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Childhood air pollutant exposure and carotid artery intima-media thickness in young adults.
ABSTRACT: 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: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:The objective of this research was to determine if prenatal exposure to two common urban air pollutants, diesel and perchloroethylene, affects children's 3rd grade standardized test scores in mathematics and English language arts (ELA). Exposure estimates consisted of annual average ambient concentrations of diesel particulate matter and perchloroethylene obtained from the Environmental Protection Agency's 1996 National Air Toxics Assessment for the residential census tract at birth. Outcome data consisted of linked birth and educational records for 201,559 singleton, non-anomalous children born between 1994 and 1998 who attended New York City public schools. Quantile regression models were used to estimate the effects of these exposures on multiple points within the continuous distribution of standardized test scores. Modified Poisson regression models were used to calculate risk ratios (RR) and 95% confidence intervals (CI) of failing to meet curricula standards, an indicator derived from test scores. Models were adjusted for a number of maternal, neighborhood and childhood factors. Results showed that math scores were approximately 6% of a standard deviation lower for children exposed to the highest levels of both pollutants as compared to children with low levels of both pollutants. Children exposed to high levels of both pollutants also had the largest risk of failing to meet math test standards when compared to children with low levels of exposure to the pollutants (RR 1.10 95%CI 1.07,1.12 RR high perchloroethylene only 1.03 95%CI 1.00,1.06; RR high diesel PM only 1.02 95%CI 0.99,1.06). There was no association observed between exposure to the pollutants and failing to meet ELA standards. This study provides preliminary evidence of associations between prenatal exposure to urban air pollutants and lower academic outcomes. Additionally, these findings suggest that individual pollutants may additively impact health and point to the need to study the collective effects of air pollutant mixtures.air toxics, academic outcomes, urban health, tetrachloroethylene, air pollutant mixtures.
Project description:BACKGROUND:Air pollution has been related to brain structural alterations, but a relationship with white matter microstructure is unclear. OBJECTIVES:We assessed whether pregnancy and childhood exposures to air pollution are related to white matter microstructure in preadolescents. METHODS:We used data of 2,954 children from the Generation R Study, a population-based birth cohort from Rotterdam, Netherlands (2002-2006). Concentrations of 17 air pollutants including nitrogen oxides (NOX), particulate matter (PM), and components of PM were estimated at participants' homes during pregnancy and childhood using land-use regression models. Diffusion tensor images were obtained at child's 9-12 years of age, and fractional anisotropy (FA) and mean diffusivity (MD) were computed. We performed linear regressions adjusting for socioeconomic and lifestyle characteristics. Single-pollutant analyses were followed by multipollutant analyses using the Deletion/Substitution/Addition (DSA) algorithm. RESULTS:In the single-pollutant analyses, higher concentrations of several air pollutants during pregnancy or childhood were associated with significantly lower FA or higher MD (p<0.05). In multipollutant models of pregnancy exposures selected by DSA, higher concentration of fine particles was associated with significantly lower FA [-0.71 (95% CI: -1.26, -0.16) per 5??g/m3 fine particles] and higher concentration of elemental silicon with significantly higher MD [0.06 (95% CI: 0.01, 0.11) per 100?ng/m3 silicon]. Multipollutant models of childhood exposures selected by DSA indicated significant associations of NOX with FA [-0.14 (95% CI: -0.23, -0.04) per 20-?g/m3 NOX increase], and of elemental zinc and the oxidative potential of PM with MD [0.03 (95% CI: 0.01, 0.04) per 10-ng/m3 zinc increase and 0.07 (95% CI: 0.00, 0.44) per 1-nmol?DTT/min/m3 oxidative potential increase]. Mutually adjusted models of significant exposures during pregnancy and childhood indicated significant associations of silicon during pregnancy, and zinc during childhood, with MD. DISCUSSION:Exposure in pregnancy and childhood to air pollutants from tailpipe and non-tailpipe emissions were associated with lower FA and higher MD in white matter of preadolescents. https://doi.org/10.1289/EHP4709.
Project description:BACKGROUND:The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common sources and individuals are exposed to more than one pollutant at a time. OBJECTIVE:We performed a cross-disciplinary review of the effects of multipollutant exposures on cardiovascular effects. METHODS:A broad literature search for references including at least two criteria air pollutants (particulate matter [PM], ozone [O3], oxides of nitrogen, sulfur oxides, carbon monoxide) was conducted. References were culled based on scientific discipline then searched for terms related to cardiovascular disease. Most multipollutant epidemiologic and experimental (i.e., controlled human exposure, animal toxicology) studies examined PM and O3 together. DISCUSSION:Epidemiologic and experimental studies provide some evidence for O3 concentration modifying the effect of PM, although PM did not modify O3 risk estimates. Experimental studies of combined exposure to PM and O3 provided evidence for additivity, synergism, and/or antagonism depending on the specific health endpoint. Evidence for other pollutant pairs was more limited. CONCLUSIONS:Overall, the evidence for multipollutant effects was often heterogeneous, and the limited number of studies inhibited making a conclusion about the nature of the relationship between pollutant combinations and cardiovascular disease.
Project description:Ambient air pollution is associated with adverse health outcomes including cardio-respiratory diseases. Epigenetic mechanisms such as DNA methylation may play a role in driving such associations. We investigated the effects of prenatal particulate matter (PM) exposure on DNA methylation of 178,309 promoter regions in 240 newborns using the Infinium HumanMethylation450 BeadChip, using a generalized linear regression model with a quasi-binomial link family, adjusted for gender, plate, and cell types. PM-associated CpG loci were then investigated for their associations with childhood asthma, carotid intima-media thickness (CIMT), and blood pressure (BP) using logistic or linear regression. Thirty-one loci were associated with either PM10 or PM2.5 using FDR-corrected p-values of less than 0.15. Two loci were evaluated for replication in a separate population of 280 Children's Health Study (CHS) subjects using Pyrosequencing, of which one successfully replicated (COLEC11 cg03579365). Three of the 31 loci were also associated with physician-diagnosed asthma at 6 years old, two were associated with CIMT and one with systolic BP at 10 years old. A higher methylation level in TM9SF2 (cg02015529) and UBE2S (cg00035623), respectively, was associated with a 2SD increase in prenatal PM and was also associated with 36% and 98% increased odds of asthma; whereas methylation of TDRD6 (cg22329831) was negatively associated with PM and a 24% decreased odds of asthma. Prenatal PM exposure was associated with altered DNA methylation in newborn blood in a small number of gene promoters, some of which were also associated with cardio-respiratory health outcomes later in childhood. Keywords: methylation, particulate matter, air pollution, asthma, cardiovascular.
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:Gene expression changes are linked to air pollutant exposures in in vitro and animal experiments. However, limited data are available on how these outcomes relate to ambient air pollutant exposures in humans. We performed an exploratory analysis testing whether gene expression levels were associated with air pollution exposures in a Los Angeles area cohort of elderly subjects with coronary artery disease. Candidate genes (35) were selected from published studies of gene expression-pollutant associations. Expression levels were measured weekly in 43 subjects (? 12 weeks) using quantitative PCR. Exposures included gaseous pollutants O3, nitrogen oxides (NOx), and CO; particulate matter (PM) pollutants elemental and black carbon (EC, BC); and size-fractionated PM mass. We measured organic compounds from PM filter extracts, including polycyclic aromatic hydrocarbons (PAHs), and determined the in vitro oxidative potential of particle extracts. Associations between exposures and gene expression levels were analyzed using mixed-effects regression models. We found positive associations of traffic-related pollutants (EC, BC, primary organic carbon, PM 0.25-2.5 PAH and/or PM 0.25 PAH, and NOx) with NFE2L2, Nrf2-mediated genes (HMOX1, NQO1, and SOD2), CYP1B1, IL1B, and SELP. Findings suggest that NFE2L2 gene expression links associations of traffic-related air pollution with phase I and II enzyme genes at the promoter transcription level.
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:BACKGROUND:Health effects of air pollution on anaemia have been scarcely studied worldwide. We aimed to explore the associations of long-term exposure to ambient air pollutants with anaemia prevalence and haemoglobin levels in Chinese older adults. METHODS:We used two-level linear regression models and modified Poisson regression with robust error variance to examine the associations of particulate matter (PM) and nitrogen dioxide (NO2) on haemoglobin concentrations and the prevalence of anaemia, respectively, among 10,611 older Chinese adults enrolled in World Health Organization (WHO) Study on global AGEing and adult health (SAGE) China. The average community exposure to ambient air pollutants (PM with an aerodynamic diameter of 10 ?m or less (PM10), 2.5 ?m or less (PM2.5), 1 ?m or less (PM1) and nitrogen dioxide (NO2)) for each participant was estimated using a satellite-based spatial statistical model. Haemoglobin levels were measured for participants from dried blood spots. The models were controlled for confounders. RESULTS:All the studied pollutants were significantly associated with increased anaemia prevalence in single pollutant model (e.g., the prevalence ratios associated with an increase in inter quartile range in three years moving average PM10 (1.05; 95% CI: 1.02-1.09), PM2.5 (1.11; 95% CI: 1.06-1.16), PM1 (1.13; 95% CI: 1.06-1.20) and NO2 (1.42; 95% CI: 1.34-1.49), respectively. These air pollutants were also associated with lower concentrations of haemoglobin: PM10 (-0.53; 95% CI: -0.67, -0.38); PM2.5 (-0.52; 95% CI: -0.71, -0.33); PM1 (-0.55; 95% CI: -0.69, -0.41); NO2 (-1.71; 95% CI: -1.85, -1.57) respectively. CONCLUSIONS:Air pollution exposure was significantly associated with increased prevalence of anaemia and decreased haemoglobin levels in a cohort of older Chinese adults.
Project description:Objectives: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC). Methods: We used baseline (2000–2003) and 5-y follow-up (2006–2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter Results: While no clear associations were observed in the full study sample (mean age 59.1 ( Conclusion: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed. https://doi.org/10.1289/EHP7077