ABSTRACT
Background: Ambient fine particulate matter (PM2.5) is among the most prevalent sources of environmentally induced inflammation and oxidative stress, both of which are implicated in the pathogenesis of most mental disorders. Evidence, however, concerning the impact of PM2.5 on mental health is just emerging.

Objective: We examined the association between PM2.5 and current level of depressive and anxiety symptoms using a nationally representative probability sample (n = 4,008) of older, community-dwelling individuals living across the United States (the National Social Life, Health and Aging project).

Methods: Mental health was evaluated using validated, standardized questionnaires and clinically relevant cases were identified using well-established cutoffs; daily PM2.5 estimates were obtained using spatiotemporal models. We used generalized linear mixed models, adjusting for potential confounders, and explored effect modification.

Results: An increase in PM2.5 was significantly associated with anxiety symptoms, with the largest increase for 180-days moving average (OR = 1.61; 95% CI: 1.35, 1.92) after adjusting for socioeconomic measures (SES); PM2.5 was positively associated with depressive symptoms, and significantly for 30-day moving average (OR = 1.16; 95% CI: 1.05, 1.29) upon SES adjustment. The observed associations were enhanced among individuals who had low SES and history of comorbidity. When considering mental health as chronic conditions, PM2.5 was significantly associated with incident depressive symptoms for all exposure windows examined, but with incident anxiety symptoms only for shorter exposure windows, which may be due to a drop in power resulting from the decreased between-subject variability in chronic PM2.5 exposure.

Conclusion: PM2.5 was associated with depressive and anxiety symptoms, with associations the strongest among individuals with lower SES or among those with certain health-related characteristics.

ABSTRACT

Background
There is growing evidence to suggest that living near major roads (and suffering from the air pollution of urban streets) can have an adverse effect on bone health. However, little is known about its relationship to fractures caused by osteoporosis.

Objective
This study was designed to investigate the relationship between residents living near major roads and the incidence of osteoporotic fractures.

Methods
A retrospective cohort of 529 subjects was established based on community populations in older women aged 65–91. All participants lived in Beijing between September 27, 2007 and September 26, 2017. The distance between the residential sites of the subjects and the main roads was determined by the authors. Osteoporotic fracture diagnosis was based on medical histories and imaging examinations (DXA and X-rays). The Cox proportional hazard model was used to assess the association between traffic proximity and osteoporotic fractures, with suitable adjustments for individual and background factors.

Results
The age range of all participants was 65–91 years, with an average age of 75.8 years (and a standard deviation 6.8 years). Of these, 19 (3.59%) suffered from diabetes, and 48 (9%) had hypertension; 85 (14%) families had annual incomes below US $30,000 and 402 (76%) had received a secondary school education or higher. Nearly 25% of people lived within 50 m of a main road, while 50% lived within 300 m. Between 2007 and 2017, a total of 96 osteoporotic fractures were observed. For people living <50 m from a main road, the adjusted hazard ratio (HR) for osteoporotic fractures was 2.509 (95% CI 1.345–4.680), while it was 1.830 (95% CI 1.029–3.255) for those living at a distance of 50–300 m from a main road vs. those living further than 300 m away.

Conclusion
In this community-based cohort, living near a major road was associated with a higher incidence of osteoporotic fractures.

Authors' concluding statement:

"In the Province of Padua, MS prevalence is strongly associated with PM2.5 exposure suggesting that air pollutants may be one of the possible environmental risk factors for MS."
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ABSTRACT
Background: Incidence and prevalence trends of multiple sclerosis (MS) in the Province of Padua, North-East Italy, suggest that environmental factors may be associated with increased MS risk.

Objective: To investigate the association of PM2.5 with MS prevalence in one of the most polluted geographical area of Italy.

Methods: In total, 1435 Italian MS patients residing in the Province of Padua were enrolled. The province surface was classified into urban areas, isolated villages, industrialized places, and countryside. Satellite-derived dust-free and sea salt-free PM2.5 concentrations (annual average 1998-2015, μg/m3) allowed the identification of 18 classes of territorial sections with statistically evaluable numbers of inhabitants. Possible correlations between residential locality types, PM2.5 concentrations, and MS prevalence were investigated.

Results: MS prevalence was significantly (p < 0.0001) higher in urban areas (ranging from 219 in Padua City to 169/100,000 in other urban areas) compared to isolated villages (116/100,000) or rural domains (109/100,000) and strongly correlated with the annual average concentration of PM2.5 (r = 0.81, p < 0.001). Regression analysis further associated MS cases with PM.2.5 average concentration (β = 0.11, p < 0.001).

Conclusion: In the Province of Padua, MS prevalence is strongly associated with PM2.5 exposure suggesting that air pollutants may be one of the possible environmental risk factors for MS.

2021 study showing the dramatic increase in MS over 50 years can be seen here - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8940874/

The kidneys from 25 patients who received transplants were examined for precise levels of black carbon. The compound forms during high temperature combustion inside car and truck engines using gasoline and diesel fuel. It is emitted from tailpipes where it is breathed in higher amounts by people driving on or living near busy traffic roadways.

Kidney biopsies of transplant patients showed the black carbon particles were being inhaled by the individual and then traveling through the blood and concentrating inside the kidneys over time. Each 10% higher level of black carbon resulted in an 8.24% higher urinary levels of something called KIM-1 and CysC. These two blood markers are used as evidence of kidney damage and building kidney failure. The scientists concluded with the following statement:

"In conclusion, we were able to demonstrate, under real-life exposure conditions, the translocation of inhaled BC (black carbon) particles into the kidneys of kidney transplant recipients. Furthermore, urinary biomarkers, such as KIM-1, a biomarker to assess kidney damage, were linked to higher accumulation of kidney BC load, as well as with ambient BC exposure at the transplant recipients’ residential address and the residential proximity to a major road."
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ABSTRACT:
Background: Ultrafine particles, including black carbon (BC), can reach the systemic circulation and therefore may distribute to distant organs upon inhalation. The kidneys may be particularly vulnerable to the adverse effects of BC exposure due to their filtration function.

Objectives: We hypothesized that BC particles reach the kidneys via the systemic circulation, where the particles may reside in structural components of kidney tissue and impair kidney function.

Methods: In kidney biopsies from 25 transplant patients, we visualized BC particles using white light generation under femtosecond-pulsed illumination. The presence of urinary kidney injury molecule-1 (KIM-1) and cystatin c (CysC) were evaluated with ELISA. We assessed the association between internal and external exposure matrices and urinary biomarkers using Pearson correlation and linear regression models.

Results: BC particles could be identified in all biopsy samples with a geometric mean (5th, 95th percentile) of 1.80 × 103 (3.65 × 102, 7.50 × 103) particles/mm3 kidney tissue, predominantly observed in the interstitium (100 %) and tubules (80 %), followed by the blood vessels and capillaries (40 %), and the glomerulus (24 %). Independent from covariates and potential confounders, we found that each 10 % higher tissue BC load resulted in 8.24 % (p = 0.03) higher urinary KIM-1. In addition, residential proximity to a major road was inversely associated with urinary CysC (+10 % distance: -4.68 %; p = 0.01) and KIM-1 (+10 % distance: -3.99 %; p < 0.01). Other urinary biomarkers, e.g., the estimated glomerular filtration rate or creatinine clearance showed no significant associations.

Discussion and conclusion: Our findings that BC particles accumulate near different structural components of the kidney represent a potential mechanism explaining the detrimental effects of particle air pollution exposure on kidney function. Furthermore, urinary KIM-1 and CysC show potential as air pollution-induced kidney injury biomarkers for taking a first step in addressing the adverse effects BC might exert on kidney function.

Additional statistics on the doubling of kidney disease in all ages since 1990
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8281340/

"Traffic pollution was positively associated with growth in BMI in children aged 5–11 years. Traffic pollution may be controlled via emission restrictions; changes in land use that promote jobs-housing balance and use of public transit and hence reduce vehicle miles traveled; promotion of zero emissions vehicles; transit and car-sharing programs; or by limiting high pollution traffic, such as diesel trucks, from residential areas or places where children play outdoors, such as schools and parks. These measures may have beneficial effects in terms of reduced obesity formation in children."
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ABSTRACT
Background: Biologically plausible mechanisms link traffic-related air pollution to metabolic disorders and potentially to obesity. Here we sought to determine whether traffic density and traffic-related air pollution were positively associated with growth in body mass index (BMI = kg/m2) in children aged 5-11 years.

Methods: Participants were drawn from a prospective cohort of children who lived in 13 communities across Southern California (N = 4550). Children were enrolled while attending kindergarten and first grade and followed for 4 years, with height and weight measured annually. Dispersion models were used to estimate exposure to traffic-related air pollution. Multilevel models were used to estimate and test traffic density and traffic pollution related to BMI growth. Data were collected between 2002-2010 and analyzed in 2011-12.

Results: Traffic pollution was positively associated with growth in BMI and was robust to adjustment for many confounders. The effect size in the adjusted model indicated about a 13.6% increase in annual BMI growth when comparing the lowest to the highest tenth percentile of air pollution exposure, which resulted in an increase of nearly 0.4 BMI units on attained BMI at age 10. Traffic density also had a positive association with BMI growth, but this effect was less robust in multivariate models.

Conclusions: Traffic pollution was positively associated with growth in BMI in children aged 5-11 years. Traffic pollution may be controlled via emission restrictions; changes in land use that promote jobs-housing balance and use of public transit and hence reduce vehicle miles traveled; promotion of zero emissions vehicles; transit and car-sharing programs; or by limiting high pollution traffic, such as diesel trucks, from residential areas or places where children play outdoors, such as schools and parks. These measures may have beneficial effects in terms of reduced obesity formation in children.

ABSTRACT
Background: This systematic review and meta-analysis aimed to overview the observational studies on the association of exposure to air pollution and type 1 diabetes mellitus (T1DM).

Materials and methods: Based on PRISMA guidelines, we systematically reviewed the databases of PubMed, Scopus, Embase, and Web of Science databases to determine the association of air pollution exposure and T1DM. Quality assessment of the papers was evaluated using the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist for observational studies. The odds ratios (OR) and their 95% confidence intervals (CI) were calculated to assess the strength of the associations between air pollutants (gases and particulate matter air pollutants including PM10, PM2.5, NO2, volatile organic compound, SO4, SO2, O3) and T1DM.

Results: Out of 385 initially identified papers, 6 studies were used for this meta-analysis. Fixed effects meta-analysis showed a significant association between per 10 μg/m3 increase in O3 and PM2.5 exposures with the increased risk of T1DM (3 studies, OR = 1.51, 95% CI: 1.26, 1.80, I 2 = 83.5% for O3 and two studies, OR = 1.03, 95% CI: 1.01, 1.05, I 2 = 76.3% for PM2.5). There was no evidence of association between increased risk of T1DM and exposure to PM10 (OR = 1.02, 95% CI: 0.99-1.06, I 2 = 59.4%), SO4 (OR = 1.16, 95% CI: 0.91-1.49, I 2 = 93.8%), SO2 (OR = 0.94, 95% CI: 0.83-1.06, I 2 = 85.0%), and NO2 (OR = 0.995,95% CI: 1.05-1.04, I 2 = 24.7%).

Conclusion: Recent publications indicated that exposure to ozone and PM2.5 may be a risk factor for T1DM. However, due to limited available studies, more prospective cohort studies are needed to clarify the role of air pollutants in T1DM occurrence.

ABSTRACT
Background & aims: Evidence is sparse and inconclusive on the association between long-term fine (≤2.5 μm) particulate matter (PM2.5) exposure and esophageal cancer. We aimed to assess the association of PM2.5 with esophageal cancer risk and compared the esophageal cancer risk attributable to PM2.5 exposure and other established risk factors.

Methods: This study included 510,125 participants without esophageal cancer at baseline from China Kadoorie Biobank. A high-resolution (1 × 1 km) satellite-based model was used to estimate PM2.5 exposure during the study period. Hazard ratios (HR) and 95% CIs of PM2.5 with esophageal cancer incidence were estimated using Cox proportional hazard model. Population attributable fractions for PM2.5 and other established risk factors were estimated.

Results: There was a linear concentration-response relationship between long-term PM2.5 exposure and esophageal cancer. For each 10-μg/m3 increase in PM2.5, the HR was 1.16 (95% CI, 1.04-1.30) for esophageal cancer incidence. Compared with the first quarter of PM2.5 exposure, participants in the highest quarter had a 1.32-fold higher risk for esophageal cancer, with an HR of 1.32 (95% CI, 1.01-1.72). The population attributable risk because of annual average PM2.5 concentration ≥35 μg/m3 was 23.3% (95% CI, 6.6%-40.0%), higher than the risks attributable to lifestyle risk factors.

Conclusions: This large prospective cohort study of Chinese adults found that long-term exposure to PM2.5 was associated with an elevated risk of esophageal cancer. With stringent air pollution mitigation measures in China, a large reduction in the esophageal cancer disease burden can be expected.

MRI imaging was also done to determine brain changes from higher roadway traffic air pollution. Researchers stated shorter residential distances to major roads was consistently associated with smaller brain volumes. Below is a quote of their findings, "In conclusion, we found that the shorter residential distance to major traffic roads was consistently associated with the higher dementia risk and smaller brain structure volumes. Traffic-related air pollution was identified as the main mediating pathway linking traffic proximity and neurocognitive outcomes, rather than noise pollution. These findings support tackling traffic-related air pollution as the key to preventing dementia onset among people living near heavy traffic.
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ABSTRACT
Background: Uncertainty exists regarding the operating pathways between near-roadway exposure and dementia incidence. We intend to examine relationships between proximity to major roadways with dementia incidence and brain MRI structure measures, and potential mediation roles of air and noise pollution.

Methods: The cohort study was based on the UK Biobank. Baseline survey was conducted from 2006 to 2010, with linkage to electronic health records conducted for follow-up. Residential distance to major roadways was ascertained residential address postcode. A land use regression model was applied for estimating traffic-related air pollution at residence. Dementia incidence was ascertained using national administrative databases. Brain MRI measures were derived as image-derived phenotypes, including total brain, white matter, gray matter, and peripheral cortical gray matter.

Results: We included 460,901 participants [mean (SD) age: 57.1 (8.1) years; men: 45.7%]. Compared with individuals living >1,000 m from major traffic roads, living ≤1,000 m was associated with a 13% to 14% higher dementia risk, accounting for 10% of dementia cases. Observed association between residential distance and dementia was substantially mediated by traffic-related air pollution, mainly nitrogen dioxide (proportion mediated: 63.6%; 95% CI, 27.0 to 89.2%) and PM2.5 (60.9%, 26.8 to 87.0%). The shorter residential distance was associated with smaller volumes of brain structures, which was also mediated by traffic-related air pollutants. No significant mediation role was observed of noise pollution.

Conclusions: The shorter residential distance to major roads was associated with elevated dementia incidence and smaller brain structure volumes, which was mainly mediated by traffic-related air pollution.

ABSTRACT
Objectives: The objective of this study is to examine the relationship between measured traffic density near the homes of children and attained body mass index (BMI) over an eight-year follow up.

Methods: Children aged 9-10 years were enrolled across multiple communities in Southern California in 1993 and 1996 (n=3318). Children were followed until age 18 or high school graduation to collect longitudinal information, including annual height and weight measurements. Multilevel growth curve models were used to assess the association between BMI levels at age 18 and traffic around the home.

Results: For traffic within 150 m around the child's home, there were significant positive associations with attained BMI for both sexes at age 18. With the 300 m traffic buffer, associations for both male and female growth in BMI were positive, but significantly elevated only in females. These associations persisted even after controlling for numerous potential confounding variables.

Conclusions: This analysis yields the first evidence of significant effects from traffic density on BMI levels at age 18 in a large cohort of children. Traffic is a pervasive exposure in most cities, and our results identify traffic as a major risk factor for the development of obesity in children.

"These results demonstrate that subchronic PM2.5 exposure depletes the ovarian reserve by increasing recruitment of primordial follicles into the growing pool and increasing apoptosis (death) of growing follicles. Further, PM2.5 exposure and removal of the ovaries each increase atherosclerosis progression..... Premature loss of ovarian function is associated with increased risk of osteoporosis, cardiovascular disease and Alzheimer's disease in women. Our results thus support possible links between PM2.5 exposure and other adverse health outcomes in women."
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ABSTRACT
Background: Fine particulate matter (PM2.5) exposure accelerates atherosclerosis and contains known ovotoxic chemicals. However, effects of exposure to PM2.5 on the finite ovarian follicle pool have hardly been investigated, nor have interactions between ovarian and cardiovascular effects. We hypothesized that subchronic inhalation exposure to human-relevant concentrations of PM2.5 results in destruction of ovarian follicles via apoptosis induction, as well as accelerated recruitment of primordial follicles into the growing pool. Further, we hypothesized that destruction of ovarian follicles enhances the adverse cardiovascular effects of PM2.5 in females.

Results: Hyperlipidemic apolipoprotein E (Apoe) null ovary-intact or ovariectomized female mice and testis-intact male mice were exposed to concentrated ambient PM2.5 or filtered air for 12 weeks, 5 days/week for 4 h/day using a versatile aerosol concentration enrichment system. Primordial, primary, and secondary ovarian follicle numbers were decreased by 45%, 40%, and 17%, respectively, in PM2.5-exposed ovary-intact mice compared to controls (P < 0.05). The percentage of primary follicles with granulosa cells positive for the mitosis marker Ki67 was increased in the ovaries from PM2.5-exposed females versus controls (P < 0.05), consistent with increased recruitment of primordial follicles into the growing pool. Exposure to PM2.5 increased the percentages of primary and secondary follicles with DNA damage, assessed by γH2AX immunostaining (P < 0.05). Exposure to PM2.5 increased the percentages of apoptotic antral follicles, determined by TUNEL and activated caspase 3 immunostaining (P < 0.05). Removal of the ovaries and PM2.5-exposure exacerbated the atherosclerotic effects of hyperlipidemia in females (P < 0.05). While there were statistically significant changes in blood pressure and heart rate variability in PM2.5-compared to Air-exposed gonad-intact males and females and ovariectomized females, the changes were not consistent between exposure years and assessment methods.

Conclusions: These results demonstrate that subchronic PM2.5 exposure depletes the ovarian reserve by increasing recruitment of primordial follicles into the growing pool and increasing apoptosis of growing follicles. Further, PM2.5 exposure and removal of the ovaries each increase atherosclerosis progression in Apoe-/- females. Premature loss of ovarian function is associated with increased risk of osteoporosis, cardiovascular disease and Alzheimer's disease in women. Our results thus support possible links between PM2.5 exposure and other adverse health outcomes in women.

This study certainly raises a red flag regarding the safety of living near busy roadway traffic. Previous studies have shown the chemical benzene (common in gasoline) is linked to damaging bone marrow and increasing related cancers. This study would also suggest an increased likelihood of remission and/or life expectancy for a child with cancer could be achieved by moving away from the residence, thereby reducing exposure to benzene and other toxic fuel by-products.


ABSTRACT
Data from a recently completed case-referent study of childhood cancer were used to explore a possible role of environmental exposures from traffic exhaust. The street addresses of 328 cancer patients and 262 population-based referents were used to assign traffic density (vehicles per day) as a marker of potential exposure to motor vehicle exhaust. An odds ratio of 1.7 [95% confidence interval (95% CI) 1.0-2.8] was found for the total number of childhood cancers and 2.1 (95% CI 1.1-4.0) for leukemias in a contrast of high and low traffic density addresses (greater than or equal to 500 versus less than 500 vehicles per day). Stronger associations were found with a traffic density cutoff score of greater than or equal to 10,000 vehicles per day, with imprecise odds ratios of 3.1 (95% CI 1.2-8.0) and 4.7 (95% CI 1.6-13.5) for the total number of cancers and leukemias, respectively. Adjustment for suspected risk factors for childhood cancer did not substantially change these results. Though the results are inconclusive, the identified association warrants further evaluation.

ABSTRACT
Airway epithelium, the first defense barrier of the respiratory system, facilitates mucociliary clearance against inflammatory stimuli, such as pathogens and particulates inhaled into the airway and lung. Inhaled particulate matter 2.5 (PM2.5) can penetrate the alveolar region of the lung, and it can develop and exacerbate respiratory diseases. Although the pathophysiological effects of PM2.5 in the respiratory system are well known, its impact on mucociliary clearance of airway epithelium has yet to be clearly defined. In this study, we used two different 3D in vitro airway models, namely the EpiAirway-full-thickness (FT) model and a normal human bronchial epithelial cell (NHBE)-based air-liquid interface (ALI) system, to investigate the effect of diesel exhaust particles (DEPs) belonging to PM2.5 on mucociliary clearance. RNA-sequencing (RNA-Seq) analyses of EpiAirway-FT exposed to DEPs indicated that DEP-induced differentially expressed genes (DEGs) are related to ciliary and microtubule function and inflammatory-related pathways. The exposure to DEPs significantly decreased the number of ciliated cells and shortened ciliary length. It reduced the expression of cilium-related genes such as acetylated α-tubulin, ARL13B, DNAH5, and DNAL1 in the NHBEs cultured in the ALI system. Furthermore, DEPs significantly increased the expression of MUC5AC, whereas they decreased the expression of epithelial junction proteins, namely, ZO1, Occludin, and E-cadherin. Impairment of mucociliary clearance by DEPs significantly improved the release of epithelial-derived inflammatory and fibrotic mediators such as IL-1β, IL-6, IL-8, GM-CSF, MMP-1, VEGF, and S100A9. Taken together, it can be speculated that DEPs can cause ciliary dysfunction, hyperplasia of goblet cells, and the disruption of the epithelial barrier, resulting in the hyperproduction of lung injury mediators. Our data strongly suggest that PM2.5 exposure is directly associated with ciliary and epithelial barrier dysfunction and may exacerbate lung injury.

Results showed the inflammatory marker TNF increased 25% with each 10 μg/m3 incremental increase in PM2.5. While higher PM2.5 is known to increase heart disease and stroke, this study is one of the first to provide an explanation of why this is occurring. The following is the concluding statements by the authors in the introductory paragraph - "We found robust evidence of endothelial injury and systemic inflammation upon exposure to increased PM2.5 levels even in young healthy individuals. These findings lend support to the view that PM2.5 causes endothelial injury, potentially by establishing a mild inflammatory state. Our results are also consistent with the possibility that aberrant immune responses and endothelial injury may be early causes of endothelial dysfunction and CVD attributable to PM2.5 exposure in susceptible individuals."
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ABSTRACT
Rationale: Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.

Objective: To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.

Methods and results: Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GROα [growth-regulated protein α], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNFα [tumor necrosis factor α], IP-10 [interferon γ-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1α/β [macrophage inflammatory protein 1α/β], IL-6 [interleukin 6], and IL-1β [interleukin 1β]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.

Conclusions: Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

The most striking difference came when comparing families living the closest 10% to the freeway (less than 300 meters) to the 10% of families living the farthest away (more than 5,150 meters). Those living in the closest group had a 2.48 times greater risk of having a child with autism. A unique design of this study is scientists chose to use 10% quintiles of exposure for comparison rather than the 25% quartiles typically used in other studies. This allows for observing a more accurate consequence of exposure. Being that autism is now affecting close to 1 in 30 children today (2024), a doubling of autism rates (as seen here) would result in 1 in 15 being diagnosed with autism. This study, by extension, also raises serious concerns of higher rates of autism for pregnant mothers spending extended time driving in busy roadway traffic as well.

The scientists concluded by stating,

"Our analysis is the first step in examining a hypothesized relationship between air pollutants and autism. It has been estimated that 11% of the U.S. population lives within 100 m of a four-lane highway, so a causal link to autism or other neurodevelopmental disorders would have broad public health implications.


ABSTRACT
Background: Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects.

Objectives: We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure.

Methods: Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother's address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls.

Results: Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (≤ 309 m) for cases than for controls [odds ratio (OR)=1.86; 95% confidence interval (CI), 1.04-3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR=2.22; CI, 1.16-4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism.

Conclusions: Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.

ABSTRACT
Objectives: Animal studies suggest that air pollution is neurotoxic to a developing fetus, but evidence in humans is limited. We tested the hypothesis that higher air pollution is associated with lower child IQ and that effects vary by maternal and child characteristics, including prenatal nutrition.

Methods: We used prospective data collected from the Conditions Affecting Neurocognitive Development and Learning in Early Childhood study. Outdoor pollutant exposure during pregnancy was predicted at geocoded home addresses using a validated national universal kriging model that combines ground-based monitoring data with an extensive database of land-use covariates. Distance to nearest major roadway was also used as a proxy for traffic-related pollution. Our primary outcome was full-scale IQ measured at age 4-6. In regression models, we adjusted for multiple determinants of child neurodevelopment and assessed interactions between air pollutants and child sex, race, socioeconomic status, reported nutrition, and maternal plasma folate in second trimester.

Results: In our analytic sample (N = 1005) full-scale IQ averaged 2.5 points (95% CI: 0.1, 4.8) lower per 5 μg/m3 higher prenatal PM10, while no associations with nitrogen dioxide or road proximity were observed. Associations between PM10 and IQ were modified by maternal plasma folate (pinteraction = 0.07). In the lowest folate quartile, IQ decreased 6.8 points (95% CI: 1.4, 12.3) per 5-unit increase in PM10; no associations were observed in higher quartiles.

Conclusions: Our findings strengthen evidence that air pollution impairs fetal neurodevelopment and suggest a potentially important role of maternal folate in modifying these effects.

The human brain grows at over 4,000 cells a second begining the 4th week of pregnancy. Cells begin from the center of the brain and move outward and recieve signals not only for growth but for when to stop in their proper location. Proper growth of the human brain requires a crtical balance of communication signals between brain cells through what are called signaling pathways. If signaling pathways are interrupted by external environmental factors (such as from endocrine disrupting chemicals in vehicle exhaust) detrimental changes could be significant. Researchers here also reviewed additional studies with older children but stated a lack of studies in younger children. For example, among school-aged children, exposure in the womb to polycyclic aromatic hydrocarbons (a toxic chemical that forms during engine fuel burning), was found to reduce size of the child's left brain hemisphere white matter surface at age 8. Prenatal PM2.5 exposure was also shown to reduce cortex thickness, altered white matter organization, and reduced blood flow at 6–14 years.[12, 13, 20] Prenatal PM10 exposure was shown to reduce full-scale IQ at ages 4–6 years, and prenatal nitrogen dioxide exposure and traffic density around the home was shown to reduce verbal IQ scores at 7 years of age [10, 11]. Nitrogen dioxide is a primary gas created during fossil-fuel engine combusion. Exposure to this air pollutant resulted in poorer attentional performance in children at 4–5 years of age [14, 15]. Additionally, studies found PM2.5 exposure between weeks 12–40 in pregnancy resulted in lower IQ, slower reaction time, and poorer memory at 6–7 years. [16] In addition, PM10, PM2.5, and NO2 exposure in the late-prenatal and early postnatal periods Late pregnancy and immediately after birth) have been associated with an increased risk of ADHD-like behaviors in children around age 3 [22]. In summary, this research shows a child's developing brain during pregnancy can be damaged from even typical levels of air pollution in society. As this exposure is widespread in society today, the harmful behavioral and economic impacts upon society would be of great concern. The following is the concluding paragraph from the authors of the study, "Prenatal exposure to ambient air pollutants was inversely associated with functional neurodevelopmental outcomes at 2 years, raising concern for child health and future functional impairment. In addition, our findings indicate that exposures during mid to late pregnancy may be especially detrimental to neurodevelopment, which suggests the need for limiting air pollution exposure, especially during the latter half of pregnancy. In summary, this study adds to the growing body of literature cataloging the negative health consequences of both pre- and postnatal ambient air pollution exposure that should be used to inform policy efforts to limit human exposure to air pollutants."

ABSTRACT
Background: Higher prenatal ambient air pollution exposure has been associated with impaired neurodevelopment in preschoolers and school-aged children. The purpose of this study was to explore the relationships between prenatal ambient air pollution exposure and neurodevelopment during infancy.

Methods: This study examined 161 Latino mother-infant pairs from the Southern California Mother's Milk Study. Exposure assessments included prenatal nitrogen dioxide (NO2) and particulate matter smaller than 2.5 and 10 microns in diameter (PM2.5 and PM10, respectively). The pregnancy period was also examined as three windows, early, mid, and late, which describe the first, middle, and last three months of pregnancy. Infant neurodevelopmental outcomes at 2 years of age were measured using the Bayley-III Scales of Infant and Toddler Development. Multivariable linear models and distributed lag linear models (DLM) were used to examine relationships between prenatal exposures and neurodevelopmental scores, adjusting for socioeconomic status, breastfeeding frequency, time of delivery, pre-pregnancy body mass index, and infant birthweight and sex.

Results: Higher prenatal exposure to PM10 and PM2.5 was negatively associated with composite cognitive score (β = -2.01 [-3.89, -0.13] and β = -1.97 [-3.83, -0.10], respectively). In addition, higher average prenatal exposure to PM10 was negatively associated with composite motor (β = -2.35 [-3.95, -0.74]), scaled motor (β = -0.77 [-1.30, -0.24]), gross motor (β = -0.37 [-0.70, -0.04]), fine motor (β = -0.40 [-0.71, -0.09]), composite language (β = -1.87 [-3.52, -0.22]), scaled language (β = -0.61 [-1.18, -0.05]) and expressive communication scaled scores (β = -0.36 [-0.66, -0.05]). DLMs showed that higher prenatal air pollution exposure during mid and late pregnancy was inversely associated with motor, cognitive, and communication language scores.

Conclusions: Higher exposure to air pollutants during pregnancy, particularly in the mid and late prenatal periods, was inversely associated with scaled and composite motor, cognitive, and language scores at 2 years. These results indicate that prenatal ambient air pollution may negatively impact neurodevelopment in early life.

Interestingly, the type of cancers noted in women are considered estrogen enhanced cancers, meaning their growth is accelerated in relation to estrogen levels. As chemicals in traffic related air pollution are now known to mimic estrogen (meaning they can bind onto estrogen receptors), this raises the likely possibility they would accelerate abnormal cell growth in these cancers.

Another interesting finding - more than 25% of blood, brain, breast, cervical, endometrial, and ovarian cancers were observed in the highest exposure quartile (10.67–15.05 µg/m3. But normally, only 25% of cancers would be expected in this high quartile group - that is, if no harmful effects were taking place form other enivironmental sources.
As the per capita rate of these female cancers has been rising steadily the past 50 years, gasoline and diesel vehicles now appear to be a contributing factor to this female cancer epidemic.............................................

ABSTRACT
Introduction: The NIH All of Us Research Program has enrolled over 544,000 participants across the US with unprecedented racial/ethnic diversity, offering opportunities to investigate myriad exposures and diseases. This paper aims to investigate the association between PM2.5 exposure and cancer risks.

Materials and methods: This work was performed on data from 409,876 All of Us Research Program participants using the All of Us Researcher Workbench. Cancer case ascertainment was performed using data from electronic health records and the self-reported Personal Medical History questionnaire. PM2.5 exposure was retrieved from NASA's Earth Observing System Data and Information Center and assigned using participants' 3-digit zip code prefixes. Multivariate logistic regression was used to estimate the odds ratio (OR) and 95% confidence interval (CI). Generalized additive models (GAMs) were used to investigate non-linear relationships.

Results: A total of 33,387 participants and 46,176 prevalent cancer cases were ascertained from participant EHR data, while 20,297 cases were ascertained from self-reported survey data from 18,133 participants; 9,502 cancer cases were captured in both the EHR and survey data. Average PM2.5 level from 2007 to 2016 was 8.90 μg/m3 (min 2.56, max 15.05). In analysis of cancer cases from EHR, an increased odds for breast cancer (OR 1.17, 95% CI 1.09-1.25), endometrial cancer (OR 1.33, 95% CI 1.09-1.62) and ovarian cancer (OR 1.20, 95% CI 1.01-1.42) in the 4th quartile of exposure compared to the 1st. In GAM, higher PM2.5 concentration was associated with increased odds for blood cancer, bone cancer, brain cancer, breast cancer, colon and rectum cancer, endocrine system cancer, lung cancer, pancreatic cancer, prostate cancer, and thyroid cancer.

Conclusions: We found evidence of an association of PM2.5 with breast, ovarian, and endometrial cancers. There is little to no prior evidence in the literature on the impact of PM2.5 on risk of these cancers, warranting further investigation.

Other important points discussed in the article include the ability of fine air pollution particles to bypass the blood brain barrier and enter the brain. Researchers stated experimental studies have confirmed that one of the main components of air pollution, PM2.5, as well as compounds
adsorbed on its surface, causes cell cycle arrest and apoptosis of neurons. This action, together with the oxidative stress and gene damage induced by these particles, maylead to degenerative changes in the brain [6]
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ABSTRACT
Air pollution is one of the greatest public health threats worldwide. All substances appearing in excessive quantities in the atmosphere, such as particulate matter, nitrogen oxides or sulphur oxides may be its ingredients. Depending on their size and nature, these compounds may cause greater risk of suffering from respiratory or cardiovascular diseases for exposed people as well as exacerbation and increased mortality due to these illnesses. Smaller particles may penetrate the brain's blood barrier and thus affect the central nervous system. In many studies, they have been shown to have negative effects on brain structure, like diminishing white matter or neuronal degeneration, leading to the earlier onset of Alzheimer or Parkinson disease. Nevertheless, there are reports of association of air pollution with mood disorders, depression, and even suicide. There are many risk factors for these conditions, most important of which are the social situation or chronic diseases. However, it has also been confirmed that the environment may affect mental health. This article will present experimental, clinical and epidemiological studies on exposure to air pollution and its impact on depressive disorders and suicide. Our goal is to determine the relationship between air pollution and incidence of depression and suicides.

ABSTRACT
We provide a comprehensive and updated systematic review and meta-analysis of the association between air pollution exposure and depression, searching PubMed, Embase, and Web of Sciences for relevant articles published up to May 2021, and eventually including 39 studies. Meta-analyses were performed separately according to pollutant type [particulate matter with diameter ≤10 μm (PM10) and ≤2.5 μm (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO)] and exposure duration [short- (<30 days) and long-term (≥30 days)]. Test for homogeneity based on Cochran's Q and I2 statistics were calculated and the restricted maximum likelihood (REML) random effect model was applied. We assessed overall quality of pooled estimates, influence of single studies on the meta-analytic estimates, sources of between-study heterogeneity, and publication bias. We observed an increased risk of depression associated with long-term exposure to PM2.5 (relative risk: 1.074, 95% confidence interval: 1.021–1.129) and NO2 (1.037, 1.011–1.064), and with short-term exposure to PM10 (1.009, 1.006–1.012), PM2.5 (1.009, 1.007–1.011), NO2 (1.022, 1.012–1.033), SO2 (1.024, 1.010–1.037), O3 (1.011, 0.997–1.026), and CO (1.062, 1.020–1.105). The publication bias affecting half of the investigated associations and the high heterogeneity characterizing most of the meta-analytic estimates partly prevent to draw very firm conclusions. On the other hand, the coherence of all the estimates after excluding single studies in the sensitivity analysis supports the soundness of our results. This especially applies to the association between PM2.5 and depression, strengthened by the absence of heterogeneity and of relevant publication bias in both long- and short-term exposure studies. Should further investigations be designed, they should involve large sample sizes, well-defined diagnostic criteria for depression, and thorough control of potential confounding factors. Finally, studies dedicated to the comprehension of the mechanisms underlying the association between air pollution and depression remain necessary.

The common vehicle exhaust gas nitrogen dioxide was also found to increase rates of dementia, with each 10 μg/m3 increase resulting in a 2% higher risk of dementia. As dementia has a high medical cost and takes a strong emotional toll on families - this report stresses the importance of rapidly eliminating vehicle sources of these pollutants that concentrate near roadways.
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ABSTRACT
Objective
To investigate the role of air pollutants in risk of dementia, considering differences by study factors that could influence findings.

Design
Systematic review and meta-analysis.

Data sources
EMBASE, PubMed, Web of Science, Psycinfo, and OVID Medline from database inception through July 2022.

Eligibility criteria for selecting studies
Studies that included adults (≥18 years), a longitudinal follow-up, considered US Environmental Protection Agency criteria air pollutants and proxies of traffic pollution, averaged exposure over a year or more, and reported associations between ambient pollutants and clinical dementia. Two authors independently extracted data using a predefined data extraction form and assessed risk of bias using the Risk of Bias In Non-randomised Studies of Exposures (ROBINS-E) tool. A meta-analysis with Knapp-Hartung standard errors was done when at least three studies for a given pollutant used comparable approaches.

Results
2080 records identified 51 studies for inclusion. Most studies were at high risk of bias, although in many cases bias was towards the null. 14 studies could be meta-analysed for particulate matter <2.5 µm in diameter (PM2.5). The overall hazard ratio per 2 μg/m3 PM2.5 was 1.04 (95% confidence interval 0.99 to 1.09). The hazard ratio among seven studies that used active case ascertainment was 1.42 (1.00 to 2.02) and among seven studies that used passive case ascertainment was 1.03 (0.98 to 1.07). The overall hazard ratio per 10 μg/m3 nitrogen dioxide was 1.02 ((0.98 to 1.06); nine studies) and per 10 μg/m3 nitrogen oxide was 1.05 ((0.98 to 1.13); five studies). Ozone had no clear association with dementia (hazard ratio per 5 μg/m3 was 1.00 (0.98 to 1.05); four studies).

Conclusion
PM2.5 might be a risk factor for dementia, as well as nitrogen dioxide and nitrogen oxide, although with more limited data. The meta-analysed hazard ratios are subject to limitations that require interpretation with caution. Outcome ascertainment approaches differ across studies and each exposure assessment approach likely is only a proxy for causally relevant exposure in relation to clinical dementia outcomes. Studies that evaluate critical periods of exposure and pollutants other than PM2.5, and studies that actively assess all participants for outcomes are needed. Nonetheless, our results can provide current best estimates for use in burden of disease and regulatory setting efforts.

ABSTRACT
Background: The available evidence of the effects of air pollution and noise on behavioral development is limited, and it overlooks exposure at schools, where children spend a considerable amount of time.

Objective: We aimed to investigate the associations of exposure to traffic-related air pollutants (TRAPs) and noise at school on behavioral development of schoolchildren.

Methods: We evaluated children 7-11 years of age in Barcelona (Catalonia, Spain) during 2012-2013 within the BREATHE project. Indoor and outdoor concentrations of elemental carbon (EC), black carbon (BC), and nitrogen dioxide (NO2) were measured at schools in two separate 1-week campaigns. In one campaign we also measured noise levels inside classrooms. Parents filled out the strengths and difficulties questionnaire (SDQ) to assess child behavioral development, while teachers completed the attention deficit/hyperactivity disorder criteria of the DSM-IV (ADHD-DSM-IV) list to assess specific ADHD symptomatology. Negative binomial mixed-effects models were used to estimate associations between the exposures and behavioral development scores.

Results: Interquartile range (IQR) increases in indoor and outdoor EC, BC, and NO2 concentrations were positively associated with SDQ total difficulties scores (suggesting more frequent behavioral problems) in adjusted multivariate models, whereas noise was significantly associated with ADHD-DSM-IV scores.

Conclusion: In our study population of 7- to 11-year-old children residing in Barcelona, exposure to TRAPs at school was associated with increased behavioral problems in schoolchildren. Noise exposure at school was associated with more ADHD symptoms.

It is also sometimes called coronary artery disease or ischemic heart disease. About 20.5 million U.S. adults have coronary artery disease, making it the most common type of heart disease in the United States, according to the Centers for Disease Control and Prevention. Coronary artery disease affects the larger coronary arteries on the surface of the heart. Another type of heart disease, called coronary microvascular disease, affects the tiny arteries within the heart muscle.

ABSTRACT

Background: Residential proximity to road traffic is associated with increased coronary heart disease (CHD) morbidity and mortality. It is unknown, however, whether changes in residential proximity to traffic could alter the risk of CHD mortality.

Methods: We used a population-based cohort study with a 5-year exposure period and a 4-year follow-up period to explore the association between changes in residential proximity to road traffic and the risk of CHD mortality. The cohort comprised all residents aged 45-85 years who resided in metropolitan Vancouver during the exposure period and without known CHD at baseline (n = 450,283). Residential proximity to traffic was estimated using a geographic information system. CHD deaths during the follow-up period were identified using provincial death registration database. The data were analyzed using logistic regression.

Results: Compared with the subjects consistently living away from road traffic (>150 m from a highway or >50 m from a major road) during the 9-year study period, those consistently living close to traffic (
Conclusions: Living close to major roadways was associated with increased risk of coronary mortality, whereas moving away from major roadways was associated with decreased risk.

ABSTRACT
Background: Childhood and adolescence are critical periods for the development of the brain. However, a limited number of studies have explored how air pollution may associate with affective symptoms in youth.

Methods: We performed a comprehensive review of the existing research on the associations between outdoor air pollution and affective disorders, suicidality, and the evidence for brain changes in youth. PRISMA guidelines were followed and PubMed, Embase, Web of Science, Cochrane Library, and PsychINFO databases were searched from their inception to June 2022.

Results: From 2123 search records, 28 papers were identified as being relevant for studying the association between air pollution and affective disorders (n = 14), suicide (n = 5), and neuroimaging-based evidence of brain alterations (n = 9). The exposure levels and neuropsychological performance measures were highly heterogeneous and confounders including traffic-related noise, indoor air pollution, and social stressors were not consistently considered. Notwithstanding, 10 out of the 14 papers provide evidence that air pollution is associated with increased risk of depression symptoms, and 4 out of 5 papers provide evidence that air pollution might trigger suicidal attempts and behaviors. Besides, 5 neuroimaging studies revealed decreased gray-matter volume in the Cortico-Striato-Thalamo-Cortical neurocircuitry, and two found white matter hyperintensities in the prefrontal lobe.

Conclusions: Outdoor air pollution is associated with increased risks of affective disorders and suicide in youth, and there is evidence for associated structural and functional brain abnormalities. Future studies should determine the specific effects of each air pollutant, the critical exposure levels, and population susceptibility.

In this study, air pollution exposure-particularly NO2 and NOx-was associated with increased odds of adolescent psychotic experiences, which partly explained the association between urban residency and adolescent psychotic experiences. Biological (eg, neuroinflammation) and psychosocial (eg, stress) mechanisms are plausible.
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ABSTRACT
Importance: Urbanicity is a well-established risk factor for clinical (eg, schizophrenia) and subclinical (eg, hearing voices and paranoia) expressions of psychosis. To our knowledge, no studies have examined the association of air pollution with adolescent psychotic experiences, despite air pollution being a major environmental problem in cities.

Objectives: To examine the association between exposure to air pollution and adolescent psychotic experiences and test whether exposure mediates the association between urban residency and adolescent psychotic experiences.

Design, setting, and participants: The Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born during the period from January 1, 1994, through December 4, 1995, in England and Wales and followed up from birth through 18 years of age. The cohort represents the geographic and socioeconomic composition of UK households. Of the original cohort, 2066 (92.6%) participated in assessments at 18 years of age, of whom 2063 (99.9%) provided data on psychotic experiences. Generation of the pollution data was completed on October 4, 2017, and data were analyzed from May 4 to November 21, 2018.

Exposures: High-resolution annualized estimates of exposure to 4 air pollutants-nitrogen dioxide (NO2), nitrogen oxides (NOx), and particulate matter with aerodynamic diameters of less than 2.5 (PM2.5) and less than 10 μm (PM10)-were modeled for 2012 and linked to the home addresses of the sample plus 2 commonly visited locations when the participants were 18 years old.

Main outcomes and measures: At 18 years of age, participants were privately interviewed regarding adolescent psychotic experiences. Urbanicity was estimated using 2011 census data.

Results: Among the 2063 participants who provided data on psychotic experiences, sex was evenly distributed (52.5% female). Six hundred twenty-three participants (30.2%) had at least 1 psychotic experience from 12 to 18 years of age. Psychotic experiences were significantly more common among adolescents with the highest (top quartile) level of annual exposure to NO2 (odds ratio [OR], 1.71; 95% CI, 1.28-2.28), NOx (OR, 1.72; 95% CI, 1.30-2.29), and PM2.5 (OR, 1.45; 95% CI, 1.11-1.90). Together NO2 and NOx statistically explained 60% of the association between urbanicity and adolescent psychotic experiences. No evidence of confounding by family socioeconomic status, family psychiatric history, maternal psychosis, childhood psychotic symptoms, adolescent smoking and substance dependence, or neighborhood socioeconomic status, crime, and social conditions occurred.

Conclusions and relevance: In this study, air pollution exposure-particularly NO2 and NOx-was associated with increased odds of adolescent psychotic experiences, which partly explained the association between urban residency and adolescent psychotic experiences. Biological (eg, neuroinflammation) and psychosocial (eg, stress) mechanisms are plausible.

ABSTRACT
Children living near highways are exposed to higher concentrations of traffic-related carcinogenic pollutants. Several studies reported an increased risk of childhood cancer associated with traffic exposure, but the published evidence is inconclusive. We investigated whether cancer risk is associated with proximity of residence to highways in a nation-wide cohort study including all children aged <16 years from Swiss national censuses in 1990 and 2000. Cancer incidence was investigated in time to event analyses (1990-2008) using Cox proportional hazards models and incidence density analyses (1985-2008) using Poisson regression. Adjustments were made for socio-economic factors, ionising background radiation and electromagnetic fields. In time to event analysis based on 532 cases the adjusted hazard ratio for leukaemia comparing children living <100 m from a highway with unexposed children (≥500 m) was 1.43 (95 % CI 0.79, 2.61). Results were similar in incidence density analysis including 1367 leukaemia cases (incidence rate ratio (IRR) 1.57; 95 % CI 1.09, 2.25). Associations were similar for acute lymphoblastic leukaemia (IRR 1.64; 95 % CI 1.10, 2.43) and stronger for leukaemia in children aged <5 years (IRR 1.92; 95 % CI 1.22, 3.04). Little evidence of association was found for other tumours. Our study suggests that young children living close to highways are at increased risk of developing leukaemia.

ABSTRACT

Inhaled particles and gases can harm health by promoting chronic inflammation in the body. Few studies have investigated the relationship between outdoor air pollution and inflammation by race and ethnicity, socioeconomic status, and lifestyle risk factors. We examined associations of particulate matter (PM) and other markers of traffic-related air pollution with circulating levels of C-reactive protein (CRP), a biomarker of systemic inflammation. CRP was measured from blood samples obtained in 1994–2016 from 7,860 California residents participating in the Multiethnic Cohort (MEC) Study. Exposure to PM (aerodynamic diameter ≤ 2.5 μm [PM2.5], ≤ 10 μm [PM10], and between 2.5 and 10 μm [PM10–2.5]), nitrogen oxides (NOx, including nitrogen dioxide [NO2]), carbon monoxide (CO), ground-level ozone (O3), and benzene averaged over one or twelve months before blood draw were estimated based on participants’ addresses. Percent change in geometric mean CRP levels and 95% confidence intervals (CI) per standard concentration increase of each pollutant were estimated using multivariable generalized linear regression. Among 4,305 females (55%) and 3,555 males (45%) (mean age 68.1 [SD 7.5] years at blood draw), CRP levels increased with 12-month exposure to PM10 (11.0%, 95% CI: 4.2%, 18.2% per 10 µg/m3), PM10–2.5 (12.4%, 95% CI: 1.4%, 24.5% per 10 µg/m3), NOx (10.4%, 95% CI: 2.2%, 19.2% per 50 ppb), and benzene (2.9%, 95% CI: 1.1%, 4.6% per 1 ppb). In subgroup analyses, these associations were observed in Latino participants, those who lived in low socioeconomic neighborhoods, overweight or obese participants, and never or former smokers. No consistent patterns were found for 1-month pollutant exposures. This investigation identified associations of primarily traffic-related air pollutants, including PM, NOx, and benzene, with CRP in a multiethnic population. The diversity of the MEC across demographic, socioeconomic, and lifestyle factors allowed us to explore the generalizability of effects of air pollution on inflammation across subgroups.

Below is the concluding paragraph as stated by the 7 scientists involved in this University of California study,
To our knowledge, this is the first study to show that increased TRAP (Traffic Related Air Pollution) exposure is associated with the gut microbiota. This study supports the hypothesis that environmental exposures, such as TRAP, have the potential to alter the relative abundance of gut bacteria. Results from this study also suggest that increased TRAP may negatively impact metabolic health through alterations in the composition and/or function of the gut microbiome, but larger studies are needed to confirm these initial findings.
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ABSTRACT
Background
Traffic-related air pollution (TRAP) exposure has been linked to type 2 diabetes and metabolic dysfunction in humans. Animal studies suggest that air pollutants may alter the composition of the gut microbiota, which may negatively impact metabolic health through changes in the composition and/or function of the gut microbiome.

Objectives
The primary aim of this study was to determine whether elevated TRAP exposure was correlated with gut bacterial taxa in overweight and obese adolescents from the Meta-AIR (Metabolic and Asthma Incidence Research) study. The secondary aim was to examine whether gut microbial taxa correlated with TRAP was also correlated with risk factors for type 2 diabetes (e.g., fasting glucose levels). We additionally explored whether correlations between TRAP and these metabolic risk factors could be explained by the relative abundance of these taxa.

Methods
Participants (17–19 years; n=43) were enrolled between 2014–2016 from Southern California. The CALINE4 line dispersion model was used to model prior year residential concentrations of nitrogen oxides (NOx) as a marker of traffic emissions. The relative abundance of fecal microbiota was characterized by 16S rRNA sequencing and spearman partial correlations were examined after adjusting for body fat percent.

Results
Freeway TRAP was correlated with decreased Bacteroidaceae (r=−0.48; p=0.001) and increased Coriobacteriaceae (r=0.48; p<0.001). These same taxa were correlated with fasting glucose levels, including Bacteroidaceae (r=−0.34; p=0.04) and Coriobacteriaceae (r=0.41; p<0.01). Further, freeway TRAP was positively correlated fasting glucose (r=0.45; p=0.004) and Bacteroidaceae and Coriobacteriaceae explained 24% and 29% of the correlation between TRAP and fasting glucose levels.

Conclusions
Increased TRAP exposure was correlated with gut microbial taxa and fasting glucose levels. Gut microbial taxa that were correlated with TRAP partially explained the correlation between TRAP and fasting glucose levels. These results suggest that exposure to air pollutants may negatively impact metabolic health via alterations in the gut microbiota.

ABSTRACT
Motor vehicle exhaust is a major contributor to air pollution, and exposure to benzene or other carcinogenic components may increase cancer risks. We aimed to investigate the association between traffic-related air pollution and risk of childhood cancer in a nationwide cohort study in Switzerland. We identified incident cases from the Swiss Childhood Cancer Registry diagnosed < 16 years of age between 1990 and 2015 and linked them probabilistically with the census-based Swiss National Cohort study. We developed land use regression models to estimate annual mean ambient levels of nitrogen dioxide (NO2) and benzene outside 1.4 million children’s homes. We used risk-set sampling to facilitate the analysis of time-varying exposure and fitted conditional logistic regression models adjusting for neighborhood socio-economic position, level of urbanization, and background ionizing radiation. We included 2,960 cancer cases in the analyses. The adjusted hazard ratios (HR) and 95% confidence intervals for exposure to NO2 per 10 μg/m3 were 1.00 (95%-CI 0.88–1.13) for acute lymphoblastic leukemia (ALL) and 1.31 (95%-CI 1.00–1.71) for acute myeloid leukemia (AML). Using exposure lagged by 1 to 5 years instead of current exposure attenuated the effect for AML. The adjusted HR for exposure to benzene per 1 μg/m3 was 1.03 (95%-CI 0.86–1.23) for ALL and 1.29 (95%-CI 0.86–1.95) for AML. We also observed increased HRs for other diagnostic groups, notably non-Hodgkin lymphoma. Our study adds to the existing evidence that exposure to traffic-related air pollution is associated with an increased risk of childhood leukemia, particularly AML.

ABSTRACT
Background
Air pollution is involved in many pathologies. These pollutants act through several mechanisms that can affect numerous physiological functions, including reproduction: as endocrine disruptors or reactive oxygen species inducers, and through the formation of DNA adducts and/or epigenetic modifications. We conducted a systematic review of the published literature on the impact of air pollution on reproductive function.

Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included (1) ovary or follicle or oocyte or testis or testicular or sperm or spermatozoa or fertility or infertility and (2) air quality or O3 or NO2 or PM2.5 or diesel or SO2 or traffic or PM10 or air pollution or air pollutants. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the search terms and published in English. We have excluded articles whose results did not concern fertility or gamete function and those focused on cancer or allergy. We have also excluded genetic, auto-immune or iatrogenic causes of reduced reproduction function from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on fertility and the molecular pathways involved.

Conclusion
Both animal and human epidemiological studies support the idea that air pollutants cause defects during gametogenesis leading to a drop in reproductive capacities in exposed populations. Air quality has an impact on overall health as well as on the reproductive function, so increased awareness of environmental protection issues is needed among the general public and the authorities.

ABSTRACT
Background: Airborne polycyclic aromatic hydrocarbons (PAH) are widespread urban air pollutants from fossil fuel burning and other combustion sources. We previously reported that a broad spectrum of combustion-related DNA adducts in cord blood was associated with attention problems at 6–7 years of age in the Columbia Center for Children’s Environmental Health (CCCEH) longitudinal cohort study.

Objectives: We evaluated the relationship between behavioral problems and two different measures of prenatal exposure—both specific to PAH—in the same cohort.

Methods: Children of nonsmoking African-American and Dominican women in New York City (NYC) were followed from in utero to 6–7 years. Prenatal PAH exposure was estimated by personal air monitoring of the mothers during pregnancy as well as by the measurement of DNA adducts specific to benzo[a]pyrene (BaP), a representative PAH, in maternal and cord blood. At 6–7 years of age, child behavior was assessed using the Child Behavior Checklist (CBCL) (n = 253). Generalized linear models were used to test the association between prenatal PAH exposure and behavioral outcomes.

Results: In multivariate analyses, high prenatal PAH exposure, whether characterized by personal air monitoring (greater than the median of 2.27 ng/m3) or maternal and cord adducts (detectable or higher), was positively associated with symptoms of Anxious/Depressed and Attention Problems (p ≤ 0.05).

Conclusion: These results provide additional evidence that environmental levels of PAH encountered in NYC air can adversely affect child behavior.

Children’s respiratory health is vulnerable to air pollution. Based on data collected from June 2019 to June 2022 at a children’s hospital in Zhengzhou, China, this study utilized Spearman correlation analysis and a generalized additive model (GAM) to examine the relationship between daily visits for common respiratory issues in children and air pollutant concentrations. Results show that the number of upper respiratory tract infection (URTI), pneumonia (PNMN), bronchitis (BCT), and bronchiolitis (BCLT) visits in children showed a positive correlation with PM2.5, PM10, NO2, SO2, and CO while exhibiting a negative correlation with temperature and relative humidity. The highest increases in PNMN visits in children were observed at lag 07 for NO2, SO2, and CO. A rise of 10 μg/m3 in NO2, 1 μg/m3 in SO2, and 0.1 mg/m3 in CO corresponded to an increase of 9.7%, 2.91%, and 5.16% in PNMN visits, respectively. The effects of air pollutants on the number of BCT and BCLT visits were more pronounced in boys compared to girls, whereas no significant differences were observed in the number of URTI and PNMN visits based on sex. Overall, air pollutants significantly affect the prevalence of respiratory diseases in children, and it is crucial to improve air quality to protect the children’s respiratory health.

ABSTRACT

Background: Limited studies have explored the relationship between air pollution and rheumatoid arthritis (RA), with the results being somewhat inconsistent.

Methods: This was a retrospective cohort study that included 322,301 subjects aged 30-50 years, selected from the National Health Insurance Research Database in Taiwan, were followed from 2001 to 2010. We used a time-dependent extended Cox model and incorporated time-dependent variables to estimate the associations between the annual mean concentrations of air pollutants with RA, including carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), particles with an aerodynamic diameter less than 10 μm (PM10), and sulfur dioxide (SO2), and reported the hazard ratio (HR) and 95% confidence interval (CI).

Results: Newly diagnosed RA was positively associated with a 100-ppb increase in CO (adjusted HR = 1.17 [95% CI = 1.16, 1.18]), a 10-ppb increase in NO2 (1.54 [1.45, 1.64]), a 10-ppb increase in O3 (1.37 [1.33, 1.41]), and a 1 ppb in SO2 (1.02 [1.00, 1.04]). There was no association between a 10-μg/m increase in PM10 and RA (1.02 [0.99, 1.05]).

Conclusions: Our finding suggests that O3 and traffic-related air pollutants (CO and NO2) may be positively associated with incident RA. This is an important finding given that many individuals are exposed to similar levels of O3 and NO2 globally.

ABSTRACT
Background: Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. However, there has been little study of effects of traffic exposure at school on new-onset asthma.

Objectives: We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools.

Methods: Parent-reported physician diagnosis of new-onset asthma (n = 120) was identified during 3 years of follow-up of a cohort of 2,497 kindergarten and first-grade children who were asthma- and wheezing-free at study entry into the Southern California Children's Health Study. We assessed traffic-related pollution exposure based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO(2)), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. Hazard ratios (HRs) for new-onset asthma were scaled to the range of ambient central site pollutants and to the residential interquartile range for each traffic exposure metric.

Results: Asthma risk increased with modeled traffic-related pollution exposure from roadways near homes [HR 1.51; 95% confidence interval (CI), 1.25-1.82] and near schools (HR 1.45; 95% CI, 1.06-1.98). Ambient NO(2) measured at a central site in each community was also associated with increased risk (HR 2.18; 95% CI, 1.18-4.01). In models with both NO(2) and modeled traffic exposures, there were independent associations of asthma with traffic-related pollution at school and home, whereas the estimate for NO(2) was attenuated (HR 1.37; 95% CI, 0.69-2.71).

Conclusions: Traffic-related pollution exposure at school and homes may both contribute to the development of asthma.

ABSTRACT
Background
The role of traffic-related air pollution (TRAP) exposure in the development of allergic sensitization in children is unclear, and few birth cohort studies have incorporated spatiotemporal exposure assessment.

Objectives
We aimed to examine the association between TRAP and atopy in 1-year-old children from an ongoing national birth cohort study in four Canadian cities.

Methods
We identified 2,477 children of approximately 1 year of age with assessment of atopy for inhalant (Alternaria, Der p, Der f, cat, dog, cockroach) and food-related (milk, eggs, peanuts, soy) allergens. Exposure to nitrogen dioxide (NO2) was estimated from city-specific land use regression models accounting for residential mobility and temporal variability in ambient concentrations. We used mixed models to examine associations between atopy and exposure during pregnancy and the first year of life, including adjustment for covariates (maternal atopy, socioeconomic status, pets, mold, nutrition). We also conducted analyses stratified by time-location patterns, daycare attendance, and modeled home ventilation.

Results
Following spatiotemporal adjustment, TRAP exposure after birth increased the risk for development of atopy to any allergens [adjusted odds ratio (aOR) per 10 μg/m3 NO2 = 1.16; 95% CI: 1.00, 1.41], but not during pregnancy (aOR = 1.02; 95% CI: 0.86, 1.22). This association was stronger among children not attending daycare (aOR = 1.61; 95% CI: 1.28, 2.01) compared with daycare attendees (aOR = 1.05; 95% CI: 0.81, 1.28). Trends to increased risk were also found for food (aOR = 1.17; 95% CI: 0.95, 1.47) and inhalant allergens (aOR = 1.28; 95% CI: 0.93, 1.76).

Conclusion
Using refined exposure estimates that incorporated temporal variability and residential mobility, we found that traffic-related air pollution during the first year of life was associated with atopy.

ABSTRACT
The objective of this research was to determine if prenatal exposure to two common urban air pollutants, diesel and perchloroethylene, affects children's 3rd grade standardized test scores in mathematics and English language arts (ELA). Exposure estimates consisted of annual average ambient concentrations of diesel particulate matter and perchloroethylene obtained from the Environmental Protection Agency's 1996 National Air Toxics Assessment for the residential census tract at birth. Outcome data consisted of linked birth and educational records for 201,559 singleton, non-anomalous children born between 1994-1998 who attended New York City public schools. Quantile regression models were used to estimate the effects of these exposures on multiple points within the continuous distribution of standardized test scores. Modified Poisson regression models were used to calculate risk ratios (RR) and 95% confidence intervals (CI) of failing to meet curricula standards, an indicator derived from test scores. Models were adjusted for a number of maternal, neighborhood and childhood factors.

Results showed that math scores were approximately 6% of a standard deviation lower for children exposed to the highest levels of both pollutants as compared to children with low levels of both pollutants. Children exposed to high levels of both pollutants also had the largest risk of failing to meet math test standards when compared to children with low levels of exposure to the pollutants (RR 1.10 95%CI 1.07,1.12 RR high perchloroethylene only 1.03 95%CI 1.00,1.06; RR high diesel PM only 1.02 95%CI 0.99,1.06).

There was no association observed between exposure to only one of the pollutants and failing to meet ELA standards. This study provides preliminary evidence of associations between prenatal exposure to urban air pollutants and lower academic outcomes.

Additionally, these findings suggest that individual pollutants may additively impact health and point to the need to study the collective effects of air pollutant mixtures.

ABSTRACT
Background
Studies investigating the link between long-term exposure to air pollution and incidence of diabetes are still scarce and results are inconsistent, possibly due to different compositions of the particle mixture. We investigate the long-term effect of traffic-specific and total particulate matter (PM) and road proximity on cumulative incidence of diabetes mellitus (mainly type 2) in a large German cohort.

Methods
We followed prospectively 3607 individuals without diabetes at baseline (2000–2003) from the Heinz Nixdorf Recall Study in Germany (mean follow-up time 5.1 years). Mean annual exposures to total as well as traffic-specific PM10 and PM2.5 at residence were estimated using a chemistry transport model (EURAD, 1 km2 resolution). Effect estimates for an increase of 1 μg/m3 in PM were obtained with Poisson regression adjusting for sex, age, body mass index, lifestyle factors, area-level and individual-level socio-economic status, and city.

Results
331 incident cases developed. Adjusted RRs for total PM10 and PM2.5 were 1.05 (95 %-CI: 1.00;1.10) and 1.03 (95 %-CI: 0.95;1.12), respectively. Markedly higher point estimates were found for local traffic-specific PM with RRs of 1.36 (95 %-CI: 0.98;1.89) for PM10 and 1.36 (95 %-CI: 0.97;1.89) for PM2.5. Individuals living closer than 100 m to a busy road had a more than 30 % higher risk (1.37;95 %-CI: 1.04;1.81) than those living further than 200 m away.

Conclusions
Long-term exposure to total PM increases type two diabetes risk in the general population, as does living close to a major road. Local traffic-specific PM was related to higher risks for type two diabetes than total PM.