) and a decrease in LF/HF ratio (Delta=-0.74; 95% CI: -1.2 to -0.2). The effect of DE on HF power was not consistent among study participants. There was no DE effect on time domain statistics and no significant DE effect on HRV in later time points. CONCLUSIONS We did not observe a consistent DE effect on the autonomic control of the heart in a controlled-exposure experiment in young participants. Efforts are warranted to understand discrepancies between epidemiological and experimental studies of air pollutions impact on HRV.

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Adam A. Szpiro

University of Washington

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R. Graham Barr

University of Washington

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