Prenatal Air Pollution Exposure and Early Cardiovascular Phenotypes in Young Adults.
ABSTRACT: Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007-2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency's Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM10 and PM2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM2.5 was associated with CAS indices, including a 5% increase (? = 1.05, 95% CI 1.00-1.10) in carotid stiffness index beta, a 5% increase (? = 1.05, 95% CI 1.01-1.10) in Young's elastic modulus and a 5% decrease (? = 0.95, 95% CI 0.91-0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.
Project description:INTRODUCTION:Effects of more than one-year exposure to air pollution on atherosclerosis is seldom studied. This paper aims to examine the association between five-year exposure to particulate matter ?2.5??m (PM2.5), ozone (O3) and atherosclerosis observed about seven years later in late midlife women. MATERIAL AND METHODS:This study was conducted among 1188 women of the Study of Women's Health Across the Nation (SWAN) from five sites, Detroit, MI; Oakland, CA; Pittsburgh, PA; Chicago, IL; and Newark, NJ, with available data on both air pollutant exposure and carotid ultrasound scans. Five-year mean annualized exposure levels of two air pollutants, PM2.5 and ozone (O3), were collected during 5 SWAN visits (1999-2005) from monitors 20?km within the participant's residential address. Linear regression models were used to estimate the association of prior five-year mean annualized exposure to PM2.5 and O3 with common carotid intima-media thickness (cIMT) and inter-adventitial diameter (IAD) examined approximately seven years later (2009-2013). Logistic and multinomial logistic regressions were applied to assess the associations of air pollutants with plaque presence and plaque index, respectively. RESULTS:At time of carotid ultrasound scan, women were on average 59.6 (±2.7) years old and a majority was postmenopausal (88.4%). The women were White (48.4%), Black (31.2%), Chinese (13.3%) and Hispanic (7.1%). A 1??g/m3 higher 5-year mean annualized exposure to PM2.5 was associated with an 8.0??m (95% CI: 1.0-15.1) greater maximum cIMT at a later mid-life, adjusting for cardiovascular disease risk factors; but was only related to IAD after adjusting for site. No association was found between either pollutant and plaque presence or plaque index. CONCLUSIONS:Long-term exposure to PM2.5 may contribute to elevated risk of atherosclerosis in the post-menopausal period.
Project description:Although exposure to ambient air pollutants increases cardiovascular disease risk in adults little is known about the effects of prenatal exposure. Genetic variation and epigenetic alterations are two mechanisms that may influence the effects of early-life exposures on cardiovascular phenotypes.We investigated whether genetic and epigenetic variation modify associations between prenatal air pollution on markers of cardiovascular risk in childhood.We used linear regression analysis to investigate the associations between prenatal pollutants (PM2.5, PM10, NO2, O3), long interspersed nuclear elements (LINE1) and AluYb8 DNA methylation levels measured in newborn blood spot tests, and carotid intima-media thickness (CIMT) and blood pressure (BP) in 459 participants as part of the Children's Health Study. Interaction terms were also included to test for effect modification of these associations by genetic variation in methylation reprogramming genes.Prenatal exposure to NO2 in the third trimester of pregnancy was associated with higher systolic BP in 11-year-old children. Prenatal exposure to multiple air pollutants in the first trimester was associated with lower DNA methylation in LINE1, whereas later exposure to O3 was associated with higher LINE1 methylation levels in newborn blood spots. The magnitude of associations with prenatal air pollution varied according to genotype for 11 SNPs within DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3 Beta (DNMT3B), Tet methylcytosine dioxygenase 2 (TET2), and Thymine DNA glycosylase (TDG) genes. Although first-trimester O3 exposure was not associated with CIMT and systolic BP overall, associations within strata of DNMT1 or DNMT3B were observed, and the magnitude and the direction of these associations depended on DNMT1 genotypes.Genetic and epigenetic variation in DNA methylation reprogramming genes and in LINE1 retrotransposons may play important roles in downstream cardiovascular consequences of prenatal air pollution exposure. Citation: Breton CV, Yao J, Millstein J, Gao L, Siegmund KD, Mack W, Whitfield-Maxwell L, Lurmann F, Hodis H, Avol E, Gilliland FD. 2016. Prenatal air pollution exposures, DNA methyl transferase genotypes, and associations with newborn LINE1 and Alu methylation and childhood blood pressure and carotid intima-media thickness in the Children's Health Study. Environ Health Perspect 124:1905-1912;?http://dx.doi.org/10.1289/EHP181.
Project description:Exposure to ambient air pollutants increases risk for cardiovascular health outcomes in adults. The contribution of childhood air pollutant exposure to cardiovascular health has not been thoroughly evaluated.The Testing Responses on Youth study consists of 861 college students recruited from the University of Southern California in 2007 to 2009. Participants attended 1 study visit during which blood pressure, heart rate, and carotid artery intima-media thickness (CIMT) were assessed. Self-administered questionnaires collected information about health and sociodemographic characteristics, and a 12-hour fasting blood sample was drawn for lipid and biomarker analyses. Residential addresses were geocoded and used to assign cumulative air pollutant exposure estimates based on data derived from the U.S. Environmental Protection Agency's Air Quality System database. The associations between CIMT and air pollutants were assessed using linear regression analysis. Mean CIMT was 603 ?m (±54 SD). A 2 standard deviation (SD) increase in childhood (aged 0-5 years) or elementary school (aged 6-12 years) O(3) exposure was associated with a 7.8-?m (95% confidence interval, -0.3-15.9) or 10.1-?m (95% confidence interval, 1.8-18.5) higher CIMT, respectively. Lifetime exposure to O(3) showed similar but nonsignificant associations. No associations were observed for PM(2.5), PM(10), or NO(2), although adjustment for these pollutants strengthened the childhood O(3) associations.Childhood exposure to O(3) may be a novel risk factor for CIMT in a healthy population of college students. Regulation of air pollutants and efforts that focus on limiting childhood exposures continue to be important public health goals.
Project description:In four European cohorts, we investigated the cross-sectional association between long-term exposure to air pollution and intima-media thickness of the common carotid artery (CIMT), a preclinical marker of atherosclerosis.Individually assigned levels of nitrogen dioxide, nitrogen oxides, particulate matter ? 2.5 ?m (PM2.5), absorbance of PM2.5 (PM2.5abs), PM10, PMcoarse, and two indicators of residential proximity to highly trafficked roads were obtained under a standard exposure protocol (European Study of Cohorts for Air Pollution Effects-ESCAPE study) in the Stockholm area (Sweden), the Ausburg and Ruhr area (Germany), and the Girona area (Spain). We used linear regression and meta-analyses to examine the association between long-term exposure to air pollution and CIMT.The meta-analysis with 9,183 individuals resulted in an estimated increase in CIMT (geometric mean) of 0.72% (95% CI: -0.65%, 2.10%) per 5-?g/m3 increase in PM2.5 and 0.42% (95% CI: -0.46%, 1.30%) per 10-5/m increase in PM2.5abs. Living in proximity to high traffic was also positively but not significantly associated with CIMT. Meta-analytic estimates for other pollutants were inconsistent. Results were similar across different adjustment sets and sensitivity analyses. In an extended meta-analysis for PM2.5 with three other previously published studies, a 0.78% (95% CI: -0.18%, 1.75%) increase in CIMT was estimated for a 5-?g/m3 contrast in PM2.5.Using a standardized exposure and analytical protocol in four European cohorts, we found that cross-sectional associations between CIMT and the eight ESCAPE markers of long-term residential air pollution exposure did not reach statistical significance. The additional meta-analysis of CIMT and PM2.5 across all published studies also was positive but not significant.
Project description:Objective: This article aims to examine the association between long-term ambient air pollution and progression of subclinical atherosclerosis with 2-year follow-up among midlife women from the Study of Women's Health Across the Nation (SWAN). Materials and Methods: Carotid duplex ultrasonography was performed in participants from a SWAN ancillary study carried out at the Pittsburgh and Chicago sites. Mean and maximum carotid intima-media thickness (CIMT) and plaque burden were assessed throughout the common, bulb, and internal carotid artery. The yearly mean exposure to PM2.5 (particulate matter) and ozone was generated based on monitors within 20?km of the participants' home. The effect of air pollutants during follow-up on progression of CIMT was estimated using linear mixed-effects models, and the effect on progression of plaque presence and plaque index, a measure of extent of plaque, was evaluated using logistic regression. Results: This study included 417 (257 White and 160 Black) women with a mean age of 51 years at baseline. A 1??g/m3 higher yearly mean exposure to PM2.5 during follow-up was associated with a 4.28 (95% confidence interval [CI]: 0.02-8.54) ?m/year increase in maximum CIMT, after adjusting for socioeconomic and traditional cardiovascular disease (CVD) risk factors. Exposure to PM2.5 contributed to a 30% (95% CI: 3%-65%) higher odds of plaque index progression adjusting for socioeconomic factors only. Conclusions: PM2.5 independently contributed to progression of subclinical atherosclerosis, among women transitioning through menopause, a time of increasing CVD risk. Yet no significant associations between ozone and subclinical atherosclerosis were observed.
Project description:Associations between long-term exposure to air pollution and carotid intima-media thickness (CIMT) have inconsistent findings.In this study we aimed to evaluate association between 1-year average exposure to traffic-related air pollution and CIMT in middle-aged adults in Asia.CIMT was measured in Taipei, Taiwan, between 2009 and 2011 in 689 volunteers 35-65 years of age who were recruited as the control subjects of an acute coronary heart disease cohort study. We applied land-use regression models developed by the European Study of Cohorts for Air Pollution Effects (ESCAPE) to estimate each subject's 1-year average exposure to traffic-related air pollutants with particulate matter diameters ? 10 ?m (PM10) and ? 2.5 ?m (PM2.5) and the absorbance levels of PM2.5 (PM2.5abs), nitrogen dioxide (NO2), and nitrogen oxides (NOx) in the urban environment.One-year average air pollution exposures were 44.21 ± 4.19 ?g/m3 for PM10, 27.34 ± 5.12 ?g/m3 for PM2.5, and (1.97 ± 0.36) × 10-5/m for PM2.5abs. Multivariate regression analyses showed average percentage increases in maximum left CIMT of 4.23% (95% CI: 0.32, 8.13) per 1.0 × 10-5/m increase in PM2.5abs; 3.72% (95% CI: 0.32, 7.11) per 10-?g/m3 increase in PM10; 2.81% (95% CI: 0.32, 5.31) per 20-?g/m3 increase in NO2; and 0.74% (95% CI: 0.08, 1.41) per 10-?g/m3 increase in NOx. The associations were not evident for right CIMT, and PM2.5 mass concentration was not associated with the outcomes.Long-term exposures to traffic-related air pollution of PM2.5abs, PM10, NO2, and NOx were positively associated with subclinical atherosclerosis in middle-aged adults.
Project description:Previous epidemiologic studies have considered the effects of individual air pollutants on birth outcomes, whereas a multiple-pollutant approach is more relevant to public health policy.The present study compared the observed effect sizes of prenatal fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAH) (a component of PM2.5) exposures on birth outcome deficits, assessed by the single vs. two-pollutant approaches.The study sample included 455 term infants born in Krakow to non-smoking mothers, among whom personal exposures to PM2.5 and PAH were monitored in the second trimester of pregnancy. The exposure effect estimates (unstandardized and standardized regression coefficients) on birth outcomes were determined using multivariable linear regression models, accounting for relevant covariates.In the single-pollutant approach, each pollutant was inversely associated with all birth outcomes. The effect size of prenatal PAH exposure on birth weight and length was twice that of PM2.5, in terms of standardized coefficients. In the two-pollutant approach, the negative effect of PM2.5 on birth weight and length, adjusted for PAH exposure, lost its significance. The standardized effect of PAH on birth weight was 10-fold stronger (? = -0.20, p?=?0.004) than that estimated for PM2.5 (? = -0.02, p?=?0.757).The results provide evidence that PAH had a greater impact on several measures of fetal development, especially birth weight, than PM2.5. Though in the single-pollutant models PM2.5 had a significant impact on birth outcomes, this effect appears to be mediated by PAH.
Project description:BACKGROUND:Studies of air pollution exposure and arterial stiffness have reported inconsistent results and large studies employing the reference standard of arterial stiffness, carotid-femoral pulse-wave velocity (CFPWV), have not been conducted. AIM:To study long-term exposure to ambient fine particles (PM2.5), proximity to roadway, and short-term air pollution exposures in relation to multiple measures of arterial stiffness in the Framingham Heart Study. METHODS:We assessed central arterial stiffness using CFPWV, forward pressure wave amplitude, mean arterial pressure and augmentation index. We investigated long-and short-term air pollution exposure associations with arterial stiffness with linear regressions using long-term residential PM2.5 (2003 average from a spatiotemporal model using satellite data) and proximity to roadway in addition to short-term averages of PM2.5, black carbon, particle number, sulfate, nitrogen oxides, and ozone from stationary monitors. RESULTS:We examined 5842 participants (mean age 51?±?16, 54% women). Living closer to a major roadway was associated with higher arterial stiffness (0.11?m/s higher CFPWV [95% CI: 0.01, 0.22] living <50?m vs 400???1000?m). We did not observe association between arterial stiffness measures and long-term PM2.5 or short-term levels of PM2.5, particle number, sulfate or ozone. Higher levels of black carbon and nitrogen oxides in the previous days were unexpectedly associated with lower arterial stiffness. CONCLUSIONS:Long-term exposure to PM2.5 was not associated with arterial stiffness but positive associations with living close to a major road may suggest that pollutant mixtures very nearby major roads, rather than PM2.5, may affect arterial stiffness. Furthermore, short-term air pollution exposures were not associated with higher arterial stiffness.
Project description:BACKGROUND:Short-term exposure to ambient air pollution triggers acute cardiovascular events. Here, we evaluate the association of exposure to ambient air pollution with two intermediate cardiovascular endpoints: blood pressure and carotid stiffness. METHODS:In a one-year panel study, we included 20 healthy volunteers (10 male-female couples aged 59-75?years) with air pollution and health parameters measured every two months at their region of residence (Leuven, Belgium) and twice during two ten-day periods in two locations, one with higher (Milan, Italy) and one with lower (Vindeln, Sweden) air pollution levels (220 observations). We measured blood pressure, carotid arterial stiffness, personal exposure to NO2, and ambient concentrations of PM10, PM2.5, and NO2. We used linear mixed models to evaluate the associations between the health outcomes and the air pollutants. RESULTS:Compared with Leuven, exposure to pollutants was higher in Milan and lower in Vindeln, with the highest contrast for NO2 (median 20.7??g/m3 (IQR:7.4) vs 65.1??g/m3 (9.0) and 4.5?mg/m3 (0.8), respectively). We did not observe significant associations between either systolic or diastolic blood pressure and variations in air pollution. However, we found significant associations between arterial stiffness and 5?day average exposure to the studied pollutants. The strongest associations were observed for PM10 with carotid distensibility (DC) and compliance (CC) coefficients, and the young elastic modulus (YEM): 4.3% (95%CI:7.0;1.5) increase in DC, 4.7% (95%CI:7.1;2.3) increase in CC and 4.2% (95%CI:1.1;7.3) decrease in YEM for each 10??g/m3 decreases in PM10. CONCLUSIONS:Our study suggests that short-term exposure to air pollution results in reductions in carotid elasticity among elderly population.
Project description:Previous studies have explored the association between air pollution levels and adverse birth outcomes such as lower birth weight. Existing literature suggests an association, although results across studies are not consistent. Additional research is needed to confirm the effect, investigate the exposure window of importance, and distinguish which pollutants cause harm. We assessed the association between ambient pollutant concentrations and term birth weight for 1,548,904 births in TX from 1998 to 2004. Assignment of prenatal exposure to air pollutants was based on maternal county of residence at the time of delivery. Pollutants examined included particulate matter with aerodynamic diameter < or = 10 and < or = 2.5 microm (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). We applied a linear model with birth weight as a continuous variable. The model was adjusted for known risk factors and region. We assessed pollutant effects by trimester to identify biological exposure window of concern, and explored interaction due to race/ethnicity. An interquartile increase in ambient pollutant concentrations of SO2 and O3 was associated with a 4.99-g (95% confidence interval [CI], 1.87-8.11) and 2. 72-g (95% CI, 1.11-4.33) decrease in birth weight, respectively. Lower birth weight was associated with exposure to O3 in the first and second trimester; whereas results were not significant for other pollutants by trimester A positive association was exhibited for PM2.5 in the first trimester. Effects estimates for PM10 and PM2.5 were inconsistent across race/ethnic groups. Current ambient air pollution levels may be increasing the risk of lower birth weight for some pollutants. These risks may be increased for certain racial/ethnic groups. Additional research including consideration of improved methodology is needed to investigate these findings. Future studies should examine the influence of residual confounding.