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Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study.

ABSTRACT: 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.Healthy volunteers in metropolitan Vancouver, Canada.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.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.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.

SUBMITTER: Gan WQ

PROVIDER: S-EPMC3987708 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study.

Gan Wen Qi WQ Allen Ryan W RW Brauer Michael M Davies Hugh W HW Mancini G B John GB Lear Scott A SA

BMJ open 20140407 4

<h4>Objectives</h4>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.< ...[more]

PMID: 24710134

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Project description:BackgroundFine particulate matter (PM2.5) has been linked to cardiovascular disease, possibly via accelerated atherosclerosis. We examined associations between the progression of the intima-medial thickness (IMT) of the common carotid artery, as an indicator of atherosclerosis, and long-term PM2.5 concentrations in participants from the Multi-Ethnic Study of Atherosclerosis (MESA).Methods and resultsMESA, a prospective cohort study, enrolled 6,814 participants at the baseline exam (2000-2002), with 5,660 (83%) of those participants completing two ultrasound examinations between 2000 and 2005 (mean follow-up: 2.5 years). PM2.5 was estimated over the year preceding baseline and between ultrasounds using a spatio-temporal model. Cross-sectional and longitudinal associations were examined using mixed models adjusted for confounders including age, sex, race/ethnicity, smoking, and socio-economic indicators. Among 5,362 participants (5% of participants had missing data) with a mean annual progression of 14 µm/y, 2.5 µg/m(3) higher levels of residential PM2.5 during the follow-up period were associated with 5.0 µm/y (95% CI 2.6 to 7.4 µm/y) greater IMT progressions among persons in the same metropolitan area. Although significant associations were not found with IMT progression without adjustment for metropolitan area (0.4 µm/y [95% CI -0.4 to 1.2 µm/y] per 2.5 µg/m(3)), all of the six areas showed positive associations. Greater reductions in PM2.5 over follow-up for a fixed baseline PM2.5 were also associated with slowed IMT progression (-2.8 µm/y [95% CI -1.6 to -3.9 µm/y] per 1 µg/m(3) reduction). Study limitations include the use of a surrogate measure of atherosclerosis, some loss to follow-up, and the lack of estimates for air pollution concentrations prior to 1999.ConclusionsThis early analysis from MESA suggests that higher long-term PM2.5 concentrations are associated with increased IMT progression and that greater reductions in PM2.5 are related to slower IMT progression. These findings, even over a relatively short follow-up period, add to the limited literature on air pollution and the progression of atherosclerotic processes in humans. If confirmed by future analyses of the full 10 years of follow-up in this cohort, these findings will help to explain associations between long-term PM2.5 concentrations and clinical cardiovascular events.

Project description:Physical disability is common though not inevitable in older age and has direct bearing on a person's ability to perform activities essential for self-care and independent living. Air pollution appears to increase the risk of several chronic diseases that contribute to the progression of disability.We evaluated long-term exposure to traffic-related air pollution (TRAP) in relation to progression in physical disability.We conducted our investigation within the Chicago Health and Aging Project. We measured participants' exposures to TRAP using two surrogates: residential proximity to major roads (1993 onwards) and ambient concentrations of oxides of nitrogen (NOX; 1999 onwards), predicted via a geographic information systems-based spatiotemporal smoothing model (cross-validation R2 = 0.87) that incorporated community-based monitoring and resolved intraurban exposure gradients at a spatial scale of tens of meters. Participants' lower-extremity physical ability was assessed every 3 years (1993-2012) via tandem stand, chair stand, and timed walking speed.In multivariable-adjusted analyses (n = 5,708), higher long-term NOX exposure was associated with significantly faster progression in disability. Compared with the 5-year decline in physical ability score among participants in the lowest quartile of NOX exposure, decline among those in the highest exposure quartile was 1.14 units greater (95% confidence interval [CI]: -1.86, -0.42), equivalent to 3 additional years of decline among those in the lowest exposure quartile. The association was linear across the continuum of NOX exposure: per 10-ppb increment in exposure, the 5-year decline in physical ability score was 0.87 unit greater (95% CI: -1.35, -0.39). Proximity to a major road was not associated with disability progression (n = 9,994).These data join a growing body of evidence suggesting that TRAP exposures may accelerate aging-related declines in health.Weuve J, Kaufman JD, Szpiro AA, Curl C, Puett RC, Beck T, Evans DA, Mendes de Leon CF. 2016. Exposure to traffic-related air pollution in relation to progression in physical disability among older adults. Environ Health Perspect 124:1000-1008;?http://dx.doi.org/10.1289/ehp.1510089.

Project description:Importance:Epidemiologic evidence of the mechanisms of the association between long-term exposure to air pollution and coronary heart disease (CHD) is limited and relies heavily on studies performed in Europe and the United States, where air pollution levels are relatively low. In particular, the association between air pollution and CHD in patients with underlying risks for CHD is understudied. Objective:To determine whether air pollution and proximity to traffic are associated with the coronary artery calcium (CAC) score, a key atherosclerotic marker. Design, Setting, and Participants:In this prospective, population-based cross-sectional study in a large-scale setting in China, 8867 consecutive patients aged 25 to 92 years with suspected CHD were recruited between November 17, 2015, and September 13, 2017. Participants were excluded if they had previous myocardial infarction, stenting, or coronary artery bypass grafting or incomplete risk factors and exposure data. Each participant underwent assessment of CAC and CHD risk factors at baseline. Data were analyzed from December 2017 to November 2018. Exposures:Annual means of fine particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) were estimated at the participants' residences using a validated geostatistical prediction model. Exposure to a nearby roadway was also estimated. Main Outcomes and Measures:Computed tomography measurement of CAC score. Results:The mean (SD) age of the 8867 participants was 56.9 (10.4) years; 4378 (53.6%) were men. Annual mean (SD) PM2.5, NO2, and O3 measurements were 70.1 (20.0), 41.4 (14.7), and 93.9 (10.5) μg/m3, respectively. The mean (SD) CAC score was 91.4 (322.2) Agatston units. Exposure to PM2.5 and NO2, adjusting for CHD risk factors and multiple pollutants, were independently associated with increases in CAC scores of 27.2% (95% CI, 10.8% to 46.1%) per 30 μg/m3 PM2.5 and 24.5% (95% CI, 3.6% to 49.7%) per 20 μg/m3 NO2. For PM2.5, odds of both detectable CAC (Agatston score >0; odds ratio, 1.28; 95% CI, 1.13 to 1.45) and severe CAC (Agatston score >400; odds ratio, 1.59; 95% CI, 1.20 to 2.12) were increased. Associations of CAC with PM2.5 and NO2 were greater among male participants (PM2.5: 42.2%; 95% CI, 24.3% to 62.7%; NO2: 45.7%; 95% CI, 25.3% to 69.5%) and elderly participants (PM2.5: 50.1%; 95% CI, 28.8% to 75.0%; NO2: 55.5%; 95% CI, 31.8% to 83.6%) and those with diabetes (PM2.5: 62.2%; 95% CI, 30.9% to 101.0%; NO2: 31.2%; 95% CI, 13.9% to 51.0%). Independent association with CAC score was 9.0% (95% CI, -1.4% to 20.4%) for O3 per 15 μg/m3 and 2.4% (95% CI, -0.6% to 5.4%) for distance near roadway per 50% decrease. Conclusions and Relevance:In this large Chinese study, long-term exposures to PM2.5 and NO2 were independently associated with severity of CAC. This finding may provide support for the pathophysiological role of coronary atherosclerosis through which air pollution exposure may be associated with CHD.

Project description:BACKGROUND: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people's noise exposure indoors in bedrooms. OBJECTIVES: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). METHODS: We evaluated 1,926 cohort participants at baseline (years 2003-2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. RESULTS: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 ?g/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (? = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (? = 1.23; 95% CI: 0.21, 2.25), and DBP (??= 0.56; 95% CI: -0.03, 1.14) per 10 ?g/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise-SBP association was stronger and statistically significant with a threshold at 30 dB(A). CONCLUSION: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity.

Project description:BackgroundLong-term ozone ([Formula: see text]) exposure is associated with cardiovascular mortality, but little is known about the associations between [Formula: see text] and subclinical arterial disease.ObjectivesWe studied the longitudinal association of exposure to [Formula: see text] and progression of key subclinical arterial markers in adults: intima-media thickness of common carotid artery ([Formula: see text]), carotid plaque (CP) burden, and coronary artery calcification (CAC).MethodsCAC was measured one to four times at baseline and at follow-up exams (1999–2012) by computed tomography (CT) in 6,619 healthy adults, recruited at age 45-84 y without cardiovascular disease (CVD), over a mean of 6.5 y (standard deviation: 3.5 y). [Formula: see text] and CP burden were quantified in 3,392 participants using carotid artery ultrasound imaging acquired over a mean of 9 y (1.7 y). Over 91% and 89% participants had at least one follow-up [Formula: see text] and CAC measurement, respectively. Residence-specific [Formula: see text] concentrations were estimated by a validated spatiotemporal model spanning from 1999 to 2012. This model relied on comprehensive monitoring data and geographical variables to predict individualized long-term average concentrations since baseline. Linear mixed models and logistic regression model were used to evaluate relationships of long-term average exposure to [Formula: see text] with longitudinal change in [Formula: see text], CAC, and CP formation, respectively.ResultsMean progression rates of [Formula: see text] and CAC were [Formula: see text] and [Formula: see text]. CP formation was identified in 55% of the subjects. A [Formula: see text] increase in long-term average [Formula: see text] exposure was associated with a [Formula: see text] [95% confidence interval (CI): 1.4, 9.7] greater increase in [Formula: see text] over 10 y. A [Formula: see text] increase in [Formula: see text] was also associated with new CP formation [odds ratio (OR): 1.2 (95% CI: 1.1, 1.4)] but not CAC progression [[Formula: see text] (95% CI: [Formula: see text], 2)]. Associations were robust in the analysis with extended covariate adjustment, including copollutants, i.e., nitrogen oxides ([Formula: see text]) and particulate matter with diameter [Formula: see text] ([Formula: see text]).ConclusionOver almost a decade of follow-up, outdoor [Formula: see text] concentrations were associated with increased rate of carotid wall thickness progression and risk of new plaque formation, suggesting arterial injury in this cohort. https://doi.org/10.1289/EHP3325.

Project description:IntroductionStudies on the association between atherosclerosis and long-term exposure to ambient air pollution suggest that carotid intima-media thickness (CIMT), a marker of subclinical atherosclerosis, is positively associated with particulate matter (PM) exposure. However, there is heterogeneity between the different studies concerning the magnitude of this association. We performed a meta-analysis to determine the strength of the association between CIMT and particulate air pollution.MethodsWe queried PubMed citation database and Web of Knowledge up to March 2015 in order to identify studies on CIMT and particulate air pollution. Two investigators selected and computerized all relevant information, independently. Eight of the reviewed epidemiological publications provided sufficient details and met our inclusion criteria. Descriptive and quantitative information was extracted from each selected study. The meta-analysis included 18,349 participants from eight cohorts for the cross-sectional association between CIMT and PM and 7,268 participants from three cohorts for the longitudinal analysis on CIMT progression and PM exposure.ResultsThe average exposure to PM2.5 in the different study populations ranged from 4.1 to 20.8 µg/m3 and CIMT averaged (SD) 0.73 (0.14) mm. We computed a pooled estimate from a random-effects model. In the combined cross-sectional studies, an increase of 5 µg/m3 PM2.5 was associated with a 1.66% (95% CI: 0.86 to 2.46; P<0.0001) thicker CIMT, which corresponds to an average increase of 12.1 µm. None of the studies moved the combined estimate outside the confidence interval of the overall estimate. A funnel plot suggested absence of publication bias. The combined longitudinal estimate showed for each 5 µg/m3 higher PM2.5 exposure, a 1.04 µm per year (95% CI: 0.01 to 2.07; P=0.048) greater CIMT progression.ConclusionOur meta-analysis supports the evidence of a positive association between CIMT, a marker of subclinical atherosclerosis, and long-term exposure to particulate air pollution.

Dataset Information

Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study.

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Long-term exposure to traffic-related air pollution and progression of carotid artery atherosclerosis: a prospective cohort study.

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