Traffic-related Air Pollution Research Articles

Oxidative biomarkers of exhaled breath condensate in adults exposed to traffic-related air pollution: a case-control study

Traffic-related air pollution exposure (TRAP) is a major public health problem. The effects of TRAP exposure on the oxidative biomarkers of exhaled breath condensate (EBC) of adults are seldom studied. We compared the oxidative EBC biomarkers in a group of individuals exposed to TRAP with those of individuals unexposed to TRAP. We conducted a case-control study in Bhopal City (Madhya Pradesh, India). Adults with a history of exposure to TRAP were enrolled as cases and adults with less exposure to TRAP were used as a control. Based on respiratory symptoms and smoking habits, study subjects were stratified into six subgroups. EBC was collected by TURBO14 (Medivac SRL, Italy) at −5 °C. The EBC pH was measured after gas standardization with argon. EBC hydrogen peroxide (H2O2), cystenine leukotrienes (Cys-LTs), 8-isoprostane were measured by commercial ELISA kit. A total of 250 consecutive adult (male: 194) subjects were recruited. Among them, 133 were TRAP-exposed (male: 128) and 117 were non-TRAP-exposed (male: 66). The respiratory symptoms between TRAP-exposed and non-TRAP-exposed subjects were not different. The post-gas standardized EBC pH (median: 7.72; interquartile range (IQR): 7.15–7.94 vs. median: 7.60, IQR: 6.72–7.87; p = 0.09) and EBC H2O2 (median: 2.20 µmol l−1; IQR: 1.46–3.51 vs. median: 1.99, IQR: 1.41–3.10; p = 0.29) in TRAP-exposed subjects were statistically not different from the non-TRAP-exposed subjects. The EBC Cys-LTs (median: 69.81; IQR: 57.0–83.38 vs. median: 47.21 pg ml−1; IQR: 39.90–54.87, p < 0.001) and EBC 8-isoprostane (median: 12.55 pg ml−1; IQR: 5.51–18.09 vs. median: 7.12; IQR: 4.60–16.04, p = 0.026) in TRAP-exposed subjects were higher compared to those in non-TRAP-exposed subjects. The subgroup analysis showed that TRAP-exposed subjects, irrespective of their smoking habits and respiratory symptoms, had higher EBC Cys-LTs compared to the non-TRAP-exposed subjects. TRAP exposure increases oxidative biomarkers of the EBC in adults.

Land-Use Regression of Long-Term Transportation Data on Metabolic Syndrome Risk Factors in Low-Income Communities

Traffic-related air pollution has been associated with adverse cardiovascular health effects in near-road residents. Transportation parameters are important surrogate variables to determine spatial variation of air pollution and consequential health outcomes. We used land-use regression models to explore associations between cardiovascular (metabolic syndrome [MetS]) health outcomes collected from a sample of low-income participants ( N = 4,959) and transportation parameters within a defined impact zone of a participant’s residence. We hypothesize cardiovascular risk factors are associated with spatially distributed transportation parameters and land-use data. MetS risk factors (waist circumference, blood pressure, triglycerides, HDL-cholesterol, and glucose) were obtained from 4,945 participants between 2014 and 2020 across the city of El Paso, Texas. Traffic-related and land-use variables were acquired from the El Paso MPO and the U.S. Census Bureau within two impact zones of 500 m and 1,000 m radius, centered at each participant resident’s home latitude and longitude coordinates using GIS. The increase in street length within 500 m radius was found to associate with increases in BMI, waist circumference, triglycerides, and glucose ( p &lt; 0.05). Glucose showed positive relationships with inverse distance to the nearest international ports of entry ( p = 0.02). Also, as the total length of the street increases, the likelihood of a high waist ( p &lt; 0.01), high triglycerides ( p = 0.03), and low HDL-cholesterol ( p &lt; 0.01) also increased. Based on a multivariable regression model, a probability surface map was prepared to show the spatial distribution of likelihood for acquiring MetS in El Paso, TX.

Assessment and mitigation of toddlers’ personal exposure to black carbon before and during the COVID-19 pandemic: A case study in Singapore

Black carbon (BC), an important indicator of traffic-related air pollution (TRAP) in urban environments, is receiving increased attention because of its adverse health effects. Personal exposure (PE) of adults to BC has been widely studied, but little is known about the exposure of young children (toddlers) to BC in cities. We carried out a pilot study to investigate the integrated daily PE of toddlers to BC in a city-state with a high population density (Singapore). We studied the impact of urban traffic on the PE of toddlers to BC by comparing and contrasting on-road traffic flow (i.e., volume and composition) in Singapore in 2019 (before the COVID-19 pandemic) and in 2020 (during the COVID-19 pandemic). Our observations indicate that the daily BC exposure levels and inhaled doses increased by about 25% in 2020 (2.9 ± 0.3 μg m−3 and 35.5 μg day−1) compared to that in 2019 (2.3 ± 0.4 μg m−3 and 28.5 μg day−1 for exposure concentration and inhaled dose, respectively). The increased BC levels were associated with the increased traffic volume on both weekdays and weekends in 2020 compared to the same time period in 2019. Specifically, we observed an increase in the number of trucks as well as cars/taxis and motorcycles (private transport) and a decline in the number of buses (public transport) in 2020. The implementation of lockdown measures in 2020 resulted in significant changes in the time, place and duration of PE of toddlers to BC. The recorded daily time-activity patterns indicated that toddlers spent almost all the time in indoor environments during the measurement period in 2020. When we compared different ventilation options (natural ventilation (NV), air conditioning (AC), and portable air cleaner (PAC)) for mitigation of PE to BC in the home environment, we found a significant decrease (>30%) in daily BC exposure levels while using the PAC compared to the NV scenario. Our case study shows that the PE of toddlers to BC is of health concern in indoor environments in 2020 because of the migration of the increased TRAP into naturally ventilated residential homes and more time spent indoors than outdoors. Since toddlers’ immune system is weak, technological intervention is necessary to protect their health against inhalation exposure to air pollutants.

Spatiotemporal analysis of pedestrian exposure to submicron and coarse particulate matter on crosswalk at urban intersection

At the crosswalk of urban traffic intersections, vehicles frequently stop with their engines idling adjacent to it during the red-light period and accelerate with intensified emissions during the green-light period. As a result, pedestrians are inevitably at a higher risk of exposure to near-source traffic-related air pollution while walking on the crosswalk or waiting on the roadside. Therefore, this study focuses on pedestrian exposure to particulate matter on the crosswalk at urban intersections. Firstly, mobile measurements at varied locations of the crosswalk were carried out to reveal the spatial difference of particles on the whole crosswalk. The results show that the concentrations of submicron and coarse particles are higher on the parking crosswalk than that on the non-parking crosswalk. Secondly, mobile measurements at varied heights of crosswalk were carried out to discover the vertical difference of particles on the crosswalk. Particulate concentration is higher at the height of 1.5 m than that at 0.5 m. Thirdly, fixed-site measurements were conducted on the roadside to make a comparison with the crosswalk. Particulate concentration is found to be nearly 6% higher on the crosswalk than that on the roadside. Finally, pedestrian exposure to particulate matter in varied trips on the crosswalk is investigated and the exposure in trips with a 10s–20s delay after the onset of a walk signal is lower than that in other situations. The results can help fully recognize the particulate pollution at intersections and better understand the particulate exposure of pedestrians on crosswalk at urban intersections.

Commuting by car, public transport, and bike: Exposure assessment and estimation of the inhaled dose of multiple airborne pollutants

It is known that air pollution affects human health and commuting environments are significant contributors to the total daily personal exposure to air pollution. With this study we aim at assessing and comparing personal exposure to traffic-related air pollution and related estimated inhaled dose of different typical commuter profiles in real-world scenarios focusing on multimodal commuting and different transport microenvironments. A car driver and two multimodal commuters (cyclist/public transport and pedestrian/public transport commuters), which reached the same destination in the city center, leaving from the same starting point in the metropolitan area of the city, were investigated in the metropolitan area of Milan, Italy. Real-time monitors for the measurement of size-fractionated particulate matter (PM - Aerocet 831-Met One Instrument Inc., Grant Pass, Oregon, USA), equivalent Black Carbon (eBC - Aethlabs, San Francisco, CA, USA), and NO2 (CairClip NO2, Cairpol; La Roche Blanche, France) and time-integrated samplers for the measurement of NO2 and benzene were used. Inhaled dose was estimated as well by applying estimated pulmonary ventilation rates to 1-min exposure measures. The Bootstrapping method was used to resample data and perform more robust comparisons among commuters and microenvironments (MEs). Results of the study could be summarized as follows: (i) travel times of the cyclist were the shortest; (ii) the highest concentrations and estimated inhaled doses were found during morning rush hour; (iii) the cyclist and the car commuter were exposed to the highest overall median values of fractionated PM and benzene, respectively; (iv) cycling MEs presented the highest median concentrations of PM, while the overall median concentration of eBC was higher commuting by car than walking and cycling; (v) the cyclist was the commuter with the highest overall median estimated inhaled dose for fractionated PM, while benzene was the highest for the car driver, and NO2 for the pedestrian; (vi) exposure differences both among microenvironments and commuters diverged comparing morning and evening commuting. Our results suggest that a multi-pollutant approach is necessary to better represent the complexity of personal exposure to traffic-related air pollution in multimodal mobility studies. Moreover, shifting from car driving to multimodal mobility is already a valuable choice for the metropolitan area of Milan considering both exposure and commuting time. However, to further reduce personal exposure and especially estimated inhaled dose of multimodal and active commuters, exposure mitigation interventions in selected MEs, traffic calming, and innovative mobility policies are still needed.

Particulate matter pollution at traffic hotspots of Accra, Ghana: levels, exposure experiences of street traders, and associated respiratory and cardiovascular symptoms.

There are limited studies on the health effects of street trading in spite of common knowledge that individuals engaged in the trade are exposed to high levels of traffic-related air pollution per their mode of operation, and also the fact that the venture is a dominant occupation in cities of Sub-Saharan Africa (SSA) and other developing regions. We characterized particulate matter (PM) pollution levels at traffic hotspots of Accra, Ghana during the dry and wet seasons, and assessed exposure experiences of street traders. A cross-sectional study was conducted among 236 street traders operating along six selected traffic routes of Accra and a comparison group of 186 office workers. PurpleAir PA-II monitors were used to measure PM levels at the selected traffic routes. We estimated annual PM2.5 exposure of street traders using assigned seasonal PM2.5 levels, and information collected in a structured questionnaire on their activity patterns. Outcomes investigated were self-reported respiratory and cardiovascular symptoms. PM levels at Accra traffic hotspots were high in both seasons. 1 ug/m3 increase in PM2.5 exposure increased respiratory, cardiovascular, and overall symptoms by a factor of 0.00027 (95% CI: 0.00012, 0.00041), 0.00022 (95% CI: 0.00007, 0.00036), and 0.00048 (95% CI: 0.00023, 0.00073), respectively. Compared to office workers, high PM2.5 exposure among street traders was associated with increased odds of coughing, catarrh (postnasal drip), sneezing, rapid heart beating, irregular heartbeat, sharp chest pains, fainting spells, headaches, and dizziness. Low and medium PM2.5 exposure was associated with increased odds of dermatitis, rapid heart beating, and irregular heartbeat, and sharp chest pains, respectively. We found consistent evidence that PM2.5 exposure among street traders increases the occurrence of respiratory and cardiovascular symptoms. We also provide indicative measurements of PM levels at traffic hotspots of a rapidly growing SSA city with heavy vehicular traffic and yet, limited air quality monitoring capacity.

Acute cardiovascular effects of traffic-related air pollution (TRAP) exposure in healthy adults: A randomized, blinded, crossover intervention study

Exposure to traffic-related air pollution (TRAP) may enhance the risk of cardiovascular disease. However, the short-term effects of TRAP components on the cardiovascular system are not well understood. We conducted a randomized, double-blinded, crossover intervention study in which 39 healthy university students spent 2 h next to a busy road. Participants wore a powered air-purifying respirator (PAPR) or an N95 mask. PAPRs were equipped with a filter for particulate matter (PM), a PM and volatile organic compounds (VOCs) filter or a sham filter. Participants were blinded to PAPR filter type and underwent randomized exposures four times, once for each intervention mode. Blood pressure (BP), heart rate (HR) and heart rate variability (HRV) were measured before, during and for 6 h after the roadside exposure. Linear mixed-effect models were used to evaluate the effects of the interventions relative to baseline controlling for other covariates. All HRV measures increased during and following exposure for all intervention modes. Some HRV measures (SDNN and rMSSD during exposure and SDNN after exposure) were marginally affected by PM filtration. Wearing the N95 mask affected VLF power and rMSSD responses to traffic exposure differently than the PAPR interventions. Both systolic and diastolic BP increased slightly during exposure, but then were generally lower than baseline after exposure for the sham and filter interventions. HR, which fell during exposure and mostly remained lower than baseline after exposure, was lower yet with all filter interventions compared to the sham mode following exposure. Therefore, short-term exposure to traffic acutely affects HRV, BP and HR, but N95 mask and PAPR interventions generally show little efficacy in reducing these effects. Removing the PM component of TRAP has some limited effects on HRV responses to exposure but exaggerates the traffic-related decrease in HR. HRV findings from N95 mask interventions need to be interpreted cautiously.

Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage.

Relatively little is known about the transgenerational effects of chronic maternal exposure to low-level traffic-related air pollution (TRAP) on the offspring lung health, nor are the effects of removing such exposure before pregnancy. Female BALB/c mice were exposed to PM2.5 (PM2.5, 5 µg/day) for 6 weeks before mating and during gestation and lactation; in a subgroup, PM was removed when mating started to model mothers moving to cleaner areas during pregnancy to protect their unborn child (Pre-exposure). Lung pathology was characterised in both dams and offspring. A subcohort of female offspring was also exposed to ovalbumin to model allergic airways disease. PM2.5 and Pre-exposure dams exhibited airways hyper-responsiveness (AHR) with mucus hypersecretion, increased mitochondrial reactive oxygen species (ROS) and mitochondrial dysfunction in the lungs. Female offspring from PM2.5 and Pre-exposure dams displayed AHR with increased lung inflammation and mitochondrial ROS production, while males only displayed increased lung inflammation. After the ovalbumin challenge, AHR was increased in female offspring from PM2.5 dams compared with those from control dams. Using an in vitro model, the mitochondria-targeted antioxidant MitoQ reversed mitochondrial dysfunction by PM stimulation, suggesting that the lung pathology in offspring is driven by dysfunctional mitochondria. In conclusion, chronic exposure to low doses of PM2.5 exerted transgenerational impairment on lung health.

Prolonged exposure to traffic-related particulate matter and gaseous pollutants implicate distinct molecular mechanisms of lung injury in rats

BackgroundExposure to air pollution exerts direct effects on respiratory organs; however, molecular alterations underlying air pollution-induced pulmonary injury remain unclear. In this study, we investigated the effect of air pollution on the lung tissues of Sprague-Dawley rats with whole-body exposure to traffic-related PM1 (particulate matter < 1 μm in aerodynamic diameter) pollutants and compared it with that in rats exposed to high-efficiency particulate air–filtered gaseous pollutants and clean air controls for 3 and 6 months. Lung function and histological examinations were performed along with quantitative proteomics analysis and functional validation.ResultsRats in the 6-month PM1-exposed group exhibited a significant decline in lung function, as determined by decreased FEF25–75% and FEV20/FVC; however, histological analysis revealed earlier lung damage, as evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2673 proteins that highlighted the differential dysregulation of proteins involved in oxidative stress, cellular metabolism, calcium signalling, inflammatory responses, and actin dynamics under exposures to PM1 and gaseous pollutants. The presence of PM1 specifically enhanced oxidative stress and inflammatory reactions under subchronic exposure to traffic-related PM1 and suppressed glucose metabolism and actin cytoskeleton signalling. These factors might lead to repair failure and thus to lung function decline after chronic exposure to traffic-related PM1. A detailed pathogenic mechanism was proposed to depict temporal and dynamic molecular regulations associated with PM1- and gaseous pollutants-induced lung injury.ConclusionThis study explored several potential molecular features associated with early lung damage in response to traffic-related air pollution, which might be used to screen individuals more susceptible to air pollution.

Exposure to traffic-related air pollution and bacterial diversity in the lower respiratory tract of children.

BackgroundExposure to particulate matter has been shown to increase the adhesion of bacteria to human airway epithelial cells. However, the impact of traffic-related air pollution (TRAP) on the respiratory microbiome is unknown.MethodsForty children were recruited through the Cincinnati Childhood Allergy and Air Pollution Study, a longitudinal cohort followed from birth through early adolescence. Saliva and induced sputum were collected at age 14 years. Exposure to TRAP was characterized from birth through the time of sample collection using a previously validated land-use regression model. Sequencing of the bacterial 16S and ITS fungal rRNA genes was performed on sputum and saliva samples. The relative abundance of bacterial taxa and diversity indices were compared in children with exposure to high and low TRAP. We also used multiple linear regression to assess the effect of TRAP exposure, gender, asthma status, and socioeconomic status on the alpha diversity of bacteria in sputum.ResultsWe observed higher bacterial alpha diversity indices in sputum than in saliva. The diversity indices for bacteria were greater in the high TRAP exposure group than the low exposure group. These differences remained after adjusting for asthma status, gender, and mother’s education. No differences were observed in the fungal microbiome between TRAP exposure groups.ConclusionOur findings indicate that exposure to TRAP in early childhood and adolescence may be associated with greater bacterial diversity in the lower respiratory tract. Asthma status does not appear to confound the observed differences in diversity. These results demonstrate that there may be a TRAP-exposure related change in the lower respiratory microbiota that is independent of asthma status.

Prenatal exposure to traffic-related air pollution and glucose homeostasis: A cross-sectional study

Air pollution exposure has been linked with glucose dysregulation in pregnant women; however, evidence on these associations with fetal glucose homeostasis is unclear yet. We therefore aimed to evaluate the association of prenatal exposure to particulate matter (PM) and traffic indicators with fetal glucose homeostasis in cord blood samples. A total of 169 mother-infant pairs recruited from Mobini hospital of Sabzevar, Iran, were included in this cross-sectional study. Maternal exposure to PMs was estimated using land use regression models. Moreover, traffic indicators (i.e., total street length in 100, 300 and 500 m buffers and distance from residential home to the nearest major roads) were calculated based on the street map of Sabzevar. Cord blood glucose and insulin concentrations, HOMA-ꞵ, HOMA-S and HOMA-IR were used as glucose homeostasis markers. Higher maternal exposure to PM2.5 and PM10 were associated with higher cord blood glucose and insulin concentrations and HOMA-IR. Moreover, total streets length in 300 m buffer was positively associated with cord blood glucose and insulin concentrations and HOMA-IR. An increase in distance to major roads was associated with higher HOMA-ꞵ and HOMA-S and lower cord blood glucose and insulin concentrations as well as HOMA-IR. Overall, we found prenatal exposure to PMs and traffic indicators was associated with a higher risk of glucose homeostasis dysregulation in the fetus.

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

IntroductionCommuting exposes millions of people to carcinogens from traffic-related air pollution (TRAP) but is seldomly considered in epidemiologic studies of lung cancer. In the prospective United Kingdom (UK) Biobank cohort study, we investigated associations between commute patterns, residential nitrogen dioxide concentrations (NO2; a surrogate for TRAP), and lung cancer risk. MethodsWe analyzed 234,124 employed participants at baseline (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: 1–4, often: ≥5 work-bound trips/week). Annual average residential NO2 concentrations in 2005–2007 were estimated with land use regression. Multivariable Cox regression was used to estimate associations between commute patterns, NO2 quartiles, and incident lung cancer. We conducted analyses stratified by NO2 (>, ≤median = 28.3 µg/m3) and potential confounders such as sex and smoking. ResultsCompared to regular automobile use, commuting often by public transportation was associated with increased lung cancer risk (hazard ratio (HR) = 1.58, 95% confidence intervals (CI):1.08–2.33). Additionally, we found a positive exposure–response relationship with residential NO2 (HRQ2 = 1.21, 95 %CI: 0.90–1.62; HRQ3 = 1.48, 95 %CI: 1.10–1.99; HRQ4 = 1.58, 95 %CI: 1.13–2.23; p-trend = 3.1 × 10−3).The public transportation association was observed among those with higher NO2 (p-interaction = 0.02). Other commute categories were not associated with risk. ConclusionsCommuters residing in high-NO2 areas who often use public transportation could have elevated lung cancer risk compared to regular automobile users. These results warrant investigations into which component(s) of public transportation contribute to the observed association with increased lung cancer risk.

Source Apportionment and Toxicity of PM in Urban, Sub-Urban, and Rural Air Quality Network Stations in Catalonia

Air quality indicators, i.e., PM10, NO2, O3, benzo[a]pyrene, and several organic tracer compounds were evaluated in an urban traffic station, a sub-urban background station, and a rural background station of the air quality network in Catalonia (Spain) from summer to winter 2019. The main sources that contribute to the organic aerosol and PM toxicity were determined. Traffic-related air pollution dominated the air quality in the urban traffic station, while biomass burning in winter and secondary organic aerosol (SOA) in summer impact the air quality in the sub-urban and rural background stations. Health risk assessment for chronic exposure over the past decade, using WHO air quality standards, showed that NO2, PM10 and benzo[a]pyrene from traffic emissions pose an unacceptable risk to the human population in the urban traffic station. PM10 and benzo[a]pyrene from biomass burning were unacceptably high in the sub-urban and rural background stations. Toxicity tests of the PM extracts with epithelial lung cells showed higher toxicity in wintertime samples in the sub-urban and rural stations, compared to the urban traffic station. These results require different mitigation strategies for urban and rural sites in order to improve the air quality. In urban areas, traffic emissions are still dominating the air quality, despite improvements in the last years, and may directly be responsible for part of the SOA and O3 levels in sub-urban and rural areas. In these later areas, air pollution from local biomass burning emissions are dominating the air quality, essentially in the colder period of the year.

Early postnatal exposure to traffic-related air pollution and asthma in adolescents: vulnerability factors in the PARIS birth cohort

BackgroundAssociations between early traffic-related air pollution (TRAP) exposure and respiratory and allergic morbidity in adolescents are inconsistent. However, sub-groups might be more vulnerable to the health effects of this exposure. ObjectivesWe investigated associations between early exposure to TRAP and respiratory and allergic morbidity at age 13 years in the PARIS birth cohort, and potential modifying effects of sex, parental allergy, stressful family event and lower respiratory tract infections (LRTI). MethodsThis study deals with data from 732 children of the PARIS birth cohort followed up using repeated questionnaires until 13 years of age. Prenatal TRAP exposure was assessed by measuring daily concentrations of nitrogen dioxide at the nearest station to mother's home. Early postnatal TRAP exposure was calculated for each child during the first year of life by a nitrogen oxides (NOx) air dispersion model taking into account both residence and daycare. Associations between TRAP exposures and asthma, rhinitis and related symptoms were assessed using multivariable logistic regression models adjusted for potential confounding factors. Effect modification was explored by testing multiplicative interactions. ResultsAn increase in interquartile range (17.0 μg/m3) of early postnatal NOx exposure was positively related to current asthma (adjusted odds ratio aOR = 1.21; 95% confidence interval CI: 1.02, 1.43), severe wheeze (aOR = 1.23; 95% CI: 1.02, 1.47) and persistent asthma at 13 years old (aOR = 1.26; 95% CI: 1.03, 1.55) and tended to be associated with asthma ever. Parental history of allergy, asthma, early stressful family event and LRTI modified these associations with TRAP exposure. No relationship with rhinitis was found. Prenatal TRAP exposure did not show any association with respiratory and allergic morbidity. DiscussionThis study is one of the first to show several modifiers of the association between early postnatal TRAP exposure and asthma at adolescence. Not all adolescents seem equally affected by early postnatal TRAP exposure: those presenting parental history of allergy, especially asthma, those with early stressful family event or LRTI appear to be more vulnerable.

Assessing the Impact of Wildfires on the Use of Black Carbon as an Indicator of Traffic Exposures in Environmental Epidemiology Studies.

Epidemiological studies frequently use black carbon (BC) as a proxy for traffic‐related air pollution (TRAP). However, wildfire smoke (WFS) represents an important source of BC not often considered when using BC as a proxy for TRAP. Here, we examined the potential for WFS to bias TRAP exposure assessments based on BC measurements. Weekly integrated BC samples were collected across the Denver, CO region from May to November 2018. We collected 609 filters during our sampling campaigns, 35% of which were WFS‐impacted. For each filter we calculated an average BC concentration. We assessed three GIS‐based indicators of TRAP for each sampling location: annual average daily traffic within a 300 m buffer, the minimum distance to a highway, and the sum of the lengths of roadways within 300 m. Median BC concentrations were 9% higher for WFS‐impacted filters (median = 1.14 μg/m3, IQR = 0.23 μg/m3) than nonimpacted filters (median = 1.04 μg/m3, IQR = 0.48 μg/m3). During WFS events, BC concentrations were elevated and expected spatial gradients in BC were reduced. We conducted a simulation study to estimate TRAP exposure misclassification as the result of regional WFS. Our results suggest that linear health effect estimates were biased away from the null when WFS was present. Thus, exposure assessments relying on BC as a proxy for TRAP may be biased by wildfire events. Alternative metrics that account for the influence of “brown” carbon associated with biomass burning may better isolate the effects of traffic emissions from those of other black carbon sources.

Commuter types identified using clustering and their associations with source-specific PM2.5

Traffic-related fine particulate matter air pollution (tr-PM2.5) has been associated with adverse health outcomes such as cardiopulmonary morbidity and mortality, with in-vehicle tr-PM2.5 exposure contributing to total personal pollution exposure. Trip characteristics, including time of day, day of the week, and traffic congestion, are associated with in-vehicle PM2.5 exposures. We hypothesized that some commuter characteristics, such as whether commuters travel primarily during rush hour, would also be associated with increased tr-PM2.5 exposures. The commute data consisted of unscripted personal vehicle trips of 46 commuters in the Washington, D.C. metro area over 48-h, with a total of 320 trips. We identified commuter types using sparse K-means clustering, which identifies the hours throughout the day important for clustering commuters. Source-specific PM2.5 over 48 h was estimated using Positive Matrix Factorization. Linear regression was used to estimate differences in source-specific PM2.5 by commuter cluster. Two commuter clusters were identified using the clustering approach: rush hour commuters, who primarily travelled during rush hour, and sporadic commuters, who travelled throughout the day. The hours given the largest weights by sparse K-means were 7–8 a.m. and 6–7 p.m., corresponding to peak travel times. Integrated black carbon (BC) was higher for rush hour commuters (median = 3.1 μg/m3 (IQR = 1.5)) compared to sporadic commuters (2.0 μg/m3 (IQR = 1.9)). Mobile PM2.5, consisting primarily of tailpipe emissions and brake/tire wear, was also higher for rush hour commuters (2.9 μg/m3 (IQR = 1.6)) compared to sporadic commuters (2.1 μg/m3 (IQR = 2.4)), though this difference was not statistically significant in regression models. Estimated differences between commuter types for secondary/mixed PM2.5 and road salt PM2.5 were smaller. Further research may elucidate whether commuter characteristics are an efficient way to identify individuals with highest tr-PM2.5 exposures associated with commuting and to develop effective mitigation strategies.

Scalable penalized spatiotemporal land-use regression for ground-level nitrogen dioxide.

Nitrogen dioxide (NO2) is a primary constituent of traffic-related air pollution and has well established harmful environmental and human-health impacts. Knowledge of the spatiotemporal distribution of NO2 is critical for exposure and risk assessment. A common approach for assessing air pollution exposure is linear regression involving spatially referenced covariates, known as land-use regression (LUR). We develop a scalable approach for simultaneous variable selection and estimation of LUR models with spatiotemporally correlated errors, by combining a general-Vecchia Gaussian-process approximation with a penalty on the LUR coefficients. In comparisons to existing methods using simulated data, our approach resulted in higher model-selection specificity and sensitivity and in better prediction in terms of calibration and sharpness, for a wide range of relevant settings. In our spatiotemporal analysis of daily, US-wide, ground-level NO2 data, our approach was more accurate, and produced a sparser and more interpretable model. Our daily predictions elucidate spatiotemporal patterns of NO2 concentrations across the United States, including significant variations between cities and intra-urban variation. Thus, our predictions will be useful for epidemiological and risk-assessment studies seeking daily, national-scale predictions, and they can be used in acute-outcome health-risk assessments.

Hyper-localized measures of air pollution and risk of preterm birth in Oakland and San Jose, California.

US preterm-birth rates are 1.6 times higher for Black mothers than for White mothers. Although traffic-related air pollution (TRAP) may increase the risk of preterm birth, evaluating its effect on preterm birth and disparities has been challenging because TRAP is often measured inaccurately. This study sought to estimate the effect of TRAP exposure, measured at the street level, on the prevalence of preterm birth by race/ethnicity. We linked birth-registry data with TRAP measured at the street level for singleton births in sampled communities during 2013-2015 in Oakland and San Jose, California. Using logistic regression and marginal standardization, we estimated the effects of exposure to black carbon, nitrogen dioxide and ultrafine particles on preterm birth after confounder adjustment and stratification by race/ethnicity. There were 8823 singleton births, of which 760 (8.6%) were preterm. Shifting black-carbon exposure from the 10th to the 90th percentile was associated with: 6.8%age point higher risk of preterm birth (95% confidence interval = 0.1 to 13.5) among Black women; 2.1%age point higher risk (95% confidence interval = -1.1 to 5.2) among Latinas; and inconclusive null findings among Asian and White women. For Latinas, there was evidence of a positive association between the other pollutants and risk of preterm birth, although effect sizes were attenuated in models that co-adjusted for other TRAP. Exposure to TRAP, especially black carbon, may increase the risk of preterm birth for Latina and Black women but not for Asian and White women.

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.

Breast cancer risk in relation to ambient concentrations of nitrogen dioxide and particulate matter: results of a population-based case-control study corrected for potential selection bias (the CECILE study)

BackgroundThere is only scant evidence that air pollution increases the risk of breast cancer. ObjectivesWe investigated this relationship for three air pollutants: nitrogen dioxide (NO2) and particulate matter with an aerodynamical diameter below 10 µm (PM10) and 2.5 µm (PM2.5). MethodsWe conducted a population-based case-control study on breast cancer in two French départements, including 1,229 women diagnosed with breast cancer in 2005–2007 and 1,316 control women frequency-matched on age. Concentrations of NO2, PM10 and PM2.5 at participants’ addresses occupied during the last 10 years were assessed using a chemistry transport model. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using multivariable logistic regression models where each woman was assigned a weight depending on her probability of selection into the study. ResultsThe OR for breast cancer per 10-µg/m3 increase in NO2 was 1.11 (95% CI, 0.98, 1.26), and 1.41 (95% CI 1.07, 1.86) in the highest exposure quintile (Q5), compared to the first. The ORs per 10-µg/m3 NO2 did not markedly differ between pre- (OR 1.09, 95% CI 0.89, 1.35)) and post-menopausal women (OR 1.14, 95% CI 0.97, 1.33)), but the OR was substantially higher for hormone-receptor positive (ER+/PR+) breast tumor subtypes (OR 1.15, 95% CI 1.00, 1.31) than for ER–/PR– tumors (OR 0.95, 95% CI 0.72, 1.26). Breast cancer risk was not associated with either PM10 (OR per 1 µg/m3 1.01, 95% CI, 0.96, 1.06) or PM2.5 (OR per 1 µg/m3 1.02, 95% CI 0.95, 1.08), regardless of the menopausal status or of the breast tumor subtype. DiscussionOur study provides evidence that NO2 exposure, a marker of traffic-related air pollutants, may be associated with an increased risk of breast cancer, particularly ER+/PR+ tumors.