Effects Of Traffic-related Air Pollution Research Articles

Measurement of black carbon exposure in urban classrooms during rush hours

Traffic-related air pollutants are predominantly emitted in urban environments; therefore, analyzing their impact on indoor air quality (IAQ) is important. Effectively managing IAQ is vital, given the extensive duration individuals, particularly students, spend indoors. This study conducted a quantitative assessment of black carbon (BC) and indoor and outdoor particulate matter (PM2.5, particles with diameter ≤2.5 μm) concentrations in five South Korean classrooms to determine the root cause and effects of traffic-related air pollutants on indoor environments. The research specifically focused on indoor BC levels during rush hours, that is, periods marked by increased traffic volume. The analysis revealed that the mean indoor and outdoor BC concentrations in the five classrooms were measured at 1.03 (95% CI: 0.69, 1.36) and 1.38 (95% CI: 0.79, 1.96) μg/m3, respectively, while the mean PM2.5 concentrations were measured at 17.07 (95% CI: 12.92, 13.62) and 29.89 (95% CI: 10.88, 48.89) μg/m3, respectively. The indoor-to-outdoor (I/O) ratio of BC in the five classrooms during the occupied period was 0.77 (95% CI: 0.69, 0.84) and 0.62 (95% CI: 0.51, 0.72) for PM2.5. During the unoccupied period, the I/O ratio of BC was 0.68 (95% CI: 0.63, 0.72) and 0.53 (95% CI: 0.42, 0.63) for PM2.5. The rise in urban traffic increased the BC outdoor level by 47% and the PM2.5 concentration by 13%. Classrooms situated closer to roadways had higher BC levels than those located at a greater distance. During rush hours, the BC concentration in the classroom closest to the major road was 2.03 (95% CI: 1.78, 2.27) μg/m3, while the furthest classroom recorded a concentration of 0.88 (95% CI: 0.79, 0.96) μg/m3. During commuting times, classroom BC concentrations increased by up to 5.86 μg/m3 owing to student door-opening activities, increasing the I/O ratio by approximately 20%. Consequently, the average BC concentration in classrooms during rush hours was approximately double that recorded during non-rush hours (0.73 μg/m3). These findings are instrumental in developing strategies to enhance IAQ in educational settings and guiding urban planning decisions regarding the location of schools.

Diesel exhaust exposure induced squamous metaplasia of corneal epithelium via yes-associated protein activation

Atmospheric pollution has been demonstrated to be associated with ocular surface diseases characterized by corneal epithelial damage, including impaired barrier function and squamous metaplasia. However, the specific mechanisms underlying the impact of atmospheric pollution on corneal damage are still unknow. To address this gap in knowledge, we conducted a study using a whole-body exposure system to investigate the detrimental effects of traffic-related air pollution, specifically diesel exhaust (DE), on corneal epithelium in C57BL/6 mice over a 28-day period. Following DE exposure, the pathological alterations in corneal epithelium, including significant increase in corneal thickness and epithelial stratification, were observed in mice. Additionally, exposure to DE was also shown to disrupt the barrier functions of corneal epithelium, leading to excessive proliferation of basal cells and even causing squamous metaplasia in corneal epithelium. Further studies have found that the activation of yes-associated protein (YAP), characterized by nuclear translocation, may play a significant role in DE-induced corneal squamous metaplasia. In vitro assays confirmed that DE exposure triggered the YAP/β-catenin pathway, resulting in squamous metaplasia and destruction of barrier functions. These findings provide the preliminary evidence that YAP activation is one of the mechanisms of the damage to corneal epithelium caused by traffic-related air pollution. These findings contribute to the knowledge base for promoting eye health in the context of atmospheric pollution.

Joint effects of traffic-related air pollution and hypertensive disorders of pregnancy on maternal postpartum depressive and anxiety symptoms.

Ambient air pollution has been linked to postpartum depression. However, few studies have investigated the effects of traffic-related NOx on postpartum depression and whether any pregnancy-related factors might increase susceptibility. To evaluate the association between traffic-related NOx and postpartum depressive and anxiety symptoms, and effect modification by pregnancy-related hypertension. This study included 453 predominantly low-income Hispanic/Latina women in the MADRES cohort. Daily traffic-related NOx concentrations by road class were estimated using the California LINE-source dispersion model (CALINE4) at participants' residential locations and averaged across pregnancy. Postpartum depressive and anxiety symptoms were evaluated by a validated questionnaire (Postpartum Distress Measure, PDM) at 1, 3, 6 and 12 months postpartum. Multivariate linear regressions were performed to estimate the associations at each timepoint. Interaction terms were added to the linear models to assess effect modification by hypertensive disorders of pregnancy (HDPs). Repeated measurement analyses were conducted by using mixed effect models. We found prenatal traffic-related NOx was associated with increased PDM scores. Specifically, mothers exposed to an IQR (0.22 ppb) increase in NOx from major roads had 3.78% (95% CI: 0.53-7.14%) and 5.27% (95% CI: 0.33-10.45%) significantly higher 3-month and 12-month PDM scores, respectively. Similarly, in repeated measurement analyses, higher NOx from major roads was associated with 3.06% (95% CI: 0.43-5.76%) significantly higher PDM scores across the first year postpartum. Effect modification by HDPs was observed: higher freeway/highway and total NOx among mothers with HDPs were associated with significantly higher PDM scores at 12 months postpartum compared to those without HDPs. This study shows that prenatal traffic-related air pollution was associated with postpartum depressive and anxiety symptoms. The study also found novel evidence of greater susceptibility among women with HDPs, which advances the understanding of the relationships between air pollution, maternal cardiometabolic health during pregnancy and postpartum mental health. Our study has potential implications for clinical intervention to mitigate the effects of traffic-related pollution on postpartum mental health disorders. The findings can also offer valuable insights into urban planning strategies concerning the implementation of emission control measures and the creation of green spaces.

A neuro-fuzzy model to predict respiratory disease hospitalizations arising from the effects of traffic-related air pollution in São Paulo

A neuro-fuzzy model to predict respiratory disease hospitalizations arising from the effects of traffic-related air pollution in São Paulo

Different Impacts of Traffic-Related Air Pollution on Early-Onset and Late-Onset Asthma.

Early-onset asthma (EOA) and late-onset asthma (LOA) are two distinct phenotypes. Air pollution has been associated with an increase in poorer asthma outcomes. The objective of this study was to examine the effects of traffic-related air pollution (TRAP) on asthma outcomes in EOA and LOA patients. A cross-sectional study was conducted on 675 asthma patients (LOA: 415) recruited from a major medical center in Taiwan. The land-use regression (LUR) model was used to estimate the level of exposure to PM10, PM2.5, NO2, and O3 on an individual level. We investigated the association between TRAP and asthma outcomes in EOA and LOA patients, stratified by allergic sensitization status, using a regression approach. An increase in PM10 was associated with younger age of onset, increased asthma duration, and decreased lung function in EOA patients (p<0.05). An increase in PM10 was associated with older age of onset, and decreased asthma duration, eosinophil count, and Asthma Control Test (ACT) score in LOA patients. An increase in PM2.5 was associated with younger age of onset, increased asthma duration, decreased eosinophil count, and lung function in EOA patients (p<0.05). An increase in PM2.5 was associated with decreased lung function and ACT score in LOA patients. An increase in NO2 was associated with increased eosinophil count and decreased lung function in EOA patients (p<0.05). An increase in O3 was associated with decreased lung function in LOA patients (p<0.05). In addition, associations of TRAP with age of onset and eosinophil counts were mainly observed in both EOA and LOA patients with allergic sensitization, and an association with ACT was mainly observed in LOA patients without allergic sensitization. The impact of TRAP on age of onset, eosinophil count, and lung function in EOA patients, and ACT in LOA patients, was affected by the status of allergic sensitization.

Associations between traffic-related air pollution and allergic rhinitis outpatient visits in three cities of Gansu Province.

Emerging evidence indicates an increasing prevalence of allergic rhinitis (AR), potentially linked to air quality. The aim of the present study was to assess the relationship between traffic-related air pollutants (TRAPs) and outpatient visits for AR. Daily outpatient data for AR, air pollutant concentrations, and meteorological data were collected from January 2018 to December 2020 in Dingxi, Longnan, and Tianshui. Utilizing a Quasi-Poisson distribution, a generalized additive model (GAM) was employed in conjunction with distributed lag non-linear models (DLNM) to explore the association and lag effects of TRAPs on AR outpatient visits across the three cities. Stratified analyses based on gender, age, and season were conducted. A total of 11 106 outpatient visits for AR were recorded in the three cities. For an increase of 10 μg m-3 in PM2.5, the effect estimates in Dingxi, Longnan, and Tianshui reached their maximum at lag04, lag06, and lag07, respectively, with relative risk (RR) values of 4.696 (95% CI: 1.890, 11.614), 2.842 (95% CI: 2.102, 4.922), and 1.102 (95% CI: 1.066, 1.140). For NO2, the highest associations were exhibited in Dingxi (RR = 1.262, 95% CI: 1.081, 1.473) at lag07, in Longnan (RR = 2.554, 95% CI: 2.100, 4.805) at lag06, and in Tianshui (RR = 1.158, 95% CI: 1.106, 1.213) at lag07. Meanwhile, the strongest effects observed for a 1 mg m-3 increase in CO were 2.786 (95% CI: 1.467, 5.291) for Dingxi at lag07, 1.502 (95% CI: 1.096, 2.059) for Longnan at lag05, and 1.385 (95% CI: 1.137, 1.686) for Tianshui at lag04. Adults aged 15-64 years appeared to be more susceptible to TRAPs, and the associations were stronger in the cold season. The results of the present study indicate that exposure to TRAPs was positively correlated with outpatient visits for AR.

Intermodal comparison of commuters' exposure to VOCs between public, private, and active transportation.

Urban populations are exposed to a multitude of traffic-related air pollutants during daily commutes. This study assessed commuters' exposure to volatile organic compounds (VOCs) during bus, motorcycle, and bicycle commuting, and estimated the VOC inhalation dose. Benzene, toluene, ethylbenzene, and xylene (BTEX) were the main compounds detected, contributing 58 - 68% to ΣVOC (sum of the concentrations of all detected VOCs) in different travel modes. The mean ΣVOC exposure concentration was higher for motorcyclists than for cyclists and bus commuters. However, due to cyclists' higher minute ventilation rates and longer exposure time, they had the highest ΣVOC inhalation dose based on both travel time (7.09 ± 2.36μgmin-1) and distance (32.9 ± 10.8μgkm-1). Among the three travel modes, bus commuters had the lowest ΣVOC inhalation dose based on travel time (2.33 ± 1.18μgmin-1) and distance (8.91 ± 4.91μgkm-1), while motorcyclists had a moderate ΣVOC inhalation dose based on travel time (5.08 ± 1.46μgmin-1) and distance (13.4 ± 5.5μgkm-1). Health impact assessment of VOCs showed that cyclists faced the highest carcinogenic and non-carcinogenic risks, while bus commuters experienced the lowest health risk associated with VOC exposure. Our findings underscore the need to consider air quality in transportation infrastructure design and prioritize interventions to safeguard urban commuters' health, particularly cyclists, who are the most vulnerable to the adverse effects of traffic-related air pollutants.

Traffic-Related Air Pollution (TRAP) in relation to respiratory symptoms and lung function of school-aged children in Kuala Lumpur

ABSTRACT Traffic-Related Air Pollution (TRAP) exposure has been connected to significant health impacts among children. A cross-sectional comparative study was conducted among school children in Malaysia to determine the relationship between their exposure to TRAP and respiratory health effects. Air monitoring was conducted in schools and residences, while the children’s routines were investigated using a diary of daily activities. Respondents’ background and respiratory symptoms were obtained from a validated questionnaire, while a spirometry test was performed to determine their lung function status. The distances between schools and residences from the had contributed to the higher concentration of air pollutants in this study, which had associations with the children’s respiratory symptoms and lung function status. PM2.5 was the main predictor influencing the respondents’ respiratory symptoms and lung function abnormalities. In conclusion, exposure of school children to a high TRAP level might increase their risk of getting respiratory symptoms and lung function reduction.

Long-term exposure to traffic-related air pollution and non-accidental mortality: A systematic review and meta-analysis

BackgroundThe health effects of traffic-related air pollution (TRAP) continue to be of important public health interest across the globe. Following its 2010 review, the Health Effects Institute appointed a new expert Panel to systematically evaluate the epidemiological evidence regarding the associations between long-term exposure to TRAP and selected health outcomes. This paper describes the main findings of the systematic review on non-accidental mortality. MethodsThe Panel used a systematic approach to conduct the review. An extensive search was conducted of literature published between 1980 and 2019. A new exposure framework was developed to determine whether a study was sufficiently specific to TRAP, which included studies beyond the near-roadway environment. We performed random-effects meta-analysis when at least three estimates were available of an association between a specific exposure and outcome. We evaluated confidence in the evidence using a modified Office of Health Assessment and Translation (OHAT) approach, supplemented with a broader narrative synthesis. ResultsThirty-six cohort studies were included. Virtually all studies adjusted for a large number of individual and area-level covariates—including smoking, body mass index, and individual and area-level socioeconomic status—and were judged at a low or moderate risk for bias. Most studies were conducted in North America and Europe, and a few were based in Asia and Australia. The meta-analytic summary estimates for nitrogen dioxide, elemental carbon and fine particulate matter—pollutants with more than 10 studies—were 1.04 (95% CI 1.01, 1.06), 1.02 (1.00, 1.04) and 1.03 (1.01, 1.05) per 10, 1 and 5 µg/m3, respectively. Effect estimates are interpreted as the relative risk of mortality when the exposure differs with the selected increment. The confidence in the evidence for these pollutants was judged as high, because of upgrades for monotonic exposure–response and consistency across populations. The consistent findings across geographical regions, exposure assessment methods and confounder adjustment resulted in a high confidence rating using a narrative approach as well. ConclusionsThe overall confidence in the evidence for a positive association between long-term exposure to TRAP and non-accidental mortality was high.

Do neighbourhood traffic-related air pollution and socio-economic status moderate the associations of the neighbourhood physical environment with cognitive function? Findings from the AusDiab study

Characteristics of the neighbourhood environment, including the built and natural environment, area-level socio-economic status (SES) and air pollution, have been linked to cognitive health. However, most studies have focused on single neighbourhood characteristics and have not considered the extent to which the effects of environmental factors may interact. We examined the associations of measures of the neighbourhood built and natural environment, area-level SES and traffic-related air pollution (TRAP) with two cognitive function domains (memory and processing speed), and the extent to which area-level SES and TRAP moderated the associations.We used cross-sectional data from the AusDiab3 study, an Australian cohort study of adults (mean age: 61 years) in 2011–12 (N = 4141) for which geocoded residential addresses were available. Spatial data were used to create composite indices of built environment complexity (population density, intersection density, non-commercial land use mix, commercial land use) and natural environment (parkland and blue spaces). Area-level SES was obtained from national census indices and TRAP was based on estimates of annual average levels of nitrogen dioxide (NO2). Confounder-adjusted generalised additive mixed models were used to estimate the independent associations of the environmental measures with cognitive function and the moderating effects of area-level SES and TRAP. The positive associations between built environment complexity and memory were stronger in those living in areas with higher SES and lower NO2 concentrations. A positive association between the natural environment and memory was found only in those living in areas with lower NO2 concentrations and average or below-average SES. Built environment complexity and the natural environment were positively related to processing speed. Complex urban environments and access to nature may benefit cognitive health in ageing populations. For higher-order cognitive abilities, such as memory, these positive effects may be stronger in areas with lower levels of TRAP.

Characterization of plasma-derived exosomal miRNA changes following traffic-related air pollution exposure: A randomized, crossover trial based on small RNA sequencing.

The underlying mechanisms for health effects of traffic-related air pollution (TRAP) are still unclear. Small RNA sequencing (RNA-seq) in exosomes represents as a powerful approach to elucidate biological pathways in response to environmental exposure. We therefore aimed to explore impact of TRAP exposure on exosomal miRNAs. We performed a randomized, crossover study among 35 healthy college students in Shanghai, China. Participants were randomly assigned to 4-hour exposure in a traffic-polluted Road and in a traffic-free Park, respectively, intermitted by a washout period (at least 2weeks). RNA-seq was conducted to identify plasma-derived exosomal miRNAs and the differential miRNAs were explored using linear mixed-effect models. Pathway enrichment was conducted using ingenuity pathway analysis. Further, we validated several selected miRNAs by droplet digital PCR (ddPCR). The average concentrations of air pollutants including ultrafine particles, black carbon, nitrogen dioxide, and carbon dioxide were 2-3 times higher in the Road compared to those in the Park. We identified 271 exosomal miRNAs (212 up-regulated and 59 down-regulated) that were significantly associated with TRAP. We found 5 miRNAs with 242 experimentally validated mRNA targets that were involved in cardiovascular pathway, cytokine signaling, and immune response. The ddPCR analysis suggested that miR-3612, miR-21-5p, and miR-195-5p were significantly changed following TRAP exposure. For the first time this trial characterized the genome-wide changes of exosomal miRNA associated with TRAP exposure. The molecular profiling of exosomal miRNAs and "novel" associations of some miRNAs were useful for understanding on biological mechanisms for the adverse effects of TRAP.

226 Evidence for a role of ambient temperature on skin aging: A cross-sectional analysis from three metropolitan cities of India

Skin aging is driven to a large extent by environmental factors such as air pollution. Air pollution is a major cause of global warming. It is currently not known if increasing ambient temperature (AT) per se contributes to skin aging and/or if it modifies air pollution-induced skin aging. In order to address this topic, we analyzed the association between skin aging traits and AT using an ordinal multiple logistic regression model. This study was conducted in three metropolitan Indian cities: Delhi, Mumbai, and Bangalore. All together 1,510 women aged between 20-91 years were investigated. The data on skin aging traits were collected between May 2018 to Feb 2019 using SCINEXA™, a validated visual score to measure extrinsic facial skin aging. Five-year mean exposure to average AT was calculated using gridded temperature data from India Meteorological Department (0.5 x 0.5 km resolution). The long-term exposure to traffic-related air pollutants including fine particulates (PM2.5) and NO2 was collected using on-ground measurements. We here report a positive and significant association between AT and skin aging parameters including wrinkles on the forehead (OR: 1.13, 95% CI; 1.06, 1.21), wrinkles under the eyes (OR: 1.11, 95% CI; 1.04 1.19), laxity on cheeks (OR: 1.10, 95%CI; 1.02, 1.18), hyperpigmentation on the forehead (OR: 1.28, 95% CI; 1.16, 1.42), and dark circles under eye (OR: 1.92, 95% CI; 1.76,2.09). The association of wrinkles under the eyes and dark circles under the eye with mean AT increased after adjusting for the confounding effect of PM2.5. Thus, the study provides epidemiological evidence that long-term exposure to high AT may contribute to skin aging and increase the effect of traffic-related air pollution on skin aging.

Long-term exposure to traffic-related air pollution and selected health outcomes: A systematic review and meta-analysis.

The health effects of traffic-related air pollution (TRAP) continue to be of important public health interest. Following its well-cited 2010 critical review, the Health Effects Institute (HEI) appointed a new expert Panel to systematically evaluate the epidemiological evidence regarding the associations between long-term exposure to TRAP and selected adverse health outcomes. Health outcomes were selected based on evidence of causality for general air pollution (broader than TRAP) cited in authoritative reviews, relevance for public health and policy, and resources available. The Panel used a systematic approach to search the literature, select studies for inclusion in the review, assess study quality, summarize results, and reach conclusions about the confidence in the evidence. An extensive search was conducted of literature published between January 1980 and July 2019 on selected health outcomes. A new exposure framework was developed to determine whether a study was sufficiently specific to TRAP. In total, 353 studies were included in the review. Respiratory effects in children (118 studies) and birth outcomes (86 studies) were the most commonly studied outcomes. Fewer studies investigated cardiometabolic effects (57 studies), respiratory effects in adults (50 studies), and mortality (48 studies). The findings from the systematic review, meta-analyses, and evaluation of the quality of the studies and potential biases provided an overall high or moderate-to-high level of confidence in an association between long-term exposure to TRAP and the adverse health outcomes all-cause, circulatory, ischemic heart disease and lung cancer mortality, asthma onsetin chilldren and adults, and acute lower respiratory infections in children. The evidence was considered moderate, low or very low for the other selected outcomes. In light of the large number of people exposed to TRAP - both in and beyond the near-road environment - the Panel concluded that the overall high or moderate-to-high confidence in the evidence for an association between long-term exposure to TRAP and several adverse health outcomes indicates that exposures to TRAP remain an important public health concern and deserve greater attention from the public and from policymakers.

Toxicological effects of traffic-related air pollution on the lungs: Evidence, biomarkers and intervention

BackgroundNumerous epidemiological studies have recently observed that exposure to traffic-related air pollution (TRAP) is associated with increased risk of various respiratory diseases. Major gaps in knowledge remain regarding the toxicological effects. ObjectivesWe examined the toxicological effects of the gasoline exhaust particles (GEP), a paradigm of TRAP, in rats, with an objective to provide the evidence, obtain the biomarkers, and suggest effective intervention measure. MethodsWe measured the airway hyperresponsiveness (AHR), inflammatory cells in the bronchoalveolar lavage (BAL) fluid, histological changes in the lung tissues, and the biomarkers so as to systematically examine the toxicological effects of GEPs at different dose levels (0.5, 2.5, 5 mg/kg BW). The intervention of vitamin E (VE), a natural antioxidant, on the toxicological effects was investigated. ResultsThe lung injury caused by GEP exposure was first indicated by the airway hyperresponsiveness (AHR). Compared with the control group, GEP exposure significantly increased the airway resistances and decreased the lung compliance; the higher the dose of GEP, the more serious the lung injury. Lung injury was also revealed by the increase of inflammatory cells, including the lymphocytes and neutrophils, in the BAL fluid. With the increase of GEP dose, histological changes in the lung tissues were further observed: inflammatory cell infiltration increased and alveolar wall thickened. The toxicology of GEP was demonstrated by the increase of the biomarkers of the oxidative stress, the pro-inflammatory cytokines and the apoptosis cytokine. However, administration of VE was found to be effective in restoring airway injury. ConclusionThe toxicological effects of traffic-related air pollution (TRAP) on rat lungs are supported by evidence and biomarkers, and vitamin E intervention is feasible.

Cardiovascular effects of traffic-related air pollution: A multi-omics analysis from a randomized, crossover trial

A system-wide cardiovascular response to traffic-related air pollution (TRAP) has been rarely described. To systemically understand the mechanisms underlying cardiovascular effects of TRAP, we conducted a randomized, crossover trial in 56 young adults, who engaged in two 4-hour exposure sessions on a main road and in a park, alternately. We measured personal exposures to traffic-related air pollutants (TRAPs), including fine and ultrafine particulate matter, black carbon, nitrogen dioxide, and carbon monoxide. Lipidomics, targeted proteomics, urine metabolomics, targeted biomarkers, ambulatory blood pressure and electrocardiogram were measured. We used linear mixed-effects models to estimate the associations. The exposures to TRAPs except for fine particulate matter in the road session were 2–3 times higher. We observed elevated blood pressure and decreased heart rate variability (HRV) after TRAP exposure, accompanied by dozens of molecular alterations involving systemic inflammation, oxidative stress, endothelial dysfunction, coagulation, and lipid metabolism. Pathways like vascular smooth muscle cell proliferation and biomarkers like trimethylamine N-Oxide might also be disturbed. Some of these TRAP-related molecular biomarkers were also associated with changes of blood pressure or HRV. Our results provided systematical mechanistic profiling for the cardiovascular effects of TRAP using multi omics, which may have implications in TRAP control.

Hippocampal but Not Serum Cytokine Levels Are Altered by Traffic-Related Air Pollution in TgF344-AD and Wildtype Fischer 344 Rats in a Sex- and Age-Dependent Manner.

Epidemiological studies have demonstrated that air pollution is a significant risk factor for age-related dementia, including Alzheimer’s disease (AD). It has been posited that traffic-related air pollution (TRAP) promotes AD neuropathology by exacerbating neuroinflammation. To test this hypothesis, serum and hippocampal cytokines were quantified in male and female TgF344-AD rats and wildtype (WT) Fischer 344 littermates exposed to TRAP or filtered air (FA) from 1 to 15 months of age. Luminex™ rat 23-cytokine panel assays were used to measure the levels of hippocampal and serum cytokines in 3-, 6-, 10-, and 15-month-old rats (corresponding to 2, 5, 9, and 14 months of exposure, respectively). Age had a pronounced effect on both serum and hippocampal cytokines; however, age-related changes in hippocampus were not mirrored in the serum and vice versa. Age-related changes in serum cytokine levels were not influenced by sex, genotype, or TRAP exposure. However, in the hippocampus, in 3-month-old TgF344-AD and WT animals, TRAP increased IL-1ß in females while increasing TNF ɑin males. In 6-month-old animals, TRAP increased hippocampal levels of M-CSF in TgF344-AD and WT females but had no significant effect in males. At 10 and 15 months of age, there were minimal effects of TRAP, genotype or sex on hippocampal cytokines. These observations demonstrate that TRAP triggers an early inflammatory response in the hippocampus that differs with sex and age and is not reflected in the serum cytokine profile. The relationship of TRAP effects on cytokines to disease progression remains to be determined.

Effects of air pollution exposure on inflammatory and endurance performance in recreationally trained cyclists adapted to traffic-related air pollution.

The aim of the present study was to analyze the effects of traffic-related air pollution (TRAP) on markers of inflammatory, neuroplasticity, and endurance performance-related parameters in recreationally trained cyclists who were adapted to TRAP during a 50-km cycling time trial (50-km cycling TT). Ten male cyclists performed a 50-km cycling TT inside an environmental chamber located in downtown Sao Paulo (Brazil), under TRAP or filtered air conditions. Blood samples were obtained before and after the 50-km cycling TT to measure markers of inflammatory [interleukin-6 (IL-6), C-reactive protein (CRP), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1)] and neuroplasticity [brain-derived neurotrophic factor (BDNF)]. Rating of perceived exertion (RPE), heart rate (HR), and power output (PO) were measured throughout the 50-km cycling TT. There were no significant differences between experimental conditions for responses of IL-6, CRP, and IL-10 (P > 0.05). When compared with exercise-induced changes in filtered air condition, TRAP provoked greater exercise-induced increase in BDNF levels (TRAP = 3.3 ± 2.4-fold change; Filtered = 1.3 ± 0.5-fold change; P = 0.04) and lower exercise-induced increase in ICAM-1 (Filtered = 1.1 ± 0.1-fold change; TRAP = 1.0 ± 0.1-fold change; P = 0.01). The endurance performance-related parameters (RPE, HR, PO, and time to complete the 50-km cycling TT) were not different between TRAP and filtered air conditions (P > 0.05). These findings suggest that the potential negative impacts of exposure to pollution on inflammatory, neuroplasticity, and performance-related parameters do not occur in recreationally trained cyclists who are adapted to TRAP.

Defining the effects of traffic-related air pollution on the human plasma proteome using an aptamer proteomic array: A dose-dependent increase in atherosclerosis-related proteins

BackgroundTraffic-related air pollution (TRAP) is a critical risk factor and major contributor to respiratory and cardiovascular disease (CVD). The effects of TRAP beyond the lungs can be related to changes in circulatory proteins. However, such TRAP-mediated changes have not been defined in an unbiased manner using a controlled human model. ObjectiveTo detail global protein changes (the proteome) in plasma following exposure to inhaled diesel exhaust (DE), a paradigm of TRAP, using controlled human exposures. MethodsIn one protocol, ex-smokers and never-smokers were exposed to filtered air (FA) and DE (300 μg PM2.5/m3), on order-randomized days, for 2 h. In a second protocol, independent never-smoking participants were exposed to lower concentrations of DE (20, 50 or 150 μg PM2.5/m3) and FA, for 4 h, on order-randomized days. Each exposure was separated by 4 weeks of washout. Plasma samples obtained 24 h post-exposure from ex-smokers (n = 6) were first probed using Slow off-rate modified aptamer proteomic array. Plasma from never-smokers (n = 11) was used for independent assessment of proteins selected from the proteomics study by immunoblotting. ResultsProteomics analyses revealed that DE significantly altered 342 proteins in plasma of ex-smokers (n = 6). The top 20 proteins therein were primarily associated with inflammation and CVD. Plasma from never-smokers (n = 11) was used for independent assessment of 6 proteins, amongst the top 10 proteins increased by DE in the proteomics study, for immunoblotting. The abundance of all six proteins (fractalkine, apolipoproteins (APOB and APOM), IL18R1, MIP-3 and MMP-12) was significantly increased by DE in plasma of these never-smokers. DE-mediated increase was shown to be concentration-dependent for fractalkine, APOB and MMP-12, all biomarkers of atherosclerosis, which correlated with plasma levels of IL-6, a subclinical marker of CVD, in independent participants. ConclusionThis investigation details changes in the human plasma proteome due to TRAP. We identify specific atherosclerosis-related proteins that increase concentration-dependently across a range of TRAP levels applicable worldwide.

Integrated molecular response of exposure to traffic-related pollutants in the US trucking industry.

Exposure to traffic-related pollutants, including diesel exhaust, is associated with increased risk of cardiopulmonary disease and mortality; however, the precise biochemical pathways underlying these effects are not known. To investigate biological response mechanisms underlying exposure to traffic related pollutants, we used an integrated molecular response approach that included high-resolution metabolomic profiling and peripheral blood gene expression to identify biological responses to diesel exhaust exposure. Plasma samples were collected from 73 non-smoking males employed in the US trucking industry between February 2009 and October 2010, and analyzed using untargeted high-resolution metabolomics to characterize metabolite associations with shift- and week-averaged levels of elemental carbon (EC), organic carbon (OC) and particulate matter with diameter≤2.5μm (PM2.5). Metabolic associations with EC, OC and PM2.5 were evaluated for biochemical processes known to be associated with disease risk. Annotated metabolites associated with exposure were then tested for relationships with the peripheral blood transcriptome using multivariate selection and network correlation. Week-averaged EC and OC levels, which were averaged across multiple shifts during the workweek, resulted in the greatest exposure-associated metabolic alterations compared to shift-averaged exposure levels. Metabolic changes associated with EC exposure suggest increased lipid peroxidation products, biomarkers of oxidative stress, thrombotic signaling lipids, and metabolites associated with endothelial dysfunction from altered nitric oxide metabolism, while OC exposures were associated with antioxidants, oxidative stress biomarkers and critical intermediates in nitric oxide production. Correlation with whole blood RNA gene expression provided additional evidence of changes in processes related to endothelial function, immune response, inflammation, and oxidative stress. We did not detect metabolic associations with PM2.5. This study provides an integrated molecular assessment of human exposure to traffic-related air pollutants that includes diesel exhaust. Metabolite and transcriptomic changes associated with exposure to EC and OC are consistent with increased risk of cardiovascular diseases and the adverse health effects of traffic-related air pollution.

Effects of Traffic-Related Air Pollution on Exercise Endurance, Dyspnea, and Cardiorespiratory Responses in Health and COPD: A Randomized, Placebo-Controlled, Crossover Trial

Individuals with COPD have increased sensitivity to traffic-related air pollution (TRAP) such as diesel exhaust (DE), but little is known about the acute effects of TRAP on exercise responses in COPD. Does exposure before exercise to TRAP (DE titrated to 300 μg/m3 particulate matter< 2.5 μm in diameter [DE300]) show greater adverse effects on exercise endurance, exertional dyspnea, and cardiorespiratory responses to exercise in participants with mild to moderate COPD compared with former smokers with normal spirometry and healthy control participants? In this double-blind, randomized, placebo-controlled, crossover study, 11 healthy control participants, nine former smokers without COPD, and nine former smokers with COPD were separately exposed to filtered air (FA) and DE300 for 2h separated by a minimum of 4weeks. Participants performed symptom-limited constant load cycling tests within 2.5h of exposure with detailed cardiorespiratory and exertional symptom measurements. A significant negative effect of TRAP on exercise endurance time was found in healthy control participants (DE300 vsFA, 10.2 ± 8.2min vs12.9 ± 9.5 min, respectively; P= .03), but not in former smokers without COPD (10.1 ± 6.9min vs12.2 ± 8.0 min, respectively; P= .57) or former smokers with COPD (9.8 ± 6.4min vs8.4 ± 6.6 min, respectively; P= .31). Furthermore, significant increases in inspiratory duty cycle and absolute end-expiratory and end-inspiratory lung volumes were observed, and dyspnea ratings were elevated at select submaximal measurement times only in healthy control participants. Contrary to our hypothesis, it was the healthy control participants, rather than the former smokers with and without COPD, who were negatively impacted by TRAP during exercise. ClinicalTrials.gov; No.: NCT02236039; URL: www. gov.