Structural equation modeling of the inflammatory response to traffic air pollution.
Ontology highlight
ABSTRACT:
SUBMITTER: Baja ES
PROVIDER: S-EPMC4648554 | biostudies-literature | 2013 May-Jun
REPOSITORIES: biostudies-literature
Publications
Structural equation modeling of the inflammatory response to traffic air pollution.
Baja Emmanuel S ES Schwartz Joel D JD Coull Brent A BA Wellenius Gregory A GA Vokonas Pantel S PS Suh Helen H HH
Journal of exposure science & environmental epidemiology 20121212 3
Several epidemiological studies have reported conflicting results on the effect of traffic-related pollutants on markers of inflammation. In a Bayesian framework, we examined the effect of traffic pollution on inflammation using structural equation models (SEMs). We studied measurements of C-reactive protein (CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble intracellular adhesion molecule-1 (sICAM-1) for 749 elderly men from the Normative Aging Study. Using repeated measure ...[more]
Similar Datasets
Project description:BackgroundTraffic-related air pollution has been associated to a range of adverse health impacts, including decreased heart rate variability (HRV). The association between traffic-related pollution and HRV, however, has varied by traffic-related or HRV marker as well as by study, suggesting the need for a more comprehensive and integrative approach to examining air pollution-mediated biological impacts on these outcomes. In a Bayesian framework, we examined the effect of traffic pollution on HRV using structural equation models (SEMs) and looked at effect modification by participant characteristics.MethodsWe studied measurements of 5 HRV markers [high frequency (HF), low frequency (LF), 5-min standard deviation of normal-to-normal intervals (SDNN), square root of the mean squared differences of successive normal-to-normal intervals (rMSSD), and LF/HF ratio (LF/HF)] for 700 elderly men from the Normative Aging Study. Using SEMs, we fit a latent variable for traffic pollution that is reflected by levels of carbon monoxide, nitrogen monoxide, nitrogen dioxide, and black carbon (BC) to estimate its effect on latent variable for parasympathetic tone that included HF, SDNN and rMSSD, and the sympathetic tone marker, LF/HF. Exposure periods were assessed using 4-, 24-, 48-, 72-hour moving average pre-visit. We compared our main effect findings using SEMs with those obtained using linear mixed models.ResultsTraffic pollution was not associated with mean parasympathetic tone and LF/HF for all examined moving averages. In Bayesian linear mixed models, however, BC was related to increased LF/HF, an inter quartile range (IQR) increase in BC was associated with a 6.5% (95% posterior interval (PI): -0.7%, 14.2%) increase in mean LF/HF 24-hours later. The strongest association observed was for the 4-hour moving average (10.1%; 95% PI: 3.0%, 17.6%). The effect of traffic on parasympathetic tone was stronger among diabetic as compared to non-diabetic participants. Specifically, an IQR increase in traffic pollution in the 48-hr prior to the clinic visit was associated with a 44.3% (95% PI: -67.7%, -4.2%) lower mean parasympathetic tone among diabetics, and a 7.7% (95% PI: -18.0%, 41.4%) higher mean parasympathetic tone among non-diabetics.ConclusionsBC was associated with adverse changes LF/HF in the elderly. Traffic pollution may decrease parasympathetic tone among diabetic elderly.
| S-EPMC3907044 | biostudies-literature
Project description:Long-term exposure to ambient air pollution can lead to adverse health effects in children; however, underlying biological mechanisms are not fully understood.We evaluated the effect of air pollution exposure during different time periods on mRNA expression as well as circulating levels of inflammatory cytokines in children.We measured a panel of 10 inflammatory markers in peripheral blood samples from 670 8-y-old children in the Barn/Child, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) birth cohort. Outdoor concentrations of nitrogen dioxide (NO2) and particulate matter (PM) with aerodynamic diameter <10 ?m (PM10) from road traffic were estimated for residential, daycare, and school addresses using dispersion modeling. Time-weighted average exposures during infancy and at biosampling were linked to serum cytokine levels using linear regression analysis. Furthermore, gene expression data from 16-year-olds in BAMSE (n=238) were used to evaluate links between air pollution exposure and expression of genes coding for the studied inflammatory markers.A 10??g/m3 increase of NO2 exposure during infancy was associated with a 13.6% (95% confidence interval (CI): 0.8; 28.1%) increase in interleukin-6 (IL-6) levels, as well as with a 27.8% (95% CI: 4.6, 56.2%) increase in IL-10 levels, the latter limited to children with asthma. However, no clear associations were observed for current exposure. Results were similar using PM10, which showed a high correlation with NO2. The functional analysis identified several differentially expressed genes in response to air pollution exposure during infancy, including IL10, IL13, and TNF;.Our results indicate alterations in systemic inflammatory markers in 8-y-old children in relation to early-life exposure to traffic-related air pollution. https://doi.org/10.1289/EHP460.
| S-EPMC5714301 | biostudies-literature
Project description:Exposure to black carbon (BC), a tracer of vehicular-traffic pollution, is associated with increased blood pressure (BP). Identifying biological factors that attenuate BC effects on BP can inform prevention. We evaluated the role of mitochondrial abundance, an adaptive mechanism compensating for cellular-redox imbalance, in the BC-BP relationship.At ? 1 visits among 675 older men from the Normative Aging Study (observations=1252), we assessed daily BP and ambient BC levels from a stationary monitor. To determine blood mitochondrial abundance, we used whole blood to analyze mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA) using quantitative polymerase chain reaction. Every standard deviation increase in the 28-day BC moving average was associated with 1.97 mm Hg (95% confidence interval [CI], 1.23-2.72; P<0.0001) and 3.46 mm Hg (95% CI, 2.06-4.87; P<0.0001) higher diastolic and systolic BP, respectively. Positive BC-BP associations existed throughout all time windows. BC moving averages (5-day to 28-day) were associated with increased mtDNA/nDNA; every standard deviation increase in 28-day BC moving average was associated with 0.12 standard deviation (95% CI, 0.03-0.20; P=0.007) higher mtDNA/nDNA. High mtDNA/nDNA significantly attenuated the BC-systolic BP association throughout all time windows. The estimated effect of 28-day BC moving average on systolic BP was 1.95-fold larger for individuals at the lowest mtDNA/nDNA quartile midpoint (4.68 mm Hg; 95% CI, 3.03-6.33; P<0.0001), in comparison with the top quartile midpoint (2.40 mm Hg; 95% CI, 0.81-3.99; P=0.003).In older adults, short-term to moderate-term ambient BC levels were associated with increased BP and blood mitochondrial abundance. Our findings indicate that increased blood mitochondrial abundance is a compensatory response and attenuates the cardiac effects of BC.
| S-EPMC4729631 | biostudies-literature
Project description:BACKGROUND:Traffic-related air pollution has been linked to multiple adverse pregnancy outcomes. However, few studies have examined pregnancy loss, targeting losses identified by hospital records, a large limitation as it does not capture events not reported to the medical system. METHODS:We used a novel variation of the time-series design to determine the association, and identify the critical window of vulnerability, between week-to-week traffic-related air pollution and conceptions resulting in live births, using nitrogen dioxide (NO2) as a traffic emissions tracer. We used information from all live births recorded at Beth Israel Deaconess Medical Center in Boston, MA (2000-2013) and all live births in Tel Aviv District, Israel (2010-2013). RESULTS:In Boston (68,969 live births), the strongest association was during the 15th week of gestation; for every 10 ppb of NO2 increase during that week, we observed a lower rate of live births (rate ratio [RR] = 0.87; 95% confidence interval [CI], 0.78, 0.97), using live birth-identified conceptions to infer pregnancy losses. In the Tel Aviv District (95,053 live births), the strongest estimate was during the 16th gestational week gestation (RR = 0.82; 95% CI, 0.76, 0.90 per 10 ppb of NO2). CONCLUSIONS:Using weekly conceptions ending in live birth rather than identified pregnancy losses, we comprehensively analyzed the relationship between air pollution and all pregnancy loss throughout gestation. The observed results, with remarkable similarity in two independent locations, suggest that higher traffic-related air pollution levels are associated with pregnancy loss, with strongest estimates between the 10th and 20th gestational weeks.
| S-EPMC6269216 | biostudies-literature
Project description:Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments.To examine the relationship between traffic-related air pollution, air quality, and autism.This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development.Case-control study from California.A total of 279 children with autism and a total of 245 control children with typical development.Crude and multivariable adjusted odds ratios (AORs) for autism.Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 ?m in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates.Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.
| S-EPMC4019010 | biostudies-literature
Project description:BackgroundA recent meta-analysis suggested evidence for an effect of exposure to ambient air pollutants on risk of certain congenital heart defects. However, few studies have investigated the effects of traffic-related air pollutants with sufficient spatial accuracy.ObjectivesWe estimated associations between congenital anomalies and exposure to traffic-related air pollution in Barcelona, Spain.MethodCases with nonchromosomal anomalies (n = 2,247) and controls (n = 2,991) were selected from the Barcelona congenital anomaly register during 1994-2006. Land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE), were applied to residential addresses at birth to estimate spatial exposure to nitrogen oxides and dioxide (NOx, NO2), particulate matter with diameter ? 10 ?m (PM10), 10-2.5 ?m (PMcoarse), ? 2.5 ?m (PM2.5), and PM2.5 absorbance. Spatial estimates were adjusted for temporal trends using data from routine monitoring stations for weeks 3-8 of each pregnancy. Logistic regression models were used to calculate odds ratios (ORs) for 18 congenital anomaly groups associated with an interquartile-range (IQR) increase in exposure estimates.ResultsIn spatial and spatiotemporal exposure models, we estimated statistically significant associations between an IQR increase in NO2 (12.2 ?g/m3) and coarctation of the aorta (ORspatiotemporal = 1.15; 95% CI: 1.01, 1.31) and digestive system defects (ORspatiotemporal = 1.11; 95% CI: 1.00, 1.23), and between an IQR increase in PMcoarse (3.6 ?g/m3) and abdominal wall defects (ORspatiotemporal = 1.93; 95% CI: 1.37, 2.73). Other statistically significant increased and decreased ORs were estimated based on the spatial model only or the spatiotemporal model only, but not both.ConclusionsOur results overall do not indicate an association between traffic-related air pollution and most groups of congenital anomalies. Findings for coarctation of the aorta are consistent with those of the previous meta-analysis.CitationSchembari A, Nieuwenhuijsen MJ, Salvador J, de Nazelle A, Cirach M, Dadvand P, Beelen R, Hoek G, Basagaña X, Vrijheid M. 2014. Traffic-related air pollution and congenital anomalies in Barcelona. Environ Health Perspect 122:317-323;?http://dx.doi.org/10.1289/ehp.1306802.
| S-EPMC3948033 | biostudies-literature
Project description:Traffic congestion increases vehicle emissions and degrades ambient air quality, and recent studies have shown excess morbidity and mortality for drivers, commuters and individuals living near major roadways. Presently, our understanding of the air pollution impacts from congestion on roads is very limited. This study demonstrates an approach to characterize risks of traffic for on- and near-road populations. Simulation modeling was used to estimate on- and near-road NO2 concentrations and health risks for freeway and arterial scenarios attributable to traffic for different traffic volumes during rush hour periods. The modeling used emission factors from two different models (Comprehensive Modal Emissions Model and Motor Vehicle Emissions Factor Model version 6.2), an empirical traffic speed-volume relationship, the California Line Source Dispersion Model, an empirical NO2-NOx relationship, estimated travel time changes during congestion, and concentration-response relationships from the literature, which give emergency doctor visits, hospital admissions and mortality attributed to NO2 exposure. An incremental analysis, which expresses the change in health risks for small increases in traffic volume, showed non-linear effects. For a freeway, "U" shaped trends of incremental risks were predicted for on-road populations, and incremental risks are flat at low traffic volumes for near-road populations. For an arterial road, incremental risks increased sharply for both on- and near-road populations as traffic increased. These patterns result from changes in emission factors, the NO2-NOx relationship, the travel delay for the on-road population, and the extended duration of rush hour for the near-road population. This study suggests that health risks from congestion are potentially significant, and that additional traffic can significantly increase risks, depending on the type of road and other factors. Further, evaluations of risk associated with congestion must consider travel time, the duration of rush-hour, congestion-specific emission estimates, and uncertainties.
| S-EPMC4243514 | biostudies-literature
Project description:PurposeTo investigate the association between exposure to traffic-related air pollution and use of spectacles (as a surrogate measure for myopia) in schoolchildren.MethodsWe analyzed the impact of exposure to NO2 and PM2.5 light absorbance at home (predicted by land-use regression models) and exposure to NO2 and black carbon (BC) at school (measured by monitoring campaigns) on the use of spectacles in a cohort of 2727 schoolchildren (7-10 years old) in Barcelona (2012-2015). We conducted cross-sectional analyses based on lifelong exposure to air pollution and prevalent cases of spectacles at baseline data collection campaign as well as longitudinal analyses based on incident cases of spectacles use and exposure to air pollution during the three-year period between the baseline and last data collection campaigns. Logistic regression models were developed to quantify the association between spectacles use and each of air pollutants adjusted for relevant covariates.ResultsAn interquartile range increase in exposure to NO2 and PM2.5 absorbance at home was respectively associated with odds ratios (95% confidence intervals (CIs)) for spectacles use of 1.16 (1.03, 1.29) and 1.13 (0.99, 1.28) in cross-sectional analyses and 1.15 (1.00, 1.33) and 1.23 (1.03, 1.46) in longitudinal analyses. Similarly, odds ratio (95% CIs) of spectacles use associated with an interquartile range increase in exposures to NO2 and black carbon at school was respectively 1.32 (1.09, 1.59) and 1.13 (0.97, 1.32) in cross-sectional analyses and 1.12 (0.84, 1.50) and 1.27 (1.03, 1.56) in longitudinal analyses. These findings were robust to a range of sensitivity analyses that we conducted.ConclusionWe observed increased risk of spectacles use associated with exposure to traffic-related air pollution. These findings require further confirmation by future studies applying more refined outcome measures such as quantified visual acuity and separating different types of refractive errors.
| S-EPMC5378327 | biostudies-literature
Project description:While many studies have evaluated the association between acute childhood leukemia and environmental factors, knowledge is limited. Ambient air pollution has been classified as a Group 1 carcinogen, but studies have not established whether traffic-related air pollution is associated with leukemia. The goal of our study was to determine if children with acute leukemia had higher odds of exposure to traffic-related air pollution at birth compared to controls.We conducted a case-control study using the Oklahoma Central Cancer Registry to identify cases of acute leukemia in children diagnosed before 20 years of age between 1997 and 2012 (n=307). Controls were selected from birth certificates and matched to cases on week of birth (n=1013). Using a novel satellite-based land-use regression model of nitrogen dioxide (NO2) and estimating road density based on the 2010 US Census, we evaluated the association between traffic-related air pollution and childhood leukemia using conditional logistic regression.The odds of exposure to the fourth quartile of NO2 (11.19-19.89ppb) were similar in cases compared to controls after adjustment for maternal education (OR: 1.08, 95% CI: 0.75, 1.55). These estimates were stronger among children with acute myeloid leukemia (AML) than acute lymphoid leukemia, with a positive association observed among urban children with AML (4th quartile odds ratio: 5.25, 95% confidence interval: 1.09, 25.26). While we observed no significant association with road density, male cases had an elevated odds of exposure to roads at 500m from the birth residence compared to controls (OR: 1.39, 95% CI: 0.93, 2.10), which was slightly attenuated at 750m.Although we observed no association overall between NO2 or road density, this was the first study to observe an elevated odds of exposure to NO2 among children with AML compared to controls suggesting further exploration of traffic-related air pollution and AML is warranted.
| S-EPMC4874884 | biostudies-literature
Project description:BACKGROUND: Traffic-related air pollution is related with asthma, and this association may be modified by genetic factors. OBJECTIVES: We investigated the role of genetic polymorphisms potentially modifying the association between home outdoor levels of modeled nitrogen dioxide and asthma. METHODS: Adults from 13 cities of the second European Community Respiratory Health Survey (ECRHS II) were included (n = 2,920), for whom both DNA and outdoor NO(2) estimates were available. Home addresses were geocoded and linked to modeled outdoor NO(2) estimates, as a marker of local traffic-related pollution. We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NAD(P)H:quinine oxidoreductase (NQO1)], inflammatory response [tumor necrosis factor alpha (TNFA)], immunologic response [Toll-like receptor 4 (TLR4)], and airway reactivity [adrenergic receptor beta2 (ADRB2)]. RESULTS: The association between modeled NO(2) and asthma prevalence was significant for carriers of the most common genotypes of NQO1 rs2917666 [odds ratio (OR) = 1.54; 95% confidence interval (CI), 1.10-2.24], TNFA rs2844484 (OR = 2.02; 95% CI, 1.30-3.27). For new-onset asthma, the effect of NO(2) was significant for the most common genotype of NQO1 rs2917666 (OR = 1.52; 95% CI, 1.09-2.16). A significant interaction was found between NQO1 rs2917666 and NO(2) for asthma prevalence (p = 0.02) and new-onset asthma (p = 0.04). CONCLUSIONS: Genetic polymorphisms in the NQO1 gene are related to asthma susceptibility among persons exposed to local traffic-related air pollution. This points to the importance of antioxidant pathways in the protection against the effects of air pollution on asthma.
| S-EPMC2799467 | biostudies-literature