Marker Of Traffic-related Air Pollution Research Articles

Air pollution exposure and mammographic breast density in Tehran, Iran: a cross-sectional study.

BackgroundAir pollution is one of the major public health challenges in many parts of the world possibly has an association with breast cancer. However, the mechanism is still unclear. This study aimed to find an association between exposure to six criteria ambient air pollutants (PM2.5, PM10, SO2, NO2, O3, and CO) and mammographic breast density (MBD), as one of the strongest predictors for developing breast cancer, in women living in Tehran, Iran.MethodsParticipants were selected from women attending two university hospitals for screening mammography from 2019 to 2021. Breast density was rated by two expert radiologists. Individual exposures to 3-year ambient air pollution levels at the residence were estimated.ResultsThe final analysis in 791 eligible women showed that low and high breast density was detected in 34.8 and 62.2 of participants, respectively. Logistic regression analysis after considering all possible confounding factors represented that an increase in each unit of NO2 (ppb) exposure was associated with an increased risk of breast density with an OR equal to 1.04 (95CI: 1.01 to 1.07). Furthermore, CO level was associated with a decreasing breast density (OR = 0.40, 95CI = 0.19 to 0.86). None of the other pollutants were associated with breast density.ConclusionHigher MBD was associated with an increased level of NO2, as a marker of traffic-related air pollution. Furthermore, CO concentration was associated with a lower MBD, while other criteria air pollutants were not related to MBD. Further studies are needed to evaluate the association between ambient air pollutants with MBD.Supplementary informationThe online version contains supplementary material available at https://doi.org/10.1265/ehpm.22-00027.

Nitrogen oxides (NO and NO2) pollution in the Accra metropolis: Spatiotemporal patterns and the role of meteorology

Economic and urban development in sub-Saharan Africa (SSA) may be shifting the dominant air pollution sources in cities from biomass to road traffic. Considered as a marker for traffic-related air pollution in cities, we conducted a city-wide measurement of NOx levels in the Accra Metropolis and examined their spatiotemporal patterns in relation to land use and meteorological factors. Between April 2019 to June 2020, we collected weekly integrated NOx (n = 428) and NO2 (n = 472) samples at 10 fixed (year-long) and 124 rotating (week-long) sites. Data from the same time of year were compared to a previous study (2006) to assess changes in NO2 concentrations. NO and NO2 concentrations were highest in commercial/business/industrial (66 and 76 μg/m3, respectively) and high-density residential areas (47 and 59 μg/m3, respectively), compared with peri-urban locations. We observed annual means of 68 and 70 μg/m3 for NO and NO2, and a clear seasonal variation, with the mean NO2 of 63 μg/m3 (non-Harmattan) increased by 25–56% to 87 μg/m3 (Harmattan) across different site types. The NO2/NOx ratio was also elevated by 19–28%. Both NO and NO2 levels were associated with indicators of road traffic emissions (e.g. distance to major roads), but not with community biomass use (e.g. wood and charcoal). We found strong correlations between both NO2 and NO2/NOx and mixing layer depth, incident solar radiation and water vapor mixing ratio. These findings represent an increase of 25–180% when compared to a small study conducted in two high-density residential neighborhoods in Accra in 2006. Road traffic may be replacing community biomass use (major source of fine particulate matter) as the prominent source of air pollution in Accra, with policy implication for growing cities in SSA.

Environmental Exposure to Traffic Pollution and Motor Function in Adolescence

BACKGROUND AND AIM: Evidence supports the neurotoxic effects of air pollution on cognitive deficits, mental health, and behavioral outcomes in children. While heavy metal exposure has been associated with poor motor function, it is unclear whether traffic-related air pollution (TRAP) has a similar relationship. METHODS: Participants (n=332) were part of the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS). Elemental carbon attributable to traffic (ECAT), a marker of TRAP, was estimated at birth, age 12 years (current), and average exposure throughout childhood, using a validated land use regression model. Motor function was assessed with the Grooved Pegboard (GPB) test including time required to complete the task for dominant and non-dominant hand and number of dropped pegs. Associations between TRAP exposure and motor outcomes were estimated using linear (i.e., seconds to completion) and logistic (i.e, drops) regression; sex-specific effects were examined. Primary models controlled for child’s IQ, neighborhood deprivation, and total household income; secondary models included blood metals (i.e., lead, cadmium, mercury) collected at the age 12 visit. RESULTS:Children exposed to elevated current ECAT levels took on average 18 seconds longer to complete the GPB task with their non-dominant hand (95% CI 4.77, 31.14, p=0.008); ECAT was not associated with dominant hand completion. We did not observe a main effect of ECAT at any time point on probability of dropped pegs; however, girls exposed to higher childhood ECAT levels were more likely to drop pegs with their dominant hand during the GPB task (Psex*childhood ECAT = 0.03). Additionally controlling for heavy metal exposure did not alter the results. CONCLUSIONS:Higher TRAP exposure was associated with poorer motor function, and girls may be at increased risk for adverse outcomes. These findings, as well as others, suggest that air pollution is quickly becoming one of the leading threats to a child’s neurodevelopment. KEYWORDS: Children's environmental health, Neurodevelopmental outcomes, Traffic-related, Air pollution

Association of Prenatal Ambient Air Pollution Exposure With Placental Mitochondrial DNA Copy Number, Telomere Length and Preeclampsia.

Background: Studies have shown that ambient air pollution is linked to preeclampsia (PE), possibly via generation of oxidative stress in the placenta. Telomere length and mitochondrial DNA copy number (mtDNAcn) are sensitive to oxidative stress damage.Objective: To study the association between prenatal exposure to ambient nitrogen oxides (NOx, a marker for traffic-related air pollution), and PE, as well as potential mediation effects by placental telomere length and mtDNAcn.Methods: This is a cross-sectional study of 42 preeclamptic and 95 arbitrarily selected normotensive pregnant women with gestational ambient NOx exposure assessment in southern Scania, Sweden. Hourly concentrations of NOx were estimated at the residential addresses by a Gaussian-plume dispersion model with 100 × 100 m spatial resolutions and aggregated into trimester-specific mean concentrations. Placental relative mtDNAcn and telomere length were measured using qPCR. Linear and logistic regression models were used to investigate associations, adjusted for perinatal and seasonal characteristics.Results: Exposure was categorized into low and high exposures by median cut-offs during first [11.9 μg/m3; interquartile range (IQR) 7.9, 17.9], second (11.6 μg/m3; IQR: 7.1, 21.1), third trimesters (11.9 μg/m3; IQR: 7.7, 19.5) and entire pregnancy (12.0 μg/m3; IQR: 7.6, 20.1). Increased risk of PE was found for high prenatal NOx exposure during the first trimester (OR 4.0; 95% CI: 1.4, 11.1; p = 0.008), and entire pregnancy (OR 3.7; 95% CI: 1.3, 10.4; p = 0.012). High exposed group during the first trimester had lower placental relative mtDNAcn compared with low exposed group (−0.20; 95% CI: −0.36, −0.04; p = 0.01). Changes in relative mtDNAcn did not mediate the association between prenatal NOx exposure and PE. No statistically significant association was found between placental relative telomere length, prenatal NOx exposure and PE.Conclusion: In this region with relatively low levels of air pollution, ambient NOx exposure during the first trimester was associated with reduced placental relative mtDNAcn and an increased risk of PE. However, we did not find any evidence that mtDNAcn or TL mediated the association between air pollution and PE. Future research should further investigate the role of mtDNAcn for pregnancy complications in relation to exposure to ambient air pollution during pregnancy.

High traffic pollution predicts rapid decline in lung function among children with cystic fibrosis

Background: Environmental exposures and community characteristics (i.e. geomarkers) have been shown to influence pulmonary outcomes; however, the ability for geomarkers to predict rapid lung-function decline among cystic fibrosis (CF) patients has not been studied.Methods: We applied a longitudinal model to predict rapid lung function decline, defined using forced expiratory volume in 1 second (FEV1) relative to patient and center specific norms, based on registry data for 185 CF patients aged 6-20 years receiving care at Cincinnati Children’s Hospital CF Center between 2012 and 2017. Clinical and demographic characteristics (F508del alleles, sex, Medicaid insurance use and pancreatic enzymes) were used as predictors in our initial model. Residential addresses were geocoded and average exposure to elemental carbon attributable to traffic sources (ECAT), a marker of traffic-related air pollution (TRAP), was estimated for the three months prior to each clinical encounter using a previously validated spatiotemporal land-use model. Neighborhood deprivation was derived at the census-tract level using an index comprised of American Community Survey measures related to poverty, education, housing, and access to healthcare. Greenness near the home was derived from the normalized differential vegetation index. We implemented real-time prediction after including geomarkers with the clinical and demographic predictors. Covariates were selected with the likelihood ratio test (LRT). Model fit including/excluding geomarkers was assessed using Akaike information criteria (delta-AIC).Results: Including geomarkers yielded a significantly better fit and improved prediction of FEV1 compared to a model with only clinical/demographic characteristics (LRT statistic: 45.4, P<0.0001; delta-AIC=27.4). Specifically, an increase of 1 ug/m3 of ECAT was associated with a1.13% predicted/yr (95% CI: 0.33, 1.93% predicted/yr) more rapid decline.Conclusion: Exposure to TRAP is an important predictor of pulmonary decline in CF that may be used to enhance clinician assessments of prognosis and enable personalized environmental health interventions.

The impact of baseline incidence rates on burden of disease assessment of air pollution and onset childhood asthma: analysis of data from the contiguous United States

PurposeBurden of disease (BoD) assessments typically rely on national-level incidence rates for the health outcomes of interest. The impact of using a constant national-level incidence rate, versus a more granular spatially varying rate, remains unknown and understudied in the literature. There has been an increasing number of publications estimating the BoD of childhood asthma attributable to air pollution, as emerging evidence demonstrates that traffic-related air pollution (TRAP) leads to onset of the disease. In this study, we estimated the burden of incident childhood asthma cases which may be attributable to nitrogen dioxide (NO2), a criteria pollutant and a good marker of TRAP, in the contiguous United States. We used both a national-level and newly generated state-specific asthma incidence rates and compared results from the two approaches. MethodsWe estimated incident childhood asthma cases which may be attributable to NO2 using standard BoD assessment methods. We combined child (<18 years) counts with 2010 NO2 exposures at the census block level, concentration-response function, and state-specific asthma incidence rates. NO2 concentrations were obtained from a previously validated land-use regression model. We sourced the concentration-response function from a meta-analysis on TRAP and risk of childhood asthma. We estimated incidence rates using raw data collected in the 2006–2010 Behavioral Risk Factor Surveillance System and Asthma Call-back Surveys. We stratified the estimated BoD by urban versus rural status and by median household income, explored trends in BoD across 48 states and the District of Columbia, and compared our results with a published BoD analysis which used a constant national-level incidence rate across all states. ResultsThe overall mean (min–max) NO2 concentration(s) was 13.2 (1.5–58.3) ug/m3 and was highest in urbanized areas. The estimated national aggregate asthma incidence rate was 11.6 per 1000 at-risk children and ranged from 4.3 (Montana) to 17.7 (District of Columbia) per 1000 at-risk children. The 17 states that did not have data to estimate an incidence rate were assigned the national aggregate asthma incidence rate. Using the state-specific incidence rates, we estimated a total of 134,166 (95% confidence interval: 75,177–193,327) childhood asthma incident cases attributable to NO2, accounting for 17.6% of all childhood asthma incident cases. Using the national-level incidence rate, we estimated a total of 141,931 (95% confidence interval: 119,222–163,505) incident cases attributable to NO2, accounting for 17.9% of all childhood asthma incident cases. Using the state-specific incidence rates therefore reduced the attributable number of cases by 7,765 (5.5% relative reduction), compared with estimates using the national-level incidence rate. Across states, the change in the attributable number of cases ranged from −64.1% (Montana) to +33.8% (Texas). California had the largest absolute decrease (−6,190) in attributable cases, whereas Texas had the largest increase (+3,615). Stratifying by socioeconomic status and urban versus rural status produced new trends compared with the previously published BoD analysis showing high heterogeneity across the states. ConclusionsWe estimated new state-specific asthma incidence rates for the contiguous United States. Using state-specific incidence rates versus a constant national incidence rate resulted in a small change in the NO2 attributable BoD at the national level, but had a more prominent impact at the state level.

Abstract 3395: Commute patterns, residential traffic-related air pollution, and lung cancer risk in the prospective UK Biobank cohort study

Abstract Introduction: Commuting to and from work is a daily activity that exposes millions of people to lung carcinogens such as particulate matter, polycyclic aromatic hydrocarbons, and other constituents of traffic-related air pollution (TRAP). Lung cancer is a global health burden and one of the most common malignancies among industrialized western countries such as the United Kingdom (UK). Few epidemiologic studies of TRAP and lung cancer consider the contribution of commute characteristics. To further investigate, we assessed associations between commute patterns, residential nitrogen dioxide (NO2; a surrogate marker for TRAP), and lung cancer risk in the prospective UK Biobank cohort study. Methods: We analyzed 234,124 employed participants at baseline in 2006-2010. There were 493 incident lung cancer cases diagnosed over an average 7-year follow-up. Subjects were cross-classified into exclusive categories of commute mode (automobile, public transportation, walking, cycling, active mixture, and other mixture) and frequency (regular: &amp;lt;5, often: ≥5 work-bound trips/week). Annual average residential NO2 concentrations in 2005-2007 were estimated from land use regression. Cox regression models were used to estimate associations between commute patterns, quartiles of NO2, and incident lung cancer, adjusted for age, sex, smoking status, race/ethnicity, study center, body mass index, annual income, commute distance, and alcohol intake. Additional analyses were stratified by age, sex, smoking status, NO2 (&amp;gt;, ≤ median2005=28.3 µg/m3) and main job duration (&amp;gt;, ≤10 years). Effect modification was tested using interaction terms. Results: Most participants only used automobiles to commute (56.5%), while 8.3% only used public transportation (e.g., buses, light-rail, subways), 2.2% only cycled, and 5.0% only walked. Compared to regular automobile use, commuting often by public transportation was strongly associated with increased lung cancer risk (HR=1.68, 95% CI: 1.14-2.47). The association was nominally stronger among high-NO2 residences, men, and ever-smokers, while similar by job duration. There was evidence for effect modification of the association by residential NO2 (p-interaction=0.03) and sex-smoking status (p-interactions=0.03 and 0.09 for former- and current-smoking men, respectively). The other commute categories were not associated with risk. Furthermore, there was a positive exposure-response relationship with NO2 (HRQ2=1.23, 95% CI:0.91-1.65; HRQ3=1.51, 95% CI:1.12-2.03; HRQ4=1.61, 95% CI:1.15-2.27; p-trend=2.1 × 10−3). Conclusions: Our findings suggest that commuters who often use public transportation have elevated lung cancer risk, possibly driven by time spent in transit microenvironments with high TRAP-levels. Although there are health benefits of public transit use, the competing risk of lung cancer warrants consideration. Citation Format: Jason Yat-Yang Wong, Rena Jones, Bryan Bassig, Batel Blechter, Wei Hu, Bu-tian Ji, Nathaniel Rothman, Qing Lan. Commute patterns, residential traffic-related air pollution, and lung cancer risk in the prospective UK Biobank cohort study [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 3395.

Associations between incident breast cancer and ambient concentrations of nitrogen dioxide from a national land use regression model in the Canadian National Breast Screening Study

BackgroundAir pollution has been classified as a human carcinogen based largely on epidemiological studies of lung cancer. Recent research suggests that exposure to ambient air pollution increases the risk of female breast cancer especially in premenopausal women. MethodsOur objective was to determine the association between residential exposure to ambient nitrogen dioxide (NO2) and newly diagnosed cases of invasive breast cancer in a cohort of 89,247 women enrolled in the Canadian National Breast Screening Study between 1980 and 1985. Vital status and incident breast cancers through 2005 were determined through record linkage to the Canadian national mortality and cancer registries. Estimates of exposures to NO2 using participants’ addresses at time of entry into the study were derived from a national land use regression model. We classified women as reaching menopause according to information obtained at baseline. In addition, as we had no information from women on their menopausal status during the observation period, we conducted analyses using different cut-points for defining postmenopausal status (i.e., at 50 or at 52 years of age), and hence we had four non-independent cohorts. We computed rate ratios for the incidence of breast cancer and their 95% confidence intervals (CI) separately for premenopausal and postmenopausal women. Our Cox models used attained age as the time axis and the rate ratios were adjusted for several individual-level risk factors, including reproductive history, as well as census-based neighborhood-level characteristics. ResultsThe median concentration of NO2 was about 15 parts per billion (ppb). After adjusting for personal risk factors and contextual variables, we found no evidence of associations for the incidence of breast cancer in the postmenopausal cohorts. In premenopausal women, the rate ratio for an increase of 9.7 ppb (about the interquartile range) was 1.13 (95%CI: 0.94–1.37) for the 50 years of age cut-off for menopausal status and it was 1.17 (95%CI: 1.00–1.38) for the 52 years of age cut-off. ConclusionsOur findings suggest that exposure to low concentrations of NO2, a marker for traffic-related air pollution, increases the risk of premenopausal breast cancer, but not postmenopausal breast cancer.

The association of traffic-related air and noise pollution with maternal blood pressure and hypertensive disorders of pregnancy in the HOME study cohort

Traffic-related air and noise pollution may increase the risk for cardiovascular disorders, especially among susceptible populations like pregnant women. The objective of this study was to evaluate the association of exposure to traffic-related air pollution and traffic noise with blood pressure in pregnant women. We extracted systolic blood pressure (SBP) and diastolic blood pressure (DBP) at ≥20 weeks gestation, as well as hypertensive disorders of pregnancy from medical records in the HOME Study, a prospective pregnancy and birth cohort from Cincinnati, OH (n = 370). We estimated exposure to elemental carbon attributable to traffic (ECAT),11ECAT = elemental carbon attributable to traffic. a marker of traffic-related air pollution, at women's residences at ~20 weeks gestation using a validated land use regression model and traffic noise using a publicly available transportation noise model. We used linear mixed models and modified Poisson regression adjusted for covariates to examine associations of ECAT and traffic noise with blood pressure and hypertensive disorders of pregnancy risk, respectively. In adjusted models, we found a 1.6 (95% CI = 0.02, 3.3; p = 0.048) mm Hg increase in SBP associated with an interquartile range increase in ECAT concentration; the association was stronger after adjusting for traffic noise (1.9 mm Hg, 95% = 0.1, 3.7; p = 0.035). ECAT concentrations were not significantly associated with DBP or hypertensive disorders of pregnancy, and traffic noise was not associated with SBP, DBP, or hypertensive disorders of pregnancy. There was no evidence of a joint effect of traffic noise and ECAT on any outcome. In this cohort, higher residential traffic-related air pollution exposure at ~20 weeks gestation was associated with higher SBP in late pregnancy. It is important for future studies of traffic-related air or noise pollution to jointly consider both exposures and neighborhood characteristics given their correlation and potential cumulative impact on cardiovascular health.

Associations between Traffic-Related Air Pollution and Cardiovascular Disease Risk Factors Were Stronger in More Walkable Neighborhoods: The Cardiovascular Health in Ambulatory Care Research Team (CANHEART) Cohort

Introduction Studies suggest living in a more walkable neighborhood may protect against cardiovascular disease risk factors such as hypertension (HTN) and diabetes mellitus (DM) by encouraging physical activity. Walkable neighborhoods, however, often carry higher levels of traffic-related air pollution. Little is known regarding whether synergistic effects may exist between walkability and air pollution on these risk factors.Hypothesis We hypothesized that the association between traffic-related air pollution, hypertension, and diabetes mellitus would be stronger in more walkable areas.Methods We drew a cross-sectional sample of individuals ages 40-74 on January 1, 2008 from the CANHEART cohort. HTN and DM were ascertained using validated algorithms. Walkability (quintiles, Q5 highest, Q1 lowest) was measured using a validated index which has previously been shown to be inversely associated with obesity and diabetes. Exposure to nitrogen dioxide, a valid marker for traffic-related air pollution, was assessed using a land use regression models. The associations were tested using logistic regression with cluster-robust standard errors, adjusting for age, sex, area-level income, ethnicity, and comorbidities.Results 2,618,584 individuals were included in the analysis. Walkability was inversely associated with odds for HTN (Q5 vs. Q1 OR &amp;#61; 0.80, 95% CI: 0.79, 0.82) and DM (Q5 vs. Q1 OR &amp;#61; 0.89, 95% CI: 0.87, 0.91), while NO2 was positively associated with each (HTN: OR &amp;#61; 1.02 per 10 ppb (1.01, 1.03); DM: OR &amp;#61; 1.11 per 10 ppb (1.09, 1.13)). We observed significant interactions between walkability and NO2 on odds for HTN and DM, with stronger NO2 associations in the most walkable neighborhoods.Conclusions We observed significant interactions between traffic-related air pollution and walkability on odds for HTN and DM. This finding suggests that benefits from living in more walkable neighborhoods may be partially offset by stronger negative associations with air pollution.

Abstract MP55: Associations Between Traffic-Related Air Pollution and Cardiovascular Disease Risk Factors Were Stronger in More Walkable Neighborhoods: The Cardiovascular Health in Ambulatory Care Research Team Cohort

Introduction: Studies suggest living in a more walkable neighborhood may protect against cardiovascular disease risk factors such as hypertension (HTN) and diabetes mellitus (DM) by encouraging physical activity. Walkable neighborhoods, however, often carry higher levels of traffic-related air pollution. Little is known regarding whether synergistic effects may exist between walkability and air pollution on these risk factors. Hypothesis: We hypothesized that the association between traffic-related air pollution, hypertension, and diabetes mellitus would be stronger in more walkable areas. Methods: We drew a cross-sectional sample of individuals ages 40-74 on January 1, 2008 from the CANHEART cohort. HTN and DM were ascertained using validated algorithms. Walkability (quintiles, Q5 highest, Q1 lowest) was measured using a validated index which has previously been shown to be inversely associated with obesity and diabetes. Exposure to nitrogen dioxide, a valid marker for traffic-related air pollution, was assessed using a land use regression models. The associations were tested using logistic regression with cluster-robust standard errors, adjusting for age, sex, area-level income, ethnicity, and comorbidities. Results: In total, 2,618,584 individuals were included in the analysis (mean (SD) age = 53.2 (9.2), 52% female). Walkability was inversely associated with odds for HTN (Q5 vs. Q1 OR = 0.80, 95% CI: 0.79, 0.82) and DM (Q5 vs. Q1 OR = 0.89, 95% CI: 0.87, 0.91), while NO 2 was positively associated with each (HTN: OR = 1.02 per 10 ppb (1.01, 1.03); DM: OR = 1.11 per 10 ppb (1.09, 1.13)). We observed significant interactions between walkability and NO 2 on odds for HTN and DM, with stronger NO 2 associations in the most walkable neighborhoods (Fig. 1). Conclusions: We observed significant interactions between traffic-related air pollution and walkability on odds for HTN and DM. This finding suggests that benefits from living in more walkable neighborhoods may be offset by stronger negative associations with air pollution.

Quantifying the value of a clean ride: How far would you bicycle to avoid exposure to traffic-related air pollution?

While there is widespread acceptance of the health benefits of bicycling, recent research has highlighted that the benefits may be partially offset by the potential adverse health impacts asa result of bicyclists’ exposure to traffic-related air pollution. Using a stated preference experiment, data from 695 commuter cyclists was compiled through a web-based survey and analyzed using a random utility approach to evaluate whether and to what extent cyclists are willing to trade-off air pollution exposure with other attributes such as roadway characteristics, bike facilities, and travel time. Mean and maximum concentrations of nitrogen dioxide (in parts per billion or ppb), a common marker of traffic-related air pollution, were used as the attributes to represent the externality (ranging from 5 to 60ppb). Empirical results indicate that travel time and traffic volume remain the most important attributes for commuter cyclists in their route decision. We also computed a unique marginal rate of substitution called “Value of Clean Ride” (VCR). For mean exposure, the VCR is: 0.72min/ppb and for maximum exposure, the VCR is: 0.25min/ppb (95% distribution: −0.16, 0.67). This essentially suggests that if an alternative route was available with an average nitrogen dioxide concentration that is lower by 5ppb (a realistic goal in light of the high spatial variability in air pollution within urban areas), then cyclists would be willing to take it if it added no more than about 4min to their travel time. We also observed that cyclists who received information on short-term impacts of traffic-related air pollution tended to be more concerned with avoiding maximum exposure.

Maternal Exposure to Nitrogen Dioxide, Intake of Methyl Nutrients, and Congenital Heart Defects in Offspring.

Nutrients that regulate methylation processes may modify susceptibility to the effects of air pollutants. Data from the National Birth Defects Prevention Study (United States, 1997-2006) were used to estimate associations between maternal exposure to nitrogen dioxide (NO2), dietary intake of methyl nutrients, and the odds of congenital heart defects in offspring. NO2 concentrations, a marker of traffic-related air pollution, averaged across postconception weeks 2-8, were assigned to 6,160 nondiabetic mothers of cases and controls using inverse distance-squared weighting of air monitors within 50 km of maternal residences. Intakes of choline, folate, methionine, and vitamins B6 and B12 were assessed using a food frequency questionnaire. Hierarchical regression models, which accounted for similarities across defects, were constructed, and relative excess risks due to interaction were calculated. Relative to women with the lowest NO2 exposure and high methionine intake, women with the highest NO2 exposure and lowest methionine intake had the greatest odds of offspring with a perimembranous ventricular septal defect (odds ratio = 3.23, 95% confidence interval: 1.74, 6.01; relative excess risk due to interaction = 2.15, 95% confidence interval: 0.39, 3.92). Considerable departure from additivity was not observed for other defects. These results provide modest evidence of interaction between nutrition and NO2 exposure during pregnancy.

Investigating the effects of multiple NO 2 exposure measures on estimates of risk for breast and prostate cancers in two case-control studies

Background Traffic-related air pollution is associated with a range of health effects. Exposure to Nitrogen dioxide (NO2), a known marker of traffic-related air pollution, has been traditionally estimated using surfaces generated through land-use regression (LUR) models. Recently, air pollution dispersion models, with refined spatial resolution, have been used to derive NO2 exposures in urban areas. With either LUR development or dispersion modelling, there is evidence that data collection protocols and modelling assumptions can have a large effect on the resulting NO2 spatial surface. This study investigates the effects of various NO 2 exposure surfaces on the resulting risk estimates of breast cancer (BC) and prostate cancer (PC), both of which have already been associated with traffic-related air pollution. Methods We derived exposures for individuals in two case control studies (BC and PC) in Montreal, Canada using four different surfaces for NO2. Two of the surfaces were developed using LUR but employed different data collection protocols (LUR-1 and LUR-2), and the other two surfaces were generated using dispersion modelling; one with a regional model (dispersion-1) and another with a street canyon model (dispersion-2). Also, we estimated separate Odds Ratios (ORs) using concentrations of NO2 as measures of exposure, both for the BC and PC case–control studies. Results While the range of NO 2 concentrations in dispersion surfaces (4-26 ppb) is lower than the range in LUR surfaces (4-36 ppb), the four surfaces were found to be reasonably correlated, with Pearson correlation coefficients ranging between 0.52 and 0.79. The ORs for BC were estimated to be 1.26 (CI: 0.97, 1.63), 1.10 (CI: 0.89, 1.37), 1.07 (CI: 0.94, 1.23), and 1.05 (CI: 0.90, 1.22) based on LUR-1, LUR-2, dispersion-1, and dispersion-2. In contrast, the ORs for PC were estimated to be 1.39 (CI: 1.14, 1.69), 1.30 (CI: 1.08, 1.56), 1.13 (CI: 1.03, 1.24), and 1.04 (CI: 0.94, 1.16) based on LUR-1, LUR-2, dispersion-1, and dispersion-2. Conclusions Our analysis sheds light on the use of four different measures of exposure to traffic-related air pollution. We observed higher mean ORs based on the LUR surfaces but with overlapping CIs. Since LUR models capture all sources of NO 2 and dispersion models only capture traffic emissions, it is possible that this difference is due to the fact that non-road sources also contribute to the spatial distribution in NO 2 concentrations.

The Dose–Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO2 exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV1/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO2). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO2 and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases.

Proximity to a Major Road and Plasma Cytokines in School-Aged Children.

Traffic-related air pollution (TRAP) may affect immune responses, including those in the TH2 and TH17 pathways. To examine whether TRAP is associated with plasma level of TH17-, TH1-, and TH2-related cytokines in children with and without asthma, a cross-sectional study of 577 children (ages 6–14 years) with (n = 294) and without (n = 283) asthma in San Juan (Puerto Rico) was performed. Residential distance to a major road was estimated using geocoded home addresses for study participants. A panel of 14 cytokines, enriched for the TH17 pathway, was measured in plasma. Asthma was defined as physician-diagnosed asthma and current wheeze. Multivariable linear regression was used to examine the association of residential distance to a major road (a marker of TRAP), asthma, and cytokine levels. Among all participating children, residential proximity to a major road was significantly associated with increased plasma level of IL-31, even after adjustment for relevant covariates and correction for multiple testing. The presence of asthma modified the estimated effect of the residential distance to a major road on plasma TNF-α (P for interaction = 0.00047). Although living farther from a major road was significantly associated with lower TNF-α level in control subjects, no such decrease was seen in children with asthma. In a direct comparison of cases and control subjects, children with asthma had significantly higher levels of IL-1β, IL-22, and IL-33 than control subjects. TRAP is associated with increased levels of proinflammatory cytokines among Puerto Rican children, who belong to an ethnic group with high risk for asthma.

Characterizing near-road air pollution using local-scale emission and dispersion models and validation against in-situ measurements

Near-road concentrations of nitrogen dioxide (NO2), a known marker of traffic-related air pollution, were simulated along a busy urban corridor in Montreal, Quebec using a combination of microscopic traffic simulation, instantaneous emission modeling, and air pollution dispersion. In order to calibrate and validate the model, a data collection campaign was designed. For this purpose, measurements of NO2 were conducted mid-block along four segments of the corridor throughout a four-week campaign conducted between March and April 2015. The four segments were chosen to be consecutive and yet exhibiting variability in road configuration and built environment characteristics. Roadside NO2 measurements were also paired with on-site and fixed-station meteorological data. In addition, traffic volumes, composition, and routing decisions were collected using video-cameras located at upstream and downstream intersections. Dispersion of simulated emissions was conducted for eight time slots and under a range of meteorological conditions using three different models with vastly different dispersion algorithms (OSPM, CALINE 4, and SIRANE). The three models exhibited poor correlation with near-road NO2 concentrations and were better able to simulate average concentrations occurring along the roadways rather than the range of concentrations measured under diverse meteorological and traffic conditions. As hypothesized, the model SIRANE that can handle a street canyon configuration was the most sensitive to the built environment especially to the presence of tall buildings around the road. In contrast, CALINE exhibited the lowest sensitivity to the built environment.

Telomere Length, Long-Term Black Carbon Exposure, and Cognitive Function in a Cohort of Older Men: The VA Normative Aging Study.

Background:Long-term air pollution exposure has been associated with age-related cognitive impairment, possibly because of enhanced inflammation. Leukocytes with longer telomere length (TL) are more responsive to inflammatory stimuli, yet TL has not been evaluated in relation to air pollution and cognition.Objectives:We assessed whether TL modifies the association of 1-year exposure to black carbon (BC), a marker of traffic-related air pollution, with cognitive function in older men, and we examined whether this modification is independent of age and of C-reactive protein (CRP), a marker of inflammation.Methods:Between 1999 and 2007, we conducted 1–3 cognitive examinations of 428 older men in the Veterans Affairs (VA) Normative Aging Study. We used covariate-adjusted repeated-measure logistic regression to estimate associations of 1-year BC exposure with relative odds of being a low scorer (≤ 25) on the Mini-Mental State Examination (MMSE), which is a proxy of poor cognition. Confounders included age, CRP, and lifestyle and sociodemographic factors.Results:Each doubling in BC level was associated with 1.57 (95% CI: 1.20, 2.05) times higher odds of low MMSE scores. The BC-MMSE association was greater only among individuals with longer blood TL (5th quintile) (OR = 3.23; 95% CI: 1.37, 7.59; p = 0.04 for BC-by-TL-interaction). TL and CRP were associated neither with each other nor with MMSE. However, CRP modified the BC-MMSE relationship, with stronger associations only at higher CRP (5th quintile) and reference TL level (1st quintile) (OR = 2.68; 95% CI: 1.06, 6.79; p = 0.04 for BC-by-CRP-interaction).Conclusions:TL and CRP levels may help predict the impact of BC exposure on cognitive function in older men.Citation:Colicino E, Wilson A, Frisardi MC, Prada D, Power MC, Hoxha M, Dioni L, Spiro A III, Vokonas PS, Weisskopf MG, Schwartz JD, Baccarelli AA. 2017. Telomere length, long-term black carbon exposure, and cognitive function in a cohort of older men: the VA Normative Aging Study. Environ Health Perspect 125:76–81; http://dx.doi.org/10.1289/EHP241

Breast Cancer Risk in Relation to Ambient Air Pollution Exposure at Residences in the Sister Study Cohort.

Some but not all past studies reported associations between components of air pollution and breast cancer, namely fine particulate matter ≤2.5 μm (PM2.5) and nitrogen dioxide (NO2). It is yet unclear whether risks differ according to estrogen receptor (ER) and progesterone receptor (PR) status. This analysis includes 47,591 women from the Sister Study cohort enrolled from August 2003 to July 2009, in whom 1,749 invasive breast cancer cases arose from enrollment to January 2013. Using Cox proportional hazards and polytomous logistic regression, we estimated breast cancer risk associated with residential exposure to NO2, PM2.5, and PM10. Although breast cancer risk overall was not associated with PM2.5 [HR = 1.03; 95% confidence intervals (CI), 0.96-1.11], PM10 (HR = 0.99; 95% CI, 0.98-1.00), or NO2 (HR = 1.02; 95% CI, 0.97-1.07), the association with NO2 differed according to ER/PR subtype (P = 0.04). For an interquartile range (IQR) difference of 5.8 parts per billion (ppb) in NO2, the relative risk (RR) of ER(+)/PR(+) breast cancer was 1.10 (95% CI, 1.02-1.19), while there was no evidence of association with ER(-)/PR(-) (RR = 0.92; 95% CI, 0.77-1.09; Pinteraction = 0.04). Within the Sister Study cohort, we found no significant associations between air pollution and breast cancer risk overall. But we observed an increased risk of ER(+)/PR(+) breast cancer associated with NO2. Though these results suggest there is no substantial increased risk for breast cancer overall in relation to air pollution, NO2, a marker of traffic-related air pollution, may differentially affect ER(+)/PR(+) breast cancer.

Measurement and modelling of nitrogen dioxide (NO2) emissions: a marker for traffic-related air pollution in Doha, Qatar

In the State of Qatar, recent statistics show a continued increase in the motor-vehicle fleet commensurate with population growth and economic development. This trend, together with the rapid expansion of urban areas and the increased dependence on automobiles, has resulted in an increase in pollution near traffic sources, indicating that the risk of exposure to vehicles’ emissions is higher and that these emissions must be considered in terms of their spatial and temporal occurrence. So far, there are no studies conducted in Qatar to evaluate the traffic-related air pollution. This study is carried out to monitor the levels of nitrogen dioxide (NO2) as a marker of pollution related to traffic. The aim of this study is to build a baseline for traffic-related pollution in Qatar by monitoring and modelling NO2 emissions. The levels of traffic-related air pollution by NO2 were investigated at six major intersections along the C-ring road. The relationship of NO2 was established with traffic volume in each intersection during December 2012 and March–April 2013. Significant differences were established between the pollutant concentrations in each intersection. The CALifornia LINE Source Dispersion Model, version 4 air dispersion model employed had estimated the influence of the measured NO2 concentration on the predicted NO2 values by 31.12%. The low percentage may have accounted for the uncertainties brought by the vehicle emission factor and non-availability of temporal dynamics during the time of sampling. Non-parametric Spearman’s correlation test resulted in a significant correlation between measured and predicted values of NO2 concentrations, rs = 0.525 and p = 0.012.