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Residential traffic exposure, pulse pressure, and C-reactive protein: consistency and contrast among exposure characterization methods.

ABSTRACT: BACKGROUND:Traffic exposure may increase cardiovascular disease (CVD) risk via systemic inflammation and elevated blood pressure, two important clinical markers for managing disease progression. OBJECTIVES:We assessed degree and consistency of association between traffic exposure indicators as predictors of C-reactive protein (CRP) and pulse pressure (PP) in an adult U.S. Puerto Rican population (n = 1,017). METHODS:Cross-sectional information on health and demographics and blood data was collected. Using multiple linear regression, we tested for associations between CRP, PP, and six traffic exposure indicators including residential proximity to roads with > 20,000 vehicles/day and traffic density [vehicle miles traveled per square mile (VMT/mi2)]. Diabetes and obesity [body mass index (BMI) >or= 30 kg/m2] were tested as effect modifiers. RESULTS:CRP was positively associated with traffic density in the total population [36% CRP difference with 95% confidence interval (CI) 2.5-81%] for residence within the highest versus lowest VMT/mi2 level. With BMI >or= 30, CRP showed significant positive associations with five of six traffic indices including residence 200 m of a roadway [22.7% CRP difference (95% CI, 3.15-46.1)] and traffic density in the third highest versus lowest VMT/mi2 level [28.1% difference (95% CI, 1.0-62.6)]. PP was positively associated with residence within or= 30 [3.8 mmHg (95% CI, 0.88-6.8)]. Effect estimates approximately doubled for residence within or= 30, may be more susceptible to the effects of traffic exposure.

SUBMITTER: Rioux CL

PROVIDER: S-EPMC2898857 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature

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Residential traffic exposure, pulse pressure, and C-reactive protein: consistency and contrast among exposure characterization methods.

Rioux Christine L CL Tucker Katherine L KL Mwamburi Mkaya M Gute David M DM Cohen Steven A SA Brugge Doug D

Environmental health perspectives 20100202 6

<h4>Background</h4>Traffic exposure may increase cardiovascular disease (CVD) risk via systemic inflammation and elevated blood pressure, two important clinical markers for managing disease progression.<h4>Objectives</h4>We assessed degree and consistency of association between traffic exposure indicators as predictors of C-reactive protein (CRP) and pulse pressure (PP) in an adult U.S. Puerto Rican population (n = 1,017).<h4>Methods</h4>Cross-sectional information on health and demographics and ...[more]

PMID: 20123638

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Project description:BackgroundMost epidemiologic studies use traffic at residential address as a surrogate for total traffic exposure when investigating effects of traffic on respiratory health. This study used GIS (Geographical Information Systems) to estimate traffic exposure, not only on residential, but also on workplace address, in addition to survey questions on time spent in traffic during commuting or other daily activities.The aim was to investigate 1) if there is an association between traffic exposure and prevalence of adult asthma and asthma symptoms, and 2) if so, does this association become stronger using more complete traffic exposure information.MethodsThis study was conducted in two stages: A first cross-sectional survey in Southern Sweden 2004 (n = 24819, 18-80 years, response rate 59%) was followed by a case-control study in 2005 to obtain more detailed exposure and confounder information (n = 2856, asthmatics and controls (1:3), 86% response rate). In the first survey, only residential address was known. In the second survey, questions about workplace addresses and daily time spent in traffic were also included. Residential and workplace addresses were geocoded and linked with GIS to road data and dispersion modelled outdoor concentrations of NOx (annual mean, 250 × 250 m resolution).ResultsLiving within 50 m of a road (measured by GIS) with traffic intensity of >10 cars/minute (compared with no road within this distance) was associated with an increased prevalence of asthma, (OR = 1.8, 95% CI = (1.1-2.8), and with asthma symptoms last 12 months. No statistically significant effects were seen for traffic exposure at workplace address, daily time spent in traffic, or commuting time to work, after adjustment for confounders. A combined total exposure estimate did not give a stronger association with asthma prevalence or asthma symptoms.ConclusionsTraffic exposure at close proximity to residential address showed association with asthma prevalence and asthma symptoms last 12 months, among adults in southern Sweden. The associations were not stronger when accounting for total traffic exposure. This could reflect exposure misclassfication at workplace address and for other daily time in traffic, but also that residential address remains the main determinant for traffic exposure among adults.

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

Project description:Previous studies reported adverse impacts of traffic-related air pollution exposure on pregnancy outcomes. Yet, little information exists on how effect estimates are impacted by the different exposure assessment methods employed in these studies.To compare effect estimates for traffic-related air pollution exposure and preeclampsia, preterm birth (gestational age less than 37 weeks), and very preterm birth (gestational age less than 30 weeks) based on four commonly used exposure assessment methods.We identified 81,186 singleton births during 1997-2006 at four hospitals in Los Angeles and Orange Counties, California. Exposures were assigned to individual subjects based on residential address at delivery using the nearest ambient monitoring station data [carbon monoxide (CO), nitrogen dioxide (NO(2)), nitric oxide (NO), nitrogen oxides (NO(x)), ozone (O(3)), and particulate matter less than 2.5 (PM(2.5)) or less than 10 (PM(10))?m in aerodynamic diameter], both unadjusted and temporally adjusted land-use regression (LUR) model estimates (NO, NO(2), and NO(x)), CALINE4 line-source air dispersion model estimates (NO(x) and PM(2.5)), and a simple traffic-density measure. We employed unconditional logistic regression to analyze preeclampsia in our birth cohort, while for gestational age-matched risk sets with preterm and very preterm birth we employed conditional logistic regression.We observed elevated risks for preeclampsia, preterm birth, and very preterm birth from maternal exposures to traffic air pollutants measured at ambient stations (CO, NO, NO(2), and NO(x)) and modeled through CALINE4 (NO(x) and PM(2.5)) and LUR (NO(2) and NO(x)). Increased risk of preterm birth and very preterm birth were also positively associated with PM(10) and PM(2.5) air pollution measured at ambient stations. For LUR-modeled NO(2) and NO(x) exposures, elevated risks for all the outcomes were observed in Los Angeles only--the region for which the LUR models were initially developed. Unadjusted LUR models often produced odds ratios somewhat larger in size than temporally adjusted models. The size of effect estimates was smaller for exposures based on simpler traffic density measures than the other exposure assessment methods.We generally confirmed that traffic-related air pollution was associated with adverse reproductive outcomes regardless of the exposure assessment method employed, yet the size of the estimated effect depended on how both temporal and spatial variations were incorporated into exposure assessment. The LUR model was not transferable even between two contiguous areas within the same large metropolitan area in Southern California.

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Residential traffic exposure, pulse pressure, and C-reactive protein: consistency and contrast among exposure characterization methods.

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Residential traffic exposure, pulse pressure, and C-reactive protein: consistency and contrast among exposure characterization methods.

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