PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-25 (1197226)

Clipboard (0)
None

Related Articles

1.  Air Pollution and the Microvasculature: A Cross-Sectional Assessment of In Vivo Retinal Images in the Population-Based Multi-Ethnic Study of Atherosclerosis (MESA) 
PLoS Medicine  2010;7(11):e1000372.
Sara Adar and colleagues show that residing in locations with higher air pollution concentrations and experiencing daily increases in air pollution are associated with narrower retinal arteriolar diameters in older individuals, thus providing a link between air pollution and cardiovascular disease.
Background
Long- and short-term exposures to air pollution, especially fine particulate matter (PM2.5), have been linked to cardiovascular morbidity and mortality. One hypothesized mechanism for these associations involves microvascular effects. Retinal photography provides a novel, in vivo approach to examine the association of air pollution with changes in the human microvasculature.
Methods and Findings
Chronic and acute associations between residential air pollution concentrations and retinal vessel diameters, expressed as central retinal arteriolar equivalents (CRAE) and central retinal venular equivalents (CRVE), were examined using digital retinal images taken in Multi-Ethnic Study of Atherosclerosis (MESA) participants between 2002 and 2003. Study participants (46 to 87 years of age) were without clinical cardiovascular disease at the baseline examination (2000–2002). Long-term outdoor concentrations of PM2.5 were estimated at each participant's home for the 2 years preceding the clinical exam using a spatio-temporal model. Short-term concentrations were assigned using outdoor measurements on the day preceding the clinical exam. Residential proximity to roadways was also used as an indicator of long-term traffic exposures. All associations were examined using linear regression models adjusted for subject-specific age, sex, race/ethnicity, education, income, smoking status, alcohol use, physical activity, body mass index, family history of cardiovascular disease, diabetes status, serum cholesterol, glucose, blood pressure, emphysema, C-reactive protein, medication use, and fellow vessel diameter. Short-term associations were further controlled for weather and seasonality. Among the 4,607 participants with complete data, CRAE were found to be narrower among persons residing in regions with increased long- and short-term levels of PM2.5. These relationships were observed in a joint exposure model with −0.8 µm (95% confidence interval [CI] −1.1 to −0.5) and −0.4 µm (95% CI −0.8 to 0.1) decreases in CRAE per interquartile increases in long- (3 µg/m3) and short-term (9 µg/m3) PM2.5 levels, respectively. These reductions in CRAE are equivalent to 7- and 3-year increases in age in the same cohort. Similarly, living near a major road was also associated with a −0.7 µm decrease (95% CI −1.4 to 0.1) in CRAE. Although the chronic association with CRAE was largely influenced by differences in exposure between cities, this relationship was generally robust to control for city-level covariates and no significant differences were observed between cities. Wider CRVE were associated with living in areas of higher PM2.5 concentrations, but these findings were less robust and not supported by the presence of consistent acute associations with PM2.5.
Conclusions
Residing in regions with higher air pollution concentrations and experiencing daily increases in air pollution were each associated with narrower retinal arteriolar diameters in older individuals. These findings support the hypothesis that important vascular phenomena are associated with small increases in short-term or long-term air pollution exposures, even at current exposure levels, and further corroborate reported associations between air pollution and the development and exacerbation of clinical cardiovascular disease.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Cardiovascular disease (CVD)—disease that affects the heart and/or the blood vessels—is a common cause of illness and death among adults in developed countries. In the United States, for example, the leading cause of death is coronary heart disease, a CVD in which narrowing of the heart's arteries by atherosclerotic plaques (fatty deposits that build up with age) slows the blood supply to the heart and may eventually cause a heart attack (myocardial infarction). Other types of CVD include stroke (in which atherosclerotic plaques interrupt the brain's blood supply) and peripheral arterial disease (in which the blood supply to the limbs is blocked). Smoking, high blood pressure, high blood levels of cholesterol (a type of fat), having diabetes, being overweight, and being physically inactive all increase a person's risk of developing CVD. Treatments for CVD include lifestyle changes and taking drugs that lower blood pressure or blood cholesterol levels.
Why Was This Study Done?
Another risk factor for CVD is exposure to long-term and/or short-term air pollution. Fine particle pollution or PM2.5 is particularly strongly associated with an increased risk of CVD. PM2.5—particulate matter 2.5 µm in diameter or 1/30th the diameter of a human hair—is mainly produced by motor vehicles, power plants, and other combustion sources. Why PM2.5 increases CVD risk is not clear but one possibility is that it alters the body's microvasculature (fine blood vessels known as capillaries, arterioles, and venules), thereby impairing the blood flow through the heart and brain. In this study, the researchers use noninvasive digital retinal photography to investigate whether there is an association between air pollution and changes in the human microvasculature. The retina—a light-sensitive layer at the back of the eye that converts images into electrical messages and sends them to the brain—has a dense microvasculature. Retinal photography is used to check the retinal microvasculature for signs of potentially blinding eye diseases such as diabetic retinopathy. Previous studies have found that narrower than normal retinal arterioles and wider than normal retinal venules are associated with CVD.
What Did the Researchers Do and Find?
The researchers used digital retinal photography to measure the diameters of retinal blood vessels in the participants of the Multi-Ethnic Study of Atherosclerosis (MESA). This study is investigating CVD progression in people aged 45–84 years of various ethnic backgrounds who had no CVD symptoms when they enrolled in the study in 2000–2002. The researchers modeled the long-term outdoor concentration of PM2.5 at each participant's house for the 2-year period preceding the retinal examination (which was done between 2002 and 2003) using data on PM2.5 levels collected by regulatory monitoring stations as well as study-specific air samples collected outside of the homes and in the communities of study participants. Outdoor PM2.5 measurements taken the day before the examination provided short-term PM2.5 levels. Among the 4,607 MESA participants who had complete data, retinal arteriolar diameters were narrowed among those who lived in regions with increased long- and short-term PM2.5 levels. Specifically, an increase in long-term PM2.5 concentrations of 3 µg/m3 was associated with a 0.8 µm decrease in arteriolar diameter, a reduction equivalent to that seen for a 7-year increase in age in this group of people. Living near a major road, another indicator of long-term exposure to PM2.5 pollution, was also associated with narrowed arterioles. Finally, increased retinal venular diameters were weakly associated with long-term high PM2.5 concentrations.
What Do These Findings Mean?
These findings indicate that living in areas with long-term air pollution or being exposed to short-term air pollution is associated with narrowing of the retinal arterioles in older individuals. They also show that widening of retinal venules is associated with long-term (but not short-term) PM2.5 pollution. Together, these findings support the hypothesis that long- and short-term air pollution increases CVD risk through effects on the microvasculature. However, they do not prove that PM2.5 is the constituent of air pollution that drives microvascular changes—these findings could reflect the toxicity of another pollutant or the pollution mixture as a whole. Importantly, these findings show that microvascular changes can occur at the PM2.5 levels that commonly occur in developed countries, which are well below those seen in developing countries. Worryingly, they also suggest that the deleterious cardiovascular effects of air pollution could occur at levels below existing regulatory standards.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/ 10.1371/journal.pmed.1000372.
The American Heart Association provides information for patients and caregivers on all aspects of cardiovascular disease (in several languages), including information on air pollution, heart disease, and stroke
The US Centers for Disease Control and Prevention has information on heart disease and on stroke
Information is available from the British Heart Foundation on cardiovascular disease
The UK National Health Service Choices website provides information for patients and caregivers about cardiovascular disease
MedlinePlus provides links to other sources of information on heart disease and on vascular disease (in English and Spanish)
The AIRNow site provides information about US air quality and about air pollution and health
The Air Quality Archive has up-to-date information about air pollution in the UK and information about the health effects of air pollution
The US Environmental Protection Agency has information on PM2.5
The following Web sites contain information available on the MESA and MESA Air studies
doi:10.1371/journal.pmed.1000372
PMCID: PMC2994677  PMID: 21152417
2.  Association of resting heart rate with carotid and aortic arterial stiffness: Multi-Ethnic Study of Atherosclerosis (MESA) 
Hypertension  2013;62(3):10.1161/HYPERTENSIONAHA.113.01605.
Resting heart rate is an easily measured, non-invasive vital sign that is associated with cardiovascular disease events. The pathophysiology of this association is not known. We investigated the relationship between resting heart rate and stiffness of the carotid (a peripheral artery) and the aorta (a central artery) in an asymptomatic multi-ethnic population. Resting heart rate was recorded at baseline in the Multi-Ethnic Study of Atherosclerosis (MESA). Distensibility was used as a measure of arterial elasticity, with a lower distensibility indicating an increase in arterial stiffness. Carotid distensibility was measured in 6,484 participants (98% of participants) using B-mode ultrasound and aortic distensibility was measured in 3,512 participants (53% of participants) using cardiac MRI. Heart rate was divided into quintiles and we used progressively adjusted models that included terms for physical activity and AV-nodal blocking agents. Mean resting heart rate of participants (mean age 62 years, 47% male) was 63 beats per minute (SD 9.6 beats per minute). In unadjusted and fully adjusted models, carotid distensibility and aortic distensibility decreased monotonically with increasing resting heart rate (p for trend <0.001 and 0.009 respectively). The relationship was stronger for carotid versus aortic distensibility. Similar results were seen using the resting heart rate taken at the time of MRI scanning. Our results suggest that a higher resting heart rate is associated with an increased arterial stiffness independent of AV-nodal blocker use and physical activity level, with a stronger association for a peripheral (carotid) compared to a central (aorta) artery.
doi:10.1161/HYPERTENSIONAHA.113.01605
PMCID: PMC3838105  PMID: 23836802
heart rate; cardiovascular disease; stiffness; ultrasound; cardiac magnetic resonance imaging
3.  Carotid Intima‐Media Thickness and Arterial Stiffness and the Risk of Atrial Fibrillation: The Atherosclerosis Risk in Communities (ARIC) Study, Multi‐Ethnic Study of Atherosclerosis (MESA), and the Rotterdam Study 
Background
We evaluated the association of carotid intima‐media thickness (cIMT), carotid plaque, carotid distensibility coefficient (DC), and aortic pulse wave velocity (PWV) with incident atrial fibrillation (AF) and their role in improving AF risk prediction beyond the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE)‐AF risk score.
Methods and Results
We analyzed data from 3 population‐based cohort studies: Atherosclerosis Risk in Communities (ARIC) Study (n=13 907); Multi‐Ethnic Study of Atherosclerosis (MESA; n=6640), and the Rotterdam Study (RS; n=5220). We evaluated the association of arterial indices with incident AF and computed the C‐statistic, category‐based net reclassification improvement (NRI), and relative integrated discrimination improvement (IDI) of incorporating arterial indices into the CHARGE‐AF risk score (age, race, height weight, systolic and diastolic blood pressure, antihypertensive medication use, smoking, diabetes, previous myocardial infarction, and previous heart failure). Higher cIMT (meta‐analyzed hazard ratio [95% CI] per 1‐SD increment, 1.12 [1.08–1.16]) and presence of carotid plaque (1.30 [1.19–1.42]) were associated with higher AF incidence after adjustment for CHARGE‐AF risk‐score variables. Lower DC and higher PWV were associated with higher AF incidence only after adjustment for the CHARGE‐AF risk‐score variables excepting height, weight, and systolic and diastolic blood pressure. Addition of cIMT or carotid plaque marginally improved CHARGE‐AF score prediction as assessed by the relative IDI (estimates, 0.025–0.051), but not when assessed with the C‐statistic and NRI.
Conclusions
Higher cIMT, presence of carotid plaque, and greater arterial stiffness are associated with higher AF incidence, indicating that atherosclerosis and arterial stiffness play a role in AF etiopathogenesis. However, arterial indices only modestly improve AF risk prediction.
doi:10.1161/JAHA.115.002907
PMCID: PMC4889172  PMID: 27207996
arterial stiffness; atherosclerosis; atrial fibrillation; carotid intima‐media thickness; Atrial Fibrillation; Epidemiology
4.  Particulate matter components and subclinical atherosclerosis: common approaches to estimating exposure in a Multi-Ethnic Study of Atherosclerosis cross-sectional study 
Environmental Health  2013;12:39.
Background
Concentrations of outdoor fine particulate matter (PM2.5) have been associated with cardiovascular disease. PM2.5 chemical composition may be responsible for effects of exposure to PM2.5.
Methods
Using data from the Multi-Ethnic Study of Atherosclerosis (MESA) collected in 2000–2002 on 6,256 US adults without clinical cardiovascular disease in six U.S. metropolitan areas, we investigated cross-sectional associations of estimated long-term exposure to total PM2.5 mass and PM2.5 components (elemental carbon [EC], organic carbon [OC], silicon and sulfur) with measures of subclinical atherosclerosis (coronary artery calcium [CAC] and right common carotid intima-media thickness [CIMT]). Community monitors deployed for this study from 2007 to 2008 were used to estimate exposures at baseline addresses using three commonly-used approaches: (1) nearest monitor (the primary approach), (2) inverse-distance monitor weighting and (3) city-wide average.
Results
Using the exposure estimate based on nearest monitor, in single-pollutant models, increased OC (effect estimate [95% CI] per IQR: 35.1 μm [26.8, 43.3]), EC (9.6 μm [3.6,15.7]), sulfur (22.7 μm [15.0,30.4]) and total PM2.5 (14.7 μm [9.0,20.5]) but not silicon (5.2 μm [−9.8,20.1]), were associated with increased CIMT; in two-pollutant models, only the association with OC was robust to control for the other pollutants. Findings were generally consistent across the three exposure estimation approaches. None of the PM measures were positively associated with either the presence or extent of CAC. In sensitivity analyses, effect estimates for OC and silicon were particularly sensitive to control for metropolitan area.
Conclusion
Employing commonly-used exposure estimation approaches, all of the PM2.5 components considered, except silicon, were associated with increased CIMT, with the evidence being strongest for OC; no component was associated with increased CAC. PM2.5 chemical components, or other features of the sources that produced them, may be important in determining the effect of PM exposure on atherosclerosis. These cross-sectional findings await confirmation in future work employing longitudinal outcome measures and using more sophisticated approaches to estimating exposure.
doi:10.1186/1476-069X-12-39
PMCID: PMC3663826  PMID: 23641873
Atherosclerosis; Cardiovascular diseases; Coronary artery disease; Air pollution; Particulate matter
5.  METABOLIC SYNDROME INCREASES CAROTID ARTERY STIFFNESS: THE NORTHERN MANHATTAN STUDY 
Background
Arterial Stiffness, an intermediate pre-clinical marker of atherosclerosis, has been associated with an increased risk of stroke and cardiovascular disease (CVD). The metabolic syndrome and its components are established CVD risk factors and may also increase arterial stiffness, but data on this potential relationship is limited. The goal of this study was to determine the association between the metabolic syndrome (MetSyn) and carotid artery stiffness (STIFF) in an elderly multi-ethnic cohort.
Methods
STIFF was assessed by carotid ultrasound as part of the Northern Manhattan Study (NOMAS), a prospective population-based cohort of stroke-free individuals. STIFF was calculated as [ln(systolicBP/diastolicBP)/Strain], where Strain was [(Systolic Diameter Diastolic Diameter)/Diastolic Diameter]. MetSyn was defined by the National Cholesterol Education Program: Adult Treatment Panel III (NCEP ATP III) criteria. LogSTIFF was analyzed as the dependent variable in linear regression models, adjusting for demographics, education, current smoking, presence of carotid plaque and intima-media thickness.
Results
STIFF was analyzed in 1133 NOMAS subjects (mean age 65±9 years; 61% women; 58% Hispanic, 22% Black, 20% White). The prevalence of MetSyn was 49%. The mean LogSTIFF was 2.01±0.61 among those with and 1.90±0.59 among those without MetSyn (p=0.003). MetSyn was significantly associated with increased logSTIFF in the final adjusted model (parameter estimate β=0.100, p=0.01). Among individual MetSyn components, waist circumference and elevated blood pressure were most significantly associated with a mean increase in logSTIFF (p<0.01).
Conclusion
MetSyn is significantly associated with increased carotid artery stiffness in a multiethnic population. Increased carotid artery stiffness may, in part, explain a high risk of stroke among individuals with the metabolic syndrome.
doi:10.1111/j.1747-4949.2010.00421.x
PMCID: PMC2980500  PMID: 20536608
metabolic syndrome; arterial stiffness; atherosclerosis; elderly; race-ethnicity
6.  Vascular Responses to Long- and Short-Term Exposure to Fine Particulate Matter 
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 (PM2.5), are linked with cardiovascular mortality. Short-term exposure to PM2.5 has been associated with decreased FMD and vasoconstriction, suggesting that adverse effects of PM2.5 may involve endothelial dysfunction. However, long-term effects of PM2.5 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 PM2.5 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 PM2.5 concentrations were based on daily central-site monitoring in each of the 6 cities.
Results
An interquartile increase in long-term PM2.5 concentration (3 μg/m3) 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 PM2.5 with FMD. FMD was not significantly associated with short-term variation in PM2.5 (−0.1% per 12 μg/m3 daily increase [95% CI: −0.2 to 0.04] on the day before examination).
Conclusions
Long-term PM2.5 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.
doi:10.1016/j.jacc.2012.08.973
PMCID: PMC3665082  PMID: 23103035
air pollution; atherosclerosis; cardiovascular mortality; endothelial function; flow-mediated dilation; traffic
7.  Relationship of Carotid Distensibility and Thoracic Aorta Calcification: Multi-Ethnic Study of Atherosclerosis (MESA) 
Hypertension  2009;54(6):1408-1415.
Stiffening of the central elastic arteries is one of the earliest detectable manifestations of adverse change within the vessel wall. While an association between carotid artery stiffness and adverse events has been demonstrated, little is known about the relationship between stiffness and atherosclerosis. Even less is known about the impact of age, gender, and race on this association. To elucidate this question, we used baseline data from the Multi-Ethnic Study of Atherosclerosis (MESA, 2000-2002). Carotid artery distensibility coefficient (DC) was calculated after visualization of the instantaneous waveform of common carotid diameter using high resolution B-mode ultrasound. Thoracic aorta calcification (TAC) was identified using non-contrast cardiac CT. We found a strong association between decreasing DC (increasing carotid stiffness) and increasing TAC as well as a graded increase in TAC score (p<0.001). After controlling for age, gender, race, and traditional and emerging cardiovascular risk factors, individuals in the stiffest quartile had a prevalence ratio of 1.52 (95% CI 1.15-2.00) for TAC compared to the least stiff quartile. In exploratory analysis, carotid stiffness was more highly correlated with calcification of the aorta than calcification of the coronary arteries (ρ=0.32 vs. 0.22, p<0.001 for comparison). In conclusion, there is a strong independent association between carotid stiffness and thoracic aorta calcification. Carotid stiffness is more highly correlated with calcification of the aorta, a central elastic artery, than calcification of the coronary arteries. The prognostic significance of these findings requires longitudinal follow-up of the MESA cohort.
doi:10.1161/HYPERTENSIONAHA.109.138396
PMCID: PMC4118641  PMID: 19805639
Carotid stiffness; carotid compliance; subclinical atherosclerosis; thoracic aorta calcification; coronary calcification
8.  A National Prediction Model for PM2.5 Component Exposures and Measurement Error–Corrected Health Effect Inference 
Environmental Health Perspectives  2013;121(9):1017-1025.
Background: Studies estimating health effects of long-term air pollution exposure often use a two-stage approach: building exposure models to assign individual-level exposures, which are then used in regression analyses. This requires accurate exposure modeling and careful treatment of exposure measurement error.
Objective: To illustrate the importance of accounting for exposure model characteristics in two-stage air pollution studies, we considered a case study based on data from the Multi-Ethnic Study of Atherosclerosis (MESA).
Methods: We built national spatial exposure models that used partial least squares and universal kriging to estimate annual average concentrations of four PM2.5 components: elemental carbon (EC), organic carbon (OC), silicon (Si), and sulfur (S). We predicted PM2.5 component exposures for the MESA cohort and estimated cross-sectional associations with carotid intima-media thickness (CIMT), adjusting for subject-specific covariates. We corrected for measurement error using recently developed methods that account for the spatial structure of predicted exposures.
Results: Our models performed well, with cross-validated R2 values ranging from 0.62 to 0.95. Naïve analyses that did not account for measurement error indicated statistically significant associations between CIMT and exposure to OC, Si, and S. EC and OC exhibited little spatial correlation, and the corrected inference was unchanged from the naïve analysis. The Si and S exposure surfaces displayed notable spatial correlation, resulting in corrected confidence intervals (CIs) that were 50% wider than the naïve CIs, but that were still statistically significant.
Conclusion: The impact of correcting for measurement error on health effect inference is concordant with the degree of spatial correlation in the exposure surfaces. Exposure model characteristics must be considered when performing two-stage air pollution epidemiologic analyses because naïve health effect inference may be inappropriate.
Citation: Bergen S, Sheppard L, Sampson PD, Kim SY, Richards M, Vedal S, Kaufman JD, Szpiro AA. 2013. A national prediction model for PM2.5 component exposures and measurement error–corrected health effect inference. Environ Health Perspect 121:1017–1025; http://dx.doi.org/10.1289/ehp.1206010
doi:10.1289/ehp.1206010
PMCID: PMC3764074  PMID: 23757600
9.  Evolution of aortic wall thickness and stiffness with atherosclerosis: Long-term follow up from the Multi-Ethnic Study of Atherosclerosis (MESA) 
Hypertension  2015;65(5):1015-1019.
The study was performed to determine age, gender, and time-dependent changes in aortic wall thickness (AWT), and to evaluate cross-sectional associations between AWT and arterial stiffness in older adults. Three hundred seventy-one (371) longitudinal and 426 cross-sectional measurements of AWT from cardiovascular magnetic resonance (CMR) imaging studies conducted within the Multi-Ethnic Study of Atherosclerosis (MESA) were analyzed at two points in time: in 2000-2002 and then again from follow-up examinations in 2010-2012. Aortic wall thickness was determined from a double inversion recovery black-blood fast spin-echo sequence, and aortic stiffness was measured from a phase-contrast cine gradient echo sequence. The thickness of the mid-thoracic descending aortic wall was measured and correlated to distensibility of the ascending aorta (AAD) and aortic pulse wave velocity (PWV). The average rate of AWT change was 0.032mm per year. The increase in AWT was greater for those aged 45 to 54 years relative to individuals older than age 55 years (p-trend<0.001). Ascending aortic distensibility was lower (p<0.001) and PWV was higher (p=0.012) for hypertensive subjects. After adjustment for traditional risk factors, AAD was significantly related to AWT in participants without hypertension. Hypertension was associated with increased aortic stiffness independent of aortic wall thickness.
doi:10.1161/HYPERTENSIONAHA.114.05080
PMCID: PMC4410010  PMID: 25776078
MR imaging; aortic wall thickness; longitudinal changes; arterial stiffness; hypertension
10.  Prospective Study of Particulate Air Pollution Exposures, Subclinical Atherosclerosis, and Clinical Cardiovascular Disease 
American Journal of Epidemiology  2012;176(9):825-837.
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.
doi:10.1093/aje/kws169
PMCID: PMC3571256  PMID: 23043127
air pollution; atherosclerosis; cardiovascular diseases; environmental exposure; epidemiologic methods; particulate matter
11.  Prevalence of and factors associated with myocardial scar in a U.S. Cohort 
JAMA  2015;314(18):1945-1954.
Importance
Myocardial scarring leads to cardiac dysfunction and poor prognosis. The prevalence of and factors associated with unrecognized myocardial infarction and scar have not been previously defined using current methods in a multi-ethnic US population.
Objective
To determine prevalence of and factors associated with myocardial scar in middle and older aged individuals in the United States (U.S).
Design, Setting, and Participants
Multi-Ethnic Study of Atherosclerosis (MESA) is a population based cohort in the U.S. MESA participants were 45-84 years old and free of clinical cardiovascular disease (CVD) at baseline in 2000-2002. In the 10th year examination of MESA (2010-2012), 1840 participants underwent cardiac magnetic resonance imaging (CMR) with gadolinium to detect myocardial scar. CVD risk factors and coronary artery calcium scores were measured at baseline and year 10. Logistic regression models were used to estimate adjusted odds ratios for myocardial scar.
Exposures
Cardiovascular risk factors, coronary artery calcium, left ventricle size and function, carotid intima media thickness
Main Outcome Measure
Myocardial scar detected by CMR.
Results
Of 1840 participants (mean age 68±9 yrs, 52% male), 146 had myocardial scars (7.9%). Most myocardial scars (114/146, 78%) were undetected by electrocardiogram or by clinical adjudication. In adjusted models, age, male gender, body mass index, hypertension, and current smoking at baseline were associated with myocardial scar at year 10 [OR (95% CI): 1.6 (1.4, 1.9) per 8.9 years, p<0.001; 5.8 (3.6, 9.2) men vs. women, p<0.001; 1.3 (1.1, 1.6) per 4.8 kg/m2, p=0.005, 1.6 (1.1, 2.3) for hypertension present, p=0.009; 2.0 (1.2, 3.3) current vs. never smokers, p=0.006, respectively]. Age, gender and ethnicity adjusted CAC score at baseline was also associated with myocardial scar at year 10 [CAC categories of 1-99, 100-399 and ≥ 400 vs. CAC =0: OR (95% CI): 2.4 (1.5, 3.9), 3.0 (1.7, 5.1), 3.3 (1.7, 6.1), respectively, p≤0.001]. CAC score significantly added to the association of myocardial scar with age, gender, ethnicity and traditional CVD risk factors (c-statistic: 0.81 vs. 0.79, with vs. without CAC, respectively, p=0.012).
Conclusions and Relevance
The prevalence of myocardial scars in a US community based multiethnic cohort was 7.9%, of which 78% were unrecognized by electrocardiography or clinical evaluation. Further studies are needed to understand the clinical consequences of these undetected scars and the utility of their identification.
doi:10.1001/jama.2015.14849
PMCID: PMC4774246  PMID: 26547466
12.  Association of Long-Term Air Pollution with Ventricular Conduction and Repolarization Abnormalities 
Epidemiology (Cambridge, Mass.)  2011;22(6):773-780.
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 spatio-temporal model to determine long-term average individual exposure to fine particulate matter (PM2.5) 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 msec). 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 PM2.5 was associated with an increased odds of prevalent QT prolongation (adjusted odds ratio [OR]= 1.6 [95% confidence interval (CI)= 1.2 to 2.2]) and intraventricular conduction delay (OR 1.7, 95% CI: 1.0 to 2.6, independent of coronary-artery calcium score. Living near major roadways was not associated with ventricular electrical abnormalities. No significant 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.
doi:10.1097/EDE.0b013e31823061a9
PMCID: PMC3197855  PMID: 21918454
13.  Associations between Recent Exposure to Ambient Fine Particulate Matter and Blood Pressure in the Multi-Ethnic Study of Atherosclerosis (MESA) 
Environmental Health Perspectives  2008;116(4):486-491.
Background
Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined cross-sectional associations between short-term ambient fine particles (particulate matter ≤ 2.5 μm in aerodynamic diameter; PM2.5) and BP: systolic (SBP), diastolic (DBP), mean arterial (MAP), and pulse pressure (PP).
Methods
The study sample included 5,112 persons 45–84 years of age, free of cardiovascular disease at the Multi-Ethnic Study of Atherosclerosis baseline examination (2000–2002). Data from U.S. Environmental Protection Agency monitors were used to estimate ambient PM2.5 exposures for the preceding 1, 2, 7, 30, and 60 days. Roadway data were used to estimate local exposures to traffic-related particles.
Results
Results from linear regression found PP and SBP positively associated with PM2.5. For example, a 10-μg/m3 increase in PM2.5 30-day mean was associated with 1.12 mmHg higher pulse pressure [95% confidence interval (CI), 0.28–1.97] and 0.99 mmHg higher systolic BP (95% CI, –0.15 to 2.13), adjusted for age, sex, race/ethnicity, income, education, body mass index, diabetes, cigarette smoking and environmental tobacco smoke, alcohol use, physical activity, medications, atmospheric pressure, and temperature. Results were much weaker and not statistically significant for MAP and DBP. Although traffic-related variables were not themselves associated with BP, the association between PM2.5 and BP was stronger in the presence of higher traffic exposure.
Conclusions
Higher SBP and PP were associated with ambient levels of PM2.5 and the association was stronger in the presence of roadway traffic, suggesting that impairment of blood pressure regulation may play a role in response to air pollution.
doi:10.1289/ehp.10899
PMCID: PMC2291007  PMID: 18414631
air pollution; blood pressure; cardiovascular disease; epidemiology; particulate matter
14.  Air Pollution and Percent Emphysema Identified by Computed Tomography in the Multi-Ethnic Study of Atherosclerosis 
Environmental Health Perspectives  2014;123(2):144-151.
Background: Air pollution is linked to low lung function and to respiratory events, yet little is known of associations with lung structure.
Objectives: We examined associations of particulate matter (PM2.5, PM10) and nitrogen oxides (NOx) with percent emphysema-like lung on computed tomography (CT).
Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) recruited participants (45–84 years of age) in six U.S. states. Percent emphysema was defined as lung regions < –910 Hounsfield Units on cardiac CT scans acquired following a highly standardized protocol. Spirometry was also conducted on a subset. Individual-level 1- and 20-year average air pollution exposures were estimated using spatiotemporal models that included cohort-specific measurements. Multivariable regression was conducted to adjust for traditional risk factors and study location.
Results: Among 6,515 participants, we found evidence of an association between percent emphysema and long-term pollution concentrations in an analysis leveraging between-city exposure contrasts. Higher concentrations of PM2.5 (5 μg/m3) and NOx (25 ppb) over the previous year were associated with 0.6 (95% CI: 0.1, 1.2%) and 0.5 (95% CI: 0.1, 0.9%) higher average percent emphysema, respectively. However, after adjustment for study site the associations were –0.6% (95% CI: –1.5, 0.3%) for PM2.5 and –0.5% (95% CI: –1.1, 0.02%) for NOx. Lower lung function measures (FEV1 and FVC) were associated with higher PM2.5 and NOx levels in 3,791 participants before and after adjustment for study site, though most associations were not statistically significant.
Conclusions: Associations between ambient air pollution and percentage of emphysema-like lung were inconclusive in this cross-sectional study, thus longitudinal analyses may better clarify these associations with percent emphysema.
Citation: Adar SD, Kaufman JD, Diez-Roux AV, Hoffman EA, D’Souza J, Stukovsky KH, Rich SS, Rotter JI, Guo X, Raffel LJ, Sampson PD, Oron AP, Raghunathan T, Barr RG. 2015. Air pollution and percent emphysema identified by computed tomography in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 123:144–151; http://dx.doi.org/10.1289/ehp.1307951
doi:10.1289/ehp.1307951
PMCID: PMC4314244  PMID: 25302408
15.  A Flexible Spatio-Temporal Model for Air Pollution with Spatial and Spatio-Temporal Covariates 
The development of models that provide accurate spatio-temporal predictions of ambient air pollution at small spatial scales is of great importance for the assessment of potential health effects of air pollution. Here we present a spatio-temporal framework that predicts ambient air pollution by combining data from several different monitoring networks and deterministic air pollution model(s) with geographic information system (GIS) covariates. The model presented in this paper has been implemented in an R package, SpatioTemporal, available on CRAN.
The model is used by the EPA funded Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) to produce estimates of ambient air pollution; MESA Air uses the estimates to investigate the relationship between chronic exposure to air pollution and cardiovascular disease. In this paper we use the model to predict long-term average concentrations of NOx in the Los Angeles area during a ten year period. Predictions are based on measurements from the EPA Air Quality System, MESA Air specific monitoring, and output from a source dispersion model for traffic related air pollution (Caline3QHCR). Accuracy in predicting long-term average concentrations is evaluated using an elaborate cross-validation setup that accounts for a sparse spatio-temporal sampling pattern in the data, and adjusts for temporal effects. The predictive ability of the model is good with cross-validated R2 of approximately 0.7 at subject sites.
Replacing four geographic covariate indicators of traffic density with the Caline3QHCR dispersion model output resulted in very similar prediction accuracy from a more parsimonious and more interpretable model. Adding traffic-related geographic covariates to the model that included Caline3QHCR did not further improve the prediction accuracy.
doi:10.1007/s10651-013-0261-4
PMCID: PMC4174563  PMID: 25264424
16.  APPROACH TO ESTIMATING PARTICIPANT POLLUTANT EXPOSURES IN THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS AND AIR POLLUTION (MESA AIR) 
Environmental science & technology  2009;43(13):4687-4693.
Most published epidemiology studies of long-term air pollution health effects have relied on central site monitoring to investigate regional-scale differences in exposure. Few cohort studies have had sufficient data to characterize localized variations in pollution, despite the fact that large gradients can exist over small spatial scales. Similarly, previous data have generally been limited to measurements of particle mass or several of the criteria gases. The Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) is an innovative investigation undertaken to link subclinical and clinical cardiovascular health effects with individual-level estimates of personal exposure to ambient-origin pollution. This project improves on prior work by implementing an extensive exposure assessment program to characterize long-term average concentrations of ambient-generated PM2.5, specific PM2.5 chemical components, and co-pollutants, with particular emphasis on capturing concentration gradients within cities.
This paper describes exposure assessment in MESA Air, including questionnaires, community sampling, home monitoring, and personal sampling. Summary statistics describing the performance of the sampling methods are presented along with descriptive statistics of the air pollution concentrations by city.
PMCID: PMC2727607  PMID: 19673252
17.  A Unified Spatiotemporal Modeling Approach for Predicting Concentrations of Multiple Air Pollutants in the Multi-Ethnic Study of Atherosclerosis and Air Pollution 
Environmental Health Perspectives  2014;123(4):301-309.
Background:
Cohort studies of the relationship between air pollution exposure and chronic health effects require predictions of exposure over long periods of time.
Objectives:
We developed a unified modeling approach for predicting fine particulate matter, nitrogen dioxide, oxides of nitrogen, and black carbon (as measured by light absorption coefficient) in six U.S. metropolitan regions from 1999 through early 2012 as part of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).
Methods:
We obtained monitoring data from regulatory networks and supplemented those data with study-specific measurements collected from MESA Air community locations and participants’ homes. In each region, we applied a spatiotemporal model that included a long-term spatial mean, time trends with spatially varying coefficients, and a spatiotemporal residual. The mean structure was derived from a large set of geographic covariates that was reduced using partial least-squares regression. We estimated time trends from observed time series and used spatial smoothing methods to borrow strength between observations.
Results:
Prediction accuracy was high for most models, with cross-validation R2 (R2CV) > 0.80 at regulatory and fixed sites for most regions and pollutants. At home sites, overall R2CV ranged from 0.45 to 0.92, and temporally adjusted R2CV ranged from 0.23 to 0.92.
Conclusions:
This novel spatiotemporal modeling approach provides accurate fine-scale predictions in multiple regions for four pollutants. We have generated participant-specific predictions for MESA Air to investigate health effects of long-term air pollution exposures. These successes highlight modeling advances that can be adopted more widely in modern cohort studies.
Citation:
Keller JP, Olives C, Kim SY, Sheppard L, Sampson PD, Szpiro AA, Oron AP, Lindström J, Vedal S, Kaufman JD. 2015. A unified spatiotemporal modeling approach for predicting concentrations of multiple air pollutants in the Multi-Ethnic Study of Atherosclerosis and Air Pollution. Environ Health Perspect 123:301–309; http://dx.doi.org/10.1289/ehp.1408145
doi:10.1289/ehp.1408145
PMCID: PMC4384200  PMID: 25398188
18.  Associations Between Short-term Changes in Air Pollution and Correlates of Arterial Stiffness: The Veterans Affairs Normative Aging Study, 2007–2011 
American Journal of Epidemiology  2013;179(2):192-199.
We investigated associations between short-term exposure to air pollution and central augmentation index and augmentation pressure, correlates of arterial stiffness, in a cohort of elderly men in the Boston, Massachusetts, metropolitan area. This longitudinal analysis included 370 participants from the Veterans Affairs Normative Aging Study with up to 2 visits between 2007 and 2011 (n = 445). Augmentation index (as %) and augmentation pressure (in mmHg) were measured at each visit by using radial artery applanation tonometry for pulse wave analysis and modeled in a mixed effects regression model as continuous functions of moving averages of air pollution exposures (over 4 hours and 1, 3, 7, and 14 days). The results suggest that short-term changes in air pollution were associated with augmentation index and augmentation pressure at several moving averages. Interquartile range (IQR) increases in 3-day average exposure to particles with aerodynamic diameter less than 2.5 μm (3.6-μg/m3 IQR increase) and sulfate (1.4-μg/m3 IQR increase) and 1-day average exposure to particle number counts (8,741-counts/cm3 IQR increase) were associated with augmentation index values that were 0.8% (95% confidence interval (CI): 0.2, 1.4), 0.6% (95% CI: 0.1, 1.2), and 1.7% (95% CI: 0.4, 2.9) higher, respectively. Overall, the findings were similar for augmentation pressure. The findings support the hypothesis that exposure to air pollution may affect vascular function.
doi:10.1093/aje/kwt271
PMCID: PMC3873113  PMID: 24227017
air pollution; particulate matter; pulse wave analysis
19.  Secondhand Smoke Exposure and Subclinical Cardiovascular Disease: The Multi‐Ethnic Study of Atherosclerosis 
Background
Few studies have evaluated the association between secondhand smoke (SHS) and subclinical cardiovascular disease among ethnically diverse populations. This study assesses the impact of SHS on inflammation and atherosclerosis (carotid intima‐media thickness, coronary artery calcification, and peripheral arterial disease).
Methods and Results
We examined 5032 nonsmoking adults aged 45 to 84 years without prior cardiovascular disease participating in the Multi‐Ethnic Study of Atherosclerosis (MESA) from 2000 to 2002. SHS exposure was determined by self‐report, and urinary cotinine was measured in a representative subset (n=2893). The multi‐adjusted geometric mean ratios (95% CIs) for high‐sensitivity C‐reactive protein and interleukin‐6 comparing 407 participants with SHS ≥12 h/wk versus 3035 unexposed participants were 1.13 (1.02–1.26) and 1.04 (0.98–1.11), respectively. The multi‐adjusted geometric mean ratio for carotid intima‐media thickness was 1.02 (0.97–1.07). Fibrinogen and coronary artery calcification were not associated with SHS. The prevalence of peripheral arterial disease (ankle‐brachial index ≤0.9 or ≥1.4) was associated with detectable urinary cotinine (odds ratio, 2.10; 95% CI, 1.09–4.04) but not with self‐reported SHS. Urinary cotinine was not associated with inflammation or carotid intima‐media thickness.
Conclusions
Despite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.
doi:10.1161/JAHA.115.002965
PMCID: PMC5210438  PMID: 27993830
ankle‐brachial index; atherosclerosis; carotid intima‐media thickness; coronary artery calcium; inflammation; peripheral artery disease; secondhand smoke; smoking; Cardiovascular Disease; Epidemiology; Risk Factors; Lifestyle; Primary Prevention
20.  Effects of Acute Resistance Exercise on Arterial Stiffness in Young Men 
Korean Circulation Journal  2010;40(1):16-22.
Background and Objectives
Increased central arterial stiffness is an emerging risk factor for cardiovascular disease. Acute aerobic exercise reduces arterial stiffness, while acute resistance exercise may increase arterial stiffness, but this is not a universal finding. We tested whether an acute resistance exercise program was associated with an increase in arterial stiffness in healthy young men.
Subjects and Methods
Thirteen healthy subjects were studied under parallel experimental conditions on 2 separate days. The order of experiments was randomized between resistance exercise (8 resistance exercises at 60% of 1 repeated maximal) and sham control (seated rest in the exercise room). Carotid-femoral pulse wave velocity (PWV) and aortic augmentation index as indices of aortic stiffness were measured using applanation tonometry. Measurements were made at baseline before treatments, 20 minutes, and 40 minutes after treatments (resistance exercise and sham control).
Results
There was no difference in resting heart rate or in arterial stiffness between the two experimental conditions at baseline. At 20 minutes after resistance exercise, heart rate, carotid-femoral PWV and augmentation index@75(%) were significantly increased in the resistance exercise group compared with the sham control (p<0.05). Brachial blood pressure, central blood pressure and pulse pressure were not significantly increased after resistance exercise.
Conclusion
An acute resistance exercise program can increase arterial stiffness in young healthy men. Further studies are needed to clarify the effects of long-term resistance training on arterial stiffness.
doi:10.4070/kcj.2010.40.1.16
PMCID: PMC2812793  PMID: 20111648
Arterial stiffness; Resistance training
21.  Thoracic Aortic Distensibility and Thoracic Aortic Calcium (From the Multi-ethnic Study of Atherosclerosis [MESA]) 
The American journal of cardiology  2010;106(4):575-580.
Decreased arterial distensibility is an early manifestation of adverse structural and functional changes within the vessel wall. Its correlation with thoracic aortic calcium (TAC), a marker of atherosclerosis, has not been well demonstrated. We tested the hypothesis that decreasing aortic compliance and increasing arterial stiffness is independently associated with increased TAC. We included 3,540 (61±10 years, 46% males) subjects from the Multi-ethnic Study of Atherosclerosis (MESA) study who underwent aortic distensibility (AD) assessment on MRI. TAC was calculated using modified Agatston algorithm on non-contrast cardiac CT. Multivariate regression models were calculated for the presence of TAC. Overall, 861 (24%) individuals had detectable TAC. A lower AD was observed among those with vs. without TAC (2.02±1.34 vs. 1.28±0.74, p<0.0001). The prevalence of TAC increased significantly across decreasing quartiles of AD (7%, 17%, 31%, and 42%, p<0.0001). Using multivariate analysis, TAC was independently associated with AD after adjusting for age, gender, ethnicity and other covariates. In conclusion, our analysis demonstrates that increased arterial stiffness is associated with increased TAC independent of ethnicity and other atherosclerotic risk factors.
doi:10.1016/j.amjcard.2010.03.074
PMCID: PMC4228943  PMID: 20691319
22.  Estimating Acute Air Pollution Health EFFects from Cohort Study Data 
Biometrics  2013;70(1):164-174.
Summary
Traditional studies of short-term air pollution health effects use time series data, while cohort studies generally focus on long-term effects. There is increasing interest in exploiting individual level cohort data to assess short-term health effects in order to understand the mechanisms and time scales of action. We extend semiparametric regression methods used to adjust for unmeasured confounding in time series studies to the cohort setting. Time series methods are not directly applicable since cohort data are typically collected over a prespecified time period and include exposure measurements on days without health observations. Therefore, long-time asymptotics are not appropriate, and it is possible to improve efficiency by exploiting the additional exposure data. We show that flexibility of the semiparametric adjustment model should match the complexity of the trend in the health outcome, in contrast to the time series setting where it suffices to match temporal structure in the exposure. We also demonstrate that pre-adjusting exposures concurrent with the health endpoints using trends in the complete exposure time series results in unbiased health effect estimation and can improve efficiency without additional confounding adjustment. A recently published article found evidence of an association between short-term exposure to ambient fine particulate matter (PM2.5) and retinal arteriolar diameter as measured by retinal photography in the Multi-Ethnic Study of Atherosclerosis (MESA). We reanalyze the data from this article in order to compare the methods described here, and we evaluate our methods in a simulation study based on the MESA data.
doi:10.1111/biom.12125
PMCID: PMC4080094  PMID: 24571570
Air pollution; Environmental epidemiology; Generalized least squares; Mixed models; Semiparametric regression; Time series; Unmeasured confounding.
23.  Pericardial Fat is Associated with Carotid Stiffness in the Multi-Ethnic Study of Atherosclerosis 
Background and Aims
Arterial stiffness is a prominent feature of vascular aging and a risk factor for cardiovascular disease (CVD). Fat around the heart and blood vessels (i.e. pericardial fat, Pfat) may contribute to arterial stiffness via a local paracrine effect of adipose tissue on the surrounding vasculature. Thus, we determined the association between Pfat and carotid stiffness in 5,770 participants (mean age 62 yrs, 53% female, 25% African American, 24% Hispanic, and 13% Chinese) from the Multi-Ethnic Study of Atherosclerosis.
Methods and Results
Pfat was measured by computed tomography, and ultrasonography of the common carotid artery was used to calculate the distensibility coefficient (DC) and young’s modulus (YM). Lower DC and higher YM values indicate stiffer arteries. Pfat quartile was highly associated with demographic, behavioral, anthropometric, hemodynamic, metabolic, and disease variables in both men and women. After adjusting for height, clinical site, CVD risk factors, and medications, a 1-standard deviation (41.91 cm3) increment in Pfat was associated with a 0.00007±0.00002 1/mmHg lower DC (p=0.0002) in men and a 48.1±15.1 mmHg/mm higher YM in women (p=0.002). Additional adjustment for C-reactive protein, coronary artery calcification, and carotid intima-media thickness had only modest effects. More importantly, adjusting for body mass index and waist circumference did not significantly change the overall results.
Conclusion
Higher Pfat is associated with higher carotid stiffness, independent of traditional CVD risk factors and obesity.
doi:10.1016/j.numecd.2009.10.010
PMCID: PMC2929306  PMID: 20153618
pericardial fat; arterial stiffness; distensibility; carotid artery
24.  Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study 
BMJ Open  2014;4(4):e004743.
Objectives
Epidemiological studies have demonstrated associations between long-term exposure to traffic-related air pollution and coronary heart disease (CHD). Atherosclerosis is the principal pathological process responsible for CHD events, but effects of traffic-related air pollution on progression of atherosclerosis are not clear. This study aimed to investigate associations between long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis.
Setting
Healthy volunteers in metropolitan Vancouver, Canada.
Participants and outcome measures
509 participants aged 30–65 years were recruited and followed for approximately 5 years. At baseline and end of follow-up, participants underwent carotid artery ultrasound examinations to assess atherosclerosis severity, including carotid intima-media thickness, plaque area, plaque number and total area. Annual change of each atherosclerosis marker during the follow-up period was calculated as the difference between these two measurements divided by years of follow-up. Living close to major roads was defined as ≤150 m from a highway or ≤50 m from a major road. Residential exposures to traffic-related air pollutants including black carbon, fine particles, nitrogen dioxide and nitric oxide were estimated using high-resolution land-use regression models. The data were analysed using general linear models adjusting for various covariates.
Results
At baseline, there were no significant differences in any atherosclerosis markers between participants living close to and those living away from major roads. After follow-up, the differences in annual changes of these markers between these two groups were small and not statistically significant. Also, no significant associations were observed with concentrations of traffic-related air pollutants including black carbon, fine particles, nitrogen dioxide and nitric oxide.
Conclusions
This study did not find significant associations between traffic-related air pollution and progression of carotid artery atherosclerosis in a region with lower levels and smaller contrasts of ambient air pollution.
doi:10.1136/bmjopen-2013-004743
PMCID: PMC3987708  PMID: 24710134
Occupational & Industrial Medicine; Epidemiology; Public Health; Preventive Medicine
25.  Long-Term Exposure to Air Pollution and Type 2 Diabetes Mellitus in a Multiethnic Cohort 
American Journal of Epidemiology  2015;181(5):327-336.
Although air pollution has been suggested as a possible risk factor for type 2 diabetes mellitus (DM), results from existing epidemiologic studies have been inconsistent. We investigated the associations of prevalence and incidence of DM with long-term exposure to air pollution as estimated using annual average concentrations of particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) and nitrogen oxides at baseline (2000) in the Multi-Ethnic Study of Atherosclerosis. All participants were aged 45–84 years at baseline and were recruited from 6 US sites. There were 5,839 participants included in the study of prevalent DM and 5,135 participants without DM at baseline in whom we studied incident DM. After adjustment for potential confounders, we found significant associations of prevalent DM with PM2.5 (odds ratio (OR) = 1.09, 95% confidence interval (CI): 1.00, 1.17) and nitrogen oxides (OR = 1.18, 95% CI: 1.01, 1.38) per each interquartile-range increase (2.43 µg/m3 and 47.1 ppb, respectively). Larger but nonsignificant associations were observed after further adjustment for study site (for PM2.5, OR = 1.16, 95% CI: 0.94, 1.42; for nitrogen oxides, OR = 1.29, 95% CI: 0.94, 1.76). No air pollution measures were significantly associated with incident DM over the course of the 9-year follow-up period. Results were partly consistent with a link between long-term exposure to air pollution and the risk of type 2 DM. Additional studies with a longer follow-up time and a greater range of air pollution exposures, including high levels, are warranted to evaluate the hypothesized association.
doi:10.1093/aje/kwu280
PMCID: PMC4339386  PMID: 25693777
air pollution; diabetes; nitrogen oxides; particulate matter; prospective cohort study

Results 1-25 (1197226)