Road traffic density and recurrent asthma emergency department visits among Medicaid enrollees in New York State 2005-2015.

BACKGROUND: Environmental exposures such as traffic may contribute to asthma morbidity including recurrent emergency department (ED) visits. However, these associations are often confounded by socioeconomic status and health care access. OBJECTIVE: This study aims to assess the association between traffic density and recurrence of asthma ED visits in the primarily low income Medicaid population in New York State (NYS) between 2005 and 2015. METHODS: The primary outcome of interest was a recurrent asthma ED visit within 1-year of index visit. Traffic densities (weighted for truck traffic) were spatially linked based on home addresses. Bivariate and multivariate logistic regression analyses were conducted to identify factors predicting recurrent asthma ED visits. RESULTS: In a multivariate model, Medicaid recipients living within 300-m of a high traffic density area were at a statistically significant risk of a recurrent asthma ED visit compared to those in a low traffic density area (OR = 1.31; 95% CI:1.24,1.38). Additionally, we evaluated effect measure modification for risk of recurrent asthma visits associated with traffic exposure by socio-demographic factors. The highest risk was found for those exposed to high traffic and being male (OR = 1.87; 95% CI:1.46,2.39), receiving cash assistance (OR = 2.11; 95% CI:1.65,2.72), receiving supplemental security income (OR = 2.21; 95% CI:1.66,2.96) and being in the 18.44 age group (OR = 1.59;95% CI 1.48,1.70) was associated with the highest risk of recurrent asthma ED visit. Black non-Hispanics (OR = 2.35; 95% CI:1.70,3.24), Hispanics (OR = 2.13; 95% CI:1.49,3.04) and those with race listed as "Other" (OR = 1.89 95% CI:1.13,3.16) in high traffic areas had higher risk of recurrent asthma ED visits as compared to White non-Hispanics in low traffic areas. CONCLUSION: We observed significant persistent disparities in asthma morbidity related to traffic exposure and race/ethnicity in a low-income population. Our findings suggest that even within a primarily low-income study population, socioeconomic differences persist. These differences in susceptibility in the extremely low-income group may not be apparent in health studies that use Medicaid enrollment as a proxy for low SES.

Exposure to traffic-related fine particulate matter 2.5 causes respiratory damage via peroxisome proliferator-activated receptor gamma-regulated inflammation.

Exposure to particulate matter 2.5 (PM2.5) potentially triggers airway inflammation. Peroxisome proliferator-activated receptor gamma (PPARγ) has been reported to regulate inflammatory responses in diverse cell types. Therefore, this work investigated the mechanisms of PPARγ in regulating traffic-related PM2.5-induced airway inflammation. Using the diffusion flame burner soot generation, traffic-related PM2.5 was generated and adsorbed. BALB/c male mice and human bronchial epithelial cells (16-HBE) were exposed to PM2.5 alone or co-treatment with rosiglitazone (RSG), an agonist of PPARγ. To the end of exposure, bronchoalveolar lavage fluid (BALF), venous blood and arterial blood, trachea, bronchus and lung tissues were collected. The levels of IL-1ß, IL-6, and IL-17 were detected by ELISA, and the cell types in BALF were counted. Hematoxylin-eosin (H&E) assay were used to analyze the pathological conditions of lung, bronchus, and pulmonary artery. Apoptosis was detected by TUNEL, and PPARγ expression in lung and bronchus was detected by immunohistochemical (IHC) staining. Western Blot was used to detect PPARγ, NF-kB, AP-1 and STAT3 expression in lung and bronchus. The viability was detected by MTT method. PM2.5 exposure caused pathological damage to the lung, bronchus and pulmonary artery tissue, which induced apoptosis of bronchial epithelial cells. PM2.5 exposure caused local inflammation of the whole body and airway. PPARγ expression increased after PM2.5 exposure. PM2.5 exposure regulated the downstream signaling pathways to affect the inflammatory response through PPARγ. Exposure to traffic-related PM2.5 caused respiratory damage via PPARγ-regulated inflammation.

Short-term exposure to traffic-related air pollution and STEMI events: Insights into STEMI onset and related cardiac impairment.

AIMS: Evidence on the impacts of traffic-related air pollution (TRAP) on ST-segment elevation myocardial infarction (STEMI) events is limited. We aimed to assess the acute effects of TRAP exposure on the clinical onset of STEMI and related cardiac impairments. METHODS AND RESULTS: We recruited patients who were admitted for STEMI and underwent primary percutaneous coronary intervention at Peking University Third Hospital between 2014 and 2020. Indicators relevant to cardiac impairments were measured. Concomitantly, hourly concentrations of traffic pollutants were monitored throughout the study period, including fine particulate matter, black carbon (BC), particles in size ranges of 5-560 nm, oxides of nitrogen (NOX), nitrogen dioxide, and carbon monoxide. The mean (SD) age of participants was 62.4 (12.5) years. Daily average (range) concentrations of ambient BC and NOX were 3.9 (0.1-25.0) µg/m3 and 90.8 (16.6-371.7) µg/m3. Significant increases in STEMI risks of 5.9% (95% CI: 0.1, 12.0) to 21.9% (95% CI: 6.0, 40.2) were associated with interquartile range increases in exposure to TRAP within a few hours. These changes were accompanied by significant elevations in cardiac troponin T levels of 6.9% (95% CI: 0.2, 14.1) to 41.7% (95% CI: 21.2, 65.6), as well as reductions in left ventricular ejection fraction of 1.5% (95% CI: 0.1, 2.9) to 3.7% (95% CI: 0.8, 6.4). Furthermore, the associations were attenuated in participants living in areas with higher residential greenness levels. CONCLUSIONS: Our findings extend current understanding that short-term exposure to higher levels of traffic pollution was associated with increased STEMI risks and exacerbated cardiac impairments, and provide evidence on traffic pollution control priority for protecting vulnerable populations who are at greater risks of cardiovascular events.

Controlled human exposure to diesel exhaust: results illuminate health effects of traffic-related air pollution and inform future directions.

Air pollution is an issue of increasing interest due to its globally relevant impacts on morbidity and mortality. Controlled human exposure (CHE) studies are often employed to investigate the impacts of pollution on human health, with diesel exhaust (DE) commonly used as a surrogate of traffic related air pollution (TRAP). This paper will review the results derived from 104 publications of CHE to DE (CHE-DE) with respect to health outcomes. CHE-DE studies have provided mechanistic evidence supporting TRAP's detrimental effects on related to the cardiovascular system (e.g., vasomotor dysfunction, inhibition of fibrinolysis, and impaired cardiac function) and respiratory system (e.g., airway inflammation, increased airway responsiveness, and clinical symptoms of asthma). Oxidative stress is thought to be the primary mechanism of TRAP-induced effects and has been supported by several CHE-DE studies. A historical limitation of some air pollution research is consideration of TRAP (or its components) in isolation, limiting insight into the interactions between TRAP and other environmental factors often encountered in tandem. CHE-DE studies can help to shed light on complex conditions, and several have included co-exposure to common elements such as allergens, ozone, and activity level. The ability of filters to mitigate the adverse effects of DE, by limiting exposure to the particulate fraction of polluted aerosols, has also been examined. While various biomarkers of DE exposure have been evaluated in CHE-DE studies, a definitive such endpoint has yet to be identified. In spite of the above advantages, this paradigm for TRAP is constrained to acute exposures and can only be indirectly applied to chronic exposures, despite the critical real-world impact of living long-term with TRAP. Those with significant medical conditions are often excluded from CHE-DE studies and so results derived from healthy individuals may not apply to more susceptible populations whose further study is needed to avoid potentially misleading conclusions. In spite of limitations, the contributions of CHE-DE studies have greatly advanced current understanding of the health impacts associated with TRAP exposure, especially regarding mechanisms therein, with important implications for regulation and policy.

Controlled human exposure to diesel exhaust: a method for understanding health effects of traffic-related air pollution.

Diesel exhaust (DE) is a major component of air pollution in urban centers. Controlled human exposure (CHE) experiments are commonly used to investigate the acute effects of DE inhalation specifically and also as a paradigm for investigating responses to traffic-related air pollution (TRAP) more generally. Given the critical role this model plays in our understanding of TRAP's health effects mechanistically and in support of associated policy and regulation, we review the methodology of CHE to DE (CHE-DE) in detail to distill critical elements so that the results of these studies can be understood in context. From 104 eligible publications, we identified 79 CHE-DE studies and extracted information on DE generation, exposure session characteristics, pollutant and particulate composition of exposures, and participant demographics. Virtually all studies had a crossover design, and most studies involved a single DE exposure per participant. Exposure sessions were typically 1 or 2 h in duration, with participants alternating between exercise and rest. Most CHE-DE targeted a PM concentration of 300 µg/m3. There was a wide range in commonly measured co-pollutants including nitrogen oxides, carbon monoxide, and total organic compounds. Reporting of detailed parameters of aerosol composition, including particle diameter, was inconsistent between studies, and older studies from a given lab were often cited in lieu of repeating measurements for new experiments. There was a male predominance in participants, and over half of studies involved healthy participants only. Other populations studied include those with asthma, atopy, or metabolic syndrome. Standardization in reporting exposure conditions, potentially using current versions of engines with modern emissions control technology, will allow for more valid comparisons between studies of CHE-DE, while recognizing that diesel engines in much of the world remain old and heterogeneous. Inclusion of female participants as well as populations more susceptible to TRAP will broaden the applicability of results from CHE-DE studies.

Adverse health and environmental outcomes of cycling in heavily polluted urban environments.

Cycling is a healthy habit; however, are its benefits outweighing risks when biking in heavily trafficked and air-polluted cities? Research involved studying contamination with traffic-related elements of dust collected from bike paths located in top trafficked cities of Europe in Poland. Human health risk was assessed via inhalation and ingestion pathways for adults and children. Bike path dust was heavily contaminated with Zn, Cd (Geoaccumulation index Igeo 4) and Pb (Igeo 3), sourced predominantly from nonexhaust car emissions. The concentrations of metals in dust decreased in the following descending order: Zn > Mn > Cu > Pb > Cr > Cd. A fractionation study revealed that Zn and Cd are almost entirely bioavailable (Mobility factor MF above 90%), causing hazards to humans and the environment. The highest congested intersections result in more TRAP-contaminated dust deposited on bike paths, which is easily resuspended, posing a health risk for cyclists or pedestrians. Avoiding cycling in proximity to heavily trafficked routes should be considered, when possible, as well as physical removal of dust by wet sweeping to limit dust resuspension.

Effect of heavy metals on ventricular repolarization and depolarization in the Metropolitan Manila Development Authority (MMDA) traffic enforcers' health study.

We examined the relationships between blood heavy metals [cadmium (B-Cd), mercury (B-Hg), and lead (B-Pb)] and heart rate-corrected QT interval (QTc), JT interval (JTc), and QRS complex duration (QRSc), electrocardiogram markers of ventricular repolarization and depolarization among 60 traffic enforcers in the MMDA traffic enforcers' health study. We fitted regression models to estimate the mean change effect on QTc, JTc, and QRSc, of B-Cd, B-Hg, and B-Pb concentrations, adjusted for potential confounding factors. We looked at effect modification by sex and smoking status. An interquartile range increase in B-Cd (0.9 µg/L) was related to a 6.6% increase in mean QRSc [95% confidence interval (CI): 2.5, 10.8], and a 1.7% increase in mean QTc (95% CI: 0.2, 3.3). We also found that the associations between B-Cd and QRSc and QTc were higher among participants who were never smokers than ever smokers. Moreover, the association between B-Cd and QRSc was also higher among males than females.

Prenatal and postnatal traffic pollution exposure, DNA methylation in Shank3 and MeCP2 promoter regions, H3K4me3 and H3K27me3 and sociability in rats' offspring.

BACKGROUND: Road traffic air pollution is linked with an increased risk of autistic spectrum disorder (ASD). The aim of this study is to assess the effect of exposure to prenatal or postnatal traffic-related air pollution combining concomitant noise pollution on ASD-related epigenetic and behavioral alternations on offspring. METHODS: A 2 × 2 factorial analysis experiment was designed. Wistar rats were exposed at different sites (L group: green space; H group: crossroads) and timings (E group: full gestation; P group: 21 days after birth) at the same time, and air pollutants of nitrogen dioxide (NO2) and fine particles (PM2.5) were meanwhile sampled. On postnatal day 25, brains from offspring of each group were extracted to determine the levels of DNA methylation in Shank3 (three parts: Shank3_01, Shank3_02, Shank3_03) and MeCP2 (two parts: MeCP2_01, MeCP2_02) promoter regions, H3K4me3 and H3K27me3 after three-chamber social test. Meanwhile, the Shank3 and MeCP2 levels were quantified. RESULTS: The concentrations of PM2.5 (L: 58.33 µg/m3; H: 88.33 µg/m3, P < 0.05) and NO2 (L: 52.76 µg/m3; H: 146.03 µg/m3, P < 0.01) as well as the intensity of noise pollution (L: 44.4 dB (A); H: 70.1 dB (A), P < 0.001) differed significantly from 18:00 to 19:00 between experimental sites. Traffic pollution exposure (P = 0.006) and neonatal exposure (P = 0.001) led to lower weight of male pups on PND25. Male rats under early-life exposure had increased levels of Shank3 (Shank3_02: timing P < 0.001; site P < 0.05, Shank3_03: timing P < 0.001) and MeCP2 (MeCP2_01: timing P < 0.001, MeCP2_02: timing P < 0.001) methylation and H3K4me3 (EL: 11.94 µg/mg; EH: 11.98; PL: 17.14; PH: 14.78, timing P < 0.05), and reduced levels of H3K27me3 (EL: 71.07 µg/mg; EH: 44.76; PL: 29.15; PH: 28.67, timing P < 0.001; site P < 0.05) in brain compared to those under prenatal exposure. There was, for female pups, a same pattern of Shank3 (Shank3_02: timing P < 0.001; site P < 0.05, Shank3_03: timing P < 0.001) and MeCP2 (MeCP2_01: timing P < 0.05, MeCP2_02: timing P < 0.001) methylation and H3K4me3 (EL: 11.27 µg/mg; EH: 11.55; PL: 16.11; PH: 15.44, timing P < 0.001), but the levels of H3K27me3 exhibited an inverse trend concerning exposure timing. Hypermethylation at the MeCP2 and Shank3 promoter was correlated with the less content of MeCP2 (female: EL: 32.23 ng/mg; EH: 29.58; PL: 25.01; PH: 23.03, timing P < 0.001; site P < 0.05; male: EL: 31.05 ng/mg; EH: 32.75; PL: 23.40; PH: 25.91, timing P < 0.001) and Shank3 (female: EL: 5.10 ng/mg; EH: 5.31; PL: 4.63; PH: 4.82, timing P < 0.001; male: EL: 5.40 ng/mg; EH: 5.48; PL: 4.82; PH: 4.87, timing P < 0.001). Rats with traffic pollution exposure showed aberrant sociability preference and social novelty, while those without it behaved normally. CONCLUSIONS: Our findings suggest early life under environmental risks is a crucial window for epigenetic perturbations and then abnormalities in protein expression, and traffic pollution impairs behaviors either during pregnancy or after birth.

Nanoparticulate matter exposure results in white matter damage and an inflammatory microglial response in an experimental murine model.

Exposure to ambient air pollution has been associated with white matter damage and neurocognitive decline. However, the mechanisms of this injury are not well understood and remain largely uncharacterized in experimental models. Prior studies have shown that exposure to particulate matter (PM), a sub-fraction of air pollution, results in neuroinflammation, specifically the upregulation of inflammatory microglia. This study examines white matter and axonal injury, and characterizes microglial reactivity in the corpus callosum of mice exposed to 10 weeks (150 hours) of PM. Nanoscale particulate matter (nPM, aerodynamic diameter ≤200 nm) consisting primarily of traffic-related emissions was collected from an urban area in Los Angeles. Male C57BL/6J mice were exposed to either re-aerosolized nPM or filtered air for 5 hours/day, 3 days/week, for 10 weeks (150 hours; n = 18/group). Microglia were characterized by immunohistochemical double staining of ionized calcium-binding protein-1 (Iba-1) with inducible nitric oxide synthase (iNOS) to identify pro-inflammatory cells, and Iba-1 with arginase-1 (Arg) to identify anti-inflammatory/ homeostatic cells. Myelin injury was assessed by degraded myelin basic protein (dMBP). Oligodendrocyte cell counts were evaluated by oligodendrocyte transcription factor 2 (Olig2). Axonal injury was assessed by axonal neurofilament marker SMI-312. iNOS-expressing microglia were significantly increased in the corpus callosum of mice exposed to nPM when compared to those exposed to filtered air (2.2 fold increase; p<0.05). This was accompanied by an increase in dMBP (1.4 fold increase; p<0.05) immunofluorescent density, a decrease in oligodendrocyte cell counts (1.16 fold decrease; p<0.05), and a decrease in neurofilament SMI-312 (1.13 fold decrease; p<0.05) immunofluorescent density. Exposure to nPM results in increased inflammatory microglia, white matter injury, and axonal degradation in the corpus callosum of adult male mice. iNOS-expressing microglia release cytokines and reactive oxygen/ nitrogen species which may further contribute to the white matter damage observed in this model.

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

BACKGROUND: Exposure 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. METHODS: Forty 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. RESULTS: We 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. CONCLUSION: Our 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.

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

BACKGROUND: Associations 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. OBJECTIVES: We 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). METHODS: This 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. RESULTS: An 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. DISCUSSION: This 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.

Traffic-related particulate matter aggravates ocular allergic inflammation by mediating dendritic cell maturation.

The aim of this study was to determine the effects of traffic-related particulate matter (PM) on allergic inflammation of ocular surfaces. BALB/c mice were sensitized with ovalbumin (OVA) and aluminum hydroxide via intraperitoneal injection. Two weeks later, mice were challenged with eye drops containing OVA concomitant with either traffic-related PM2.5 or vehicle eye drops. Topical OVA challenges were administered following unilateral subconjunctival injection of magnetic-bead-sorted CD11c+ dendritic cells (DC). The following were assessed: (1) clinical signs, (2) infiltration of inflammatory cells into conjunctiva, (3) serum levels of OVA-specific IgE production, and (4) T-cell cytokine secretion with topical application of PM2.5, compared to saline vehicle. PM2.5 was found to increase production of OVA-specific IgE in serum and Th2 immune response-related cytokines including interleukin (IL)-4, IL-17A, and IL-13 compared to vehicle control. It is of interest that PM2.5 treatment also elevated the population of mature DCs in draining lymph nodes (LNs). Exposure with PM2.5 was associated with a significant rise in conjunctival expression of IL-1ß, IL-6, IL-17, and TNF. After subconjunctival injection of CD11c+DCs from PM2.5-treated allergic conjunctivitis (AC) mice into naïve mice, T cell responses and OVA-specific IgE were also enhanced. Data suggest that traffic-related PM2.5 exacerbated allergic conjunctivitis as evidenced by increased infiltration of inflammatory cells into the conjunctiva and Th2 responses in the draining LNs associated with enhanced maturation of DCs. Our findings provide new insight into the hazardous potential of traffic-related PM2.5 on allergic diseases, such as asthma or atopic dermatitis.

The Effects of Chronic Exposure to Ambient Traffic-Related Air Pollution on Alzheimer's Disease Phenotypes in Wildtype and Genetically Predisposed Male and Female Rats.

BACKGROUND: Epidemiological data link traffic-related air pollution (TRAP) to increased risk of Alzheimer's disease (AD). Preclinical data corroborating this association are largely from studies of male animals exposed acutely or subchronically to high levels of isolated fractions of TRAP. What remains unclear is whether chronic exposure to ambient TRAP modifies AD risk and the influence of sex on this interaction. OBJECTIVES: This study sought to assess effects of chronic exposure to ambient TRAP on the time to onset and severity of AD phenotypes in a preclinical model and to determine whether sex or genetic susceptibility influences outcomes. METHODS: Male and female TgF344-AD rats that express human AD risk genes and wildtype littermates were housed in a vivarium adjacent to a heavily trafficked tunnel in Northern California and exposed for up to 14 months to filtered air (FA) or TRAP drawn from the tunnel and delivered to animals unchanged in real time. Refractive particles in the brain and AD phenotypes were quantified in 3-, 6-, 10-, and 15-month-old animals using hyperspectral imaging, behavioral testing, and neuropathologic measures. RESULTS: Particulate matter (PM) concentrations in TRAP exposure chambers fluctuated with traffic flow but remained below 24-h PM with aerodynamic diameter less than or equal to 2.5 micrometers (PM2.5) U.S. National Ambient Air Quality Standards limits. Ultrafine PM was a predominant component of TRAP. Nano-sized refractive particles were detected in the hippocampus of TRAP animals. TRAP-exposed animals had more amyloid plaque deposition, higher hyperphosphorylated tau levels, more neuronal cell loss, and greater cognitive deficits in an age-, genotype-, and sex-dependent manner. TRAP-exposed animals also had more microglial cell activation, but not astrogliosis. DISCUSSION: These data demonstrate that chronic exposure to ambient TRAP promoted AD phenotypes in wildtype and genetically susceptible rats. TRAP effects varied according to age, sex, and genotype, suggesting that AD progression depends on complex interactions between environment and genetics. These findings suggest current PM2.5 regulations are insufficient to protect the aging brain. https://doi.org/10.1289/EHP8905.

Early childhood traffic-related air pollution and risk of allergic rhinitis at 2-4 years of age modification by family stress and male gender: a case-control study in Shenyang, China.

BACKGROUND: Few studies have explored the modifications by family stress and male gender in the relationship between early exposure to traffic-related air pollution (TRAP) and allergic rhinitis (AR) risk in preschool children. METHODS: We conducted a case-control study of 388 children aged 2-4 years in Shenyang, China. These children AR were diagnosed by clinicians. By using measured concentrations from monitoring stations, we estimated the exposures of particulate matter less than 10 µm in diameter (PM10), nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and sulfur dioxide (SO2) in preschool children aged 2-4 years. After adjusted potential confounding factors, we used logistic regression model to evaluate the odds ratio (OR) and 95% confidence interval (CI) for childhood AR with exposure to different air pollutants according to the increasing of the interquartile range (IQR) in the exposure level. RESULTS: The prevalence of AR in children aged 2-4 years (6.4%) was related to early TRAP exposure. With an IQR (20 µg/m3) increase in PM10 levels, an adjusted OR was significantly elevated by 1.70 (95% CI, 1.19 to 2.66). Also, with an IQR (18 µg/m3) increase in NO2, an elevated adjusted OR was 1.85 (95% CI, 1.52 to 3.18). Among children with family stress and boys, PM10 and NO2 were positively related to AR symptoms. No significant association was found among children without family stress and girls. CONCLUSIONS: Family stress and male gender may increase the risk of AR in preschool children with early exposure to PM10 and NO2.

Childhood traffic-related air pollution and adverse changes in subclinical atherosclerosis measures from childhood to adulthood.

BACKGROUND: Chronic exposure to air pollutants is associated with increased risk of cardiovascular disease (CVD) among adults. However, little is known about how air pollution may affect the development of subclinical atherosclerosis in younger populations. Carotid artery intima-media thickness (CIMT) is a measure of subclinical atherosclerosis that provides insight into early CVD pathogenesis. METHODS: In a pilot study of 70 participants from the Southern California Children's Health Study, we investigated CIMT progression from childhood to adulthood. Using carotid artery ultrasound images obtained at age 10 and follow-up images at age 21-22, we examined associations between childhood ambient and traffic-related air pollutants with changes in CIMT over time and attained adult CIMT using linear mixed-effects models adjusted for potential confounders. Average residential childhood exposures (i.e., birth to time of measurement at 10-11 years) were assigned for regional, ambient pollutants (ozone, nitrogen dioxide, particulate matter, interpolated from regulatory air monitoring data) and traffic-related nitrogen oxides (NOx) by road class (modeled using the CALINE4 line source dispersion model). Traffic density was calculated within a 300-m residential buffer. RESULTS: For each 1 standard deviation (SD) increase in childhood traffic-related total NOx exposure, we observed greater yearly rate of change in CIMT from childhood to adulthood (ß: 2.17 µm/yr, 95% CI: 0.78-3.56). Increases in annual rate of CIMT change from childhood to adulthood also were observed with freeway NOx exposure (ß: 2.24 µm/yr, 95% CI: 0.84-3.63) and traffic density (ß: 2.11 µm/yr, 95% CI: 0.79-3.43). Traffic exposures were also related to increases in attained CIMT in early adulthood. No associations of CIMT change or attained level were observed with ambient pollutants. CONCLUSIONS: Overall, we observed adverse changes in CIMT over time in relation to childhood traffic-related NOx exposure and traffic density in our study population. While these results must be cautiously interpreted given the limited sample size, the observed associations of traffic measures with CIMT suggest a need for future studies to more fully explore this relationship.

The Role of Traffic-Related Air Pollution on Neurodegenerative Diseases in Older People: An Epidemiological Perspective.

Traffic-related air pollution is ubiquitous and almost impossible to avoid. It is important to understand the role that traffic-related air pollution may play in neurodegenerative diseases, such as dementia, Alzheimer's disease, and Parkinson's disease, particularly among older populations and at-risk groups. There is a growing interest in this area among the environmental epidemiology literature and the body of evidence identifying this role is emerging and strengthening. This review focuses on the principal components of traffic-related air pollutants (particulate matter and nitrogen oxides) and the epidemiological evidence of their contribution to common neurodegenerative diseases. All studies reported are currently observational in nature and there are mixed findings depending on the study design, assessment of traffic-related air pollutant levels, assessment of the neurodegenerative disease outcome, time period of assessment, and the role of confounding environmental factors and at-risk genetic characteristics. All current studies have been conducted in income-rich countries where traffic-related air pollution levels are relatively low. Additional longer-term studies are needed to confirm the levels of risk, consider other contributing environmental factors and to be conducted in settings where air pollution exposures are higher and at-risk populations reside and work. Better understanding of these relationships will help inform the development of preventive measures and reduce chronic cognitive and physical health burdens (cost, quality of life) at personal and societal levels.

Residential proximity to roadways and placental-associated stillbirth: a case-control study.

We conducted a retrospective case-control study of 1,097 women in Massachusetts and Rhode Island, USA, to examine the association between stillbirth related to placental abruption or placental insufficiency and maternal exposure to traffic-related air pollution. We utilized distance to nearest roadway proximity metrics as a proxy for traffic-related air pollution exposure. No meaningful increase in the overall odds of placental-associated stillbirths was observed (adjusted OR: 1.1, 95% CI: 0.5-2.8). However, mothers living within 50 m of a roadway had a 60% increased odds of experiencing a stillbirth related to placental abruption compared to mothers living greater than 200 m away. This suggestive finding was imprecise due to the small case number in the highest exposure category (95% CI: 0.6-4.0). Future studies of placental abruption with more precise exposure assessments are warranted.

Association Between Traffic Count and Cardiovascular Mortality: A Prospective Cohort Study in Taiwan.

BACKGROUND: Exposure to traffic-related pollution is positively associated with cardiovascular diseases (CVD), but little is known about how different sources of traffic pollution (eg, gasoline-powered cars, diesel-engine vehicles) contribute to CVD. Therefore, we evaluated the association between exposure to different types of engine exhaust and CVD mortality. METHODS: We recruited 12,098 participants from REVEAL-HBV cohort in Taiwan. The CVD mortality in 2000-2014 was ascertained by the Taiwan Death Certificates. Traffic pollution sources (2005-2013) were based on information provided by the Directorate General of Highway in 2005. Exposure to PM2.5 was based on a land-use regression model. We applied Cox proportional hazard models to assess the association of traffic vehicle exposure and CVD mortality. A causal mediation analysis was applied to evaluate the mediation effect of PM2.5 on the relationship between traffic and CVD mortality. RESULTS: A total of 382 CVD mortalities were identified from 2000 to 2014. We found participants exposed to higher volumes of small car and truck exhausts had an increased CVD mortality. The adjusted hazard ratio (HR) was 1.10 for small cars (95% confidence interval [CI], 0.94-1.27; P-value = 0.23) and 1.24 for truck (95% CI, 1.03-1.51; P-value = 0.03) per one unit increment of the logarithm scale. The findings were still robust with further adjustment for different types of vehicles. A causal mediation analysis revealed PM2.5 had an over 60% mediation effect on traffic-CVD association. CONCLUSIONS: Exposure to exhaust from trucks or gasoline-powered cars is positively associated with CVD mortality, and air pollution may play a role in this association.

Early childhood traffic-related air pollution and risk of allergic rhinitis at 2-4 years of age modification by family stress and male gender: a case-control study in Shenyang, China

BACKGROUND@#Few studies have explored the modifications by family stress and male gender in the relationship between early exposure to traffic-related air pollution (TRAP) and allergic rhinitis (AR) risk in preschool children.@*METHODS@#We conducted a case-control study of 388 children aged 2-4 years in Shenyang, China. These children AR were diagnosed by clinicians. By using measured concentrations from monitoring stations, we estimated the exposures of particulate matter less than 10 μm in diameter (PM@*RESULTS@#The prevalence of AR in children aged 2-4 years (6.4%) was related to early TRAP exposure. With an IQR (20 μg/m@*CONCLUSIONS@#Family stress and male gender may increase the risk of AR in preschool children with early exposure to PM