Mechanisms Linking Air Pollution Research Articles

The Effects of Oxidative Stress on RNA Editing with Insight into the Relationship Between Air Pollution and Alzheimer's Disease

Human interactions with the environment today add pressure on the world’s resources and ecosystems, which in turn harm human health. Many anthropogenic environmental changes, including climate change, biodiversity loss, and pollution, have accelerated morbidity and mortality. Research across multiple countries have found correlations between anthropogenic air pollution exposure and neurological degeneration, particularly with Alzheimer’s disease (AD). RNA editing induced by oxidative stress is one possible mechanism in which air pollution increases the risk of AD. To study this further, RNA adenosine-to-inosine (A-to-I) alterations were analyzed to identify a mechanism linking air pollution to neurological degeneration. These alterations occur in RNA, most prevalently in the central nervous system (CNS). Adenosine deaminase acting on RNA (ADAR) enzymes mediate A-to-I alterations and are essential for mammalian development and survival. ADAR mediated alterations have been associated with AD and the A-to-I occurrence frequency may increase in polluted environments that trigger increased oxidative stress. To test this possibility, wildtype (WT) and ADAR knockout (adr-2(-) Caenorhabditis elegans in their first larval (L1) developmental stage were exposed to juglone solution for 0, 15, and 60 minute experimental settings. For the two worm strains, WT and adr-2(-), the 0 minute treatment was the control, the 15 minute treatment represented acute oxidative stress exposure, and the 60 minute treatment represented chronic exposure. RNA was extracted from both groups and quantitative Real Time PCR (qRT-PCR) was used to measure the expression of gst-4, an Alzheimer’s associated gene (sel-12), and adr-2 normalized to the expression of gpd-3, the housekeeping gene that corrected for systemic errors. The gst-4 gene expression confirmed that oxidative stress occurred. Lack of adr-2 gene significantly decreased sel-12 expression at acute exposure, but adr-2 gene expression in WT worms did not significantly change across treatments. It remains to be determined whether oxidative stress impacts RNA editing of target mRNAs. Future studies are needed to explore the role of adr-2 in promoting sel-12 expression.

From Inhalation to Neurodegeneration: Air Pollution as a Modifiable Risk Factor for Alzheimer's Disease.

Air pollution, a growing concern for public health, has been linked to various respiratory and cardiovascular diseases. Emerging evidence also suggests a link between exposure to air pollutants and neurodegenerative diseases, particularly Alzheimer's disease (AD). This review explores the composition and sources of air pollutants, including particulate matter, gases, persistent organic pollutants, and heavy metals. The pathophysiology of AD is briefly discussed, highlighting the role of beta-amyloid plaques, neurofibrillary tangles, and genetic factors. This article also examines how air pollutants reach the brain and exert their detrimental effects, delving into the neurotoxicity of air pollutants. The molecular mechanisms linking air pollution to neurodegeneration are explored in detail, focusing on oxidative stress, neuroinflammation, and protein aggregation. Preclinical studies, including in vitro experiments and animal models, provide evidence for the direct effects of pollutants on neuronal cells, glial cells, and the blood-brain barrier. Epidemiological studies have reported associations between exposure to air pollution and an increased risk of AD and cognitive decline. The growing body of evidence supporting air pollution as a modifiable risk factor for AD underscores the importance of considering environmental factors in the etiology and progression of neurodegenerative diseases, in the face of worsening global air quality.

Air pollution, cardiovascular disease, and urban greening: an ecological blueprint.

A number of studies and systematic reviews indicate that exposure to greenness reduces of all-cause, non accidental mortality, particularly from cardiopulmonary and cancer causes. There is also some evidence that green space residence may be associated with improved pregnancy and birth outcomes, and with better school performances in children. Furthermore, because at least one third of the premature deaths are globally attributable to exposure to air pollution due household agents, particularly in fragile populations living in low-income countries (i.e., children, older and deprived people, pregnant women), that houseplants are an effective and economic mean for cleaning indoor air and thus reducing volatile organic compounds such as formaldehyde, benzene, toluene and others. On the whole more prospective studies are needed to further elucidate the mechanisms linking air pollution, greenness and health outcomes, although the multiple and interacting mechanisms depicted in this article are all biologically plausible.

Impact of Air Pollution on Atopic Dermatitis: A Comprehensive Review.

Air pollution is associated with multiple health problems worldwide, contributing to increased morbidity and mortality. Atopic dermatitis (AD) is a common allergic disease, and increasing evidence has revealed a role of air pollution in the development of atopic dermatitis. Air pollutants are derived from several sources, including harmful gases such as nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO), as well as particulate matter (PM) of various sizes, and bioaerosols. Possible mechanisms linking air pollution to atopic dermatitis include damage to the skin barrier through oxidative stress, increased water loss, physicochemical injury, and an effect on skin microflora. Furthermore, oxidative stress triggers immune dysregulation, leading to enhanced sensitization to allergens. There have been multiple studies focusing on the association between various types of air pollutants and atopic dermatitis. Since there are many confounders in the current research, such as climate, synergistic effects of mixed pollutants, and diversity of study population, it is not surprising that inconsistencies exist between different studies regarding AD and air pollution. Still, it is generally accepted that air pollution is a risk factor for AD. Future studies should focus on how air pollution leads to AD as well as effective intervention measures.

Impacts of long-term ambient particulate matter and gaseous pollutants on circulating biomarkers of inflammation in male and female health professionals

BackgroundSystemic inflammation may serve as a biological mechanism linking air pollution to poor health but supporting evidence from studies of long-term pollutant exposure and inflammatory cytokines is inconsistent. ObjectiveWe studied associations between multiple particulate matter (PM) and gaseous air pollutants and pro- and anti-inflammatory cytokines within two nationwide cohorts of men and women. MethodsData were obtained from 16,151 women in the Nurses' Health Study and 7,930 men in the Health Professionals' Follow-up Study with at least one measure of circulating adiponectin, C-Reactive Protein (CRP), Interleukin-6 (IL-6) or soluble tumor necrosis-factor receptor-2 (sTNFR-2). Exposure to PM with aerodynamic diameter ≤2.5, 2.5–10, and ≤10 μm (PM2.5, PM2.5-10, PM10) and nitrogen dioxide (NO2) was estimated using spatio-temporal models and were linked to participants’ addresses at the time of blood draw. Averages of the 1-, 3-, and 12-months prior to blood draw were examined. Associations between each biomarker and pollutant were estimated from linear regression models adjusted for individual and contextual covariates. ResultsIn adjusted models, we observed a 2.72% (95% CI: 0.43%, 5.95%), 3.11% (−0.12%, 6.45%), and 3.67% (0.19%, 7.26%) increase in CRP associated with a 10 μg/m3 increase in 1-, 3-, and 12- month averaged NO2 in women. Among men, there was a statistically significant 5.96% (95% CI: 0.07%, 12.20%), 6.99% (95% CI: 0.29%, 14.15%), and 8.33% (95% CI: 0.35%, 16.94%) increase in CRP associated with a 10 μg/m3 increase in 1-, 3-, and 12-month averaged PM2.5-10, respectively. Increasing PM2.5-10 was associated with increasing IL-6 and sTNFR-2 among men over shorter exposure durations. There were no associations with exposures to PM2.5 or PM10, or with adiponectin. Findings were robust to sensitivity analyses restricting to disease-free controls and non-movers. ConclusionsAcross multiple long-term pollutant exposures and inflammatory markers, associations were generally weak. Focusing on specific pollutant-inflammatory mechanisms may clarify pathways.

Ambient Air Pollution and Pediatric Inflammatory Bowel Diseases: An Updated Scoping Review

To review and discuss recent findings on the associations between pediatric/early-life exposures to ambient air pollution and the risk of pediatric-onset inflammatory bowel diseases (IBD). A scoping review was conducted using the Peters Micah et al. framework. We searched, selected, extracted, and reviewed information from published peer-reviewed papers from three bibliographic databases, chosen to cover a broad range of disciplines. Limits on date (last decade), language, and subject were placed on the database search. The search identified 109 papers from 2010 to June 2021. After screening, we identified nine articles with data on air pollution as a risk factor for IBD, but only four epidemiologic studies directly investigated the association between air pollution and IBD development in children and young adults. These four papers show that air pollution components have different associations with pediatric IBD (pIBD) incidence. Consequently, sulfur dioxide (SO2), nitrogen dioxide (NO2), and the oxidant capacity of air pollution (Ox) were positively associated with pIBD incidence, whereas the association effects of particulate matter (PM) and ozone (O3) exposures were not clear. Despite good scientific rationale and some studies, the evidence on the role that air pollution has in IBD development is limited, highlighting the need for further investigation. Future studies should include the epidemiology of air pollutants and its sources, identifying and understanding mechanisms linking air pollution and pIBD, and identifying signatures of biological responses to air pollutants.

DNA damage, serum metabolomic alteration and carcinogenic risk associated with low-level air pollution

Outdoor air pollution has been classified as carcinogenic to humans (Group 1) for lung cancer, but the underlying mechanism and key toxic components remain incompletely understood. Since DNA damage and metabolite alterations are associated with cancer progression, exploring potential mechanisms linking air pollution and cancer might be meaningful. In this study, a real-time ambient air exposure system was established to simulate the real-world environment of adult male SD rats in Beijing from June 13th, 2018, to October 8th, 2018. 8-OHdG in the urine, γ-H2AX in the lungs and mtDNA copy number in the peripheral blood were analyzed to explore DNA damage at different levels. Serum non-targeted metabolomics analysis was performed. Pair-wise spearman was used to explore the correlation between DNA damage biomarkers and serum differential metabolites. Carcinogenic risks of heavy metals and PAHs via inhalation were assessed according to US EPA guidelines. Results showed that PM2.5 and O3 were the major air pollutants in the exposure group and not detected in the control group. Compared with control group, higher levels of 8-OHdG, mtDNA copy number, γ-H2AX and PCNA-positive nuclei cells were observed in the exposure group. Histopathological evaluation suggested ambient air induced alveolar wall thickening and inflammatory cell infiltration in lungs. Perturbed metabolic pathways identified included glycolysis/gluconeogenesis metabolism, purine and pyrimidine metabolism, etc. γ-H2AX was positively correlated with serum ADP, 3-phospho-D-glyceroyl phosphate and N-acetyl-D-glucosamine. The BaPeq was 0.120 ng/m3. Risks of Cr(VI), As, V, BaP, BaA and BbF were above 1 × 10−6. We concluded that low-level air pollution was associated with DNA damage and serum metabolomic alterations in rats. Cr(VI) and BaP were identified as key carcinogenic components in PM2.5. Our results provided experimental evidence for hazard identification and risk assessment of low-level air pollution.

246 Air pollution and coronary plaque vulnerability and instability: an optical coherence tomography study

Abstract Aims Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. We aimed at assessing the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). Methods and results ACS patients undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case’s home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. We included 126 patients [median age 67.0 years (55.5–76.0), 97 (77.0%) male]. Sixty-six patients (52.4%) had PR as mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels compared to IFC, and PM2.5 was independently associated with PR [odds ratio per unit = 1.194, 95% CI: (1.036–1.377), P = 0.015]. Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and CO levels were positively and significantly correlated with serum levels of C-reactive protein. ROC curves were constructed to assess the ability of PM2.5 to predict the presence of plaque rupture, TCFA or MØI. The AUC for PM2.5 to predict plaque rupture was 0.62 (95% CI: 0.52–0.71, P = 0.018), for TCFA was 0.71 (95% CI: 0.61–0.80, P <0.001) and for MØI was 0.80 (95% CI: 0.71–0.88, P <0.001). Using a PM2.5 cut-off value of 13.40 μg/m3, the sensitivity and specificity for MØI were 81% and 66%, respectively. Conclusions We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is a risk factor for vulnerable plaque features and for plaque rupture as mechanism of coronary instability mediated by systemic and local plaque inflammation. Of importance, the thresholds of air pollutants that predicted the presence of vulnerable plaque features are far lower than commonly accepted safety thresholds used to start preventive measures for public health, suggesting that further efforts are needed in order to reduce the adverse effects on the cardiovascular system.

Air Pollution and Coronary Plaque Vulnerability and Instability: An Optical Coherence Tomography Study

ObjectivesWe assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). BackgroundAir pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. MethodsPatients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case’s home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. ResultsWe included 126 patients (median age: 67.0 years of age; IQR: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and Co levels were positively and significantly correlated with serum levels of C-reactive protein. ConclusionsWe provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory activation may explain these findings.

Long-term exposure to ambient air pollution portends a higher risk of coronary plaque vulnerability and instability in patients with acute coronary syndrome: an optical coherence tomography study

Abstract Background Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. Purpose We assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). Methods ACS patients undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case's home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. Results We included 136 patients [median age 67.0 years (56.2–76.0), 104 (76.5%) male]. Sixty-six patients (48.5%) had PR as mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels compared to IFC, and PM2.5 was an independent predictor for PR (OR=1.133, 95% CI [1.020–1.258], p=0.019). Moreover, exposure to higher levels of PM2.5, PM10 and CO was an independent predictor for the presence of TCFA, while PM2.5 and CO levels predicted the presence of MØI. Interestingly, PM2.5, PM10 and CO levels were positively and significantly correlated with serum levels of C-reactive protein. ROC curves were constructed to assess the ability of PM2.5 to predict the presence of plaque rupture, TCFA or MØI. The AUC for PM2.5 to predict plaque rupture was 0.62 (95% CI: 0.52–0.71, p=0.018), for TCFA was 0.71 (95% CI: 0.61–0.80, p<0.001) and for MØI was 0.80 (95% CI: 0.71–0.88, p<0.001). Using a PM2.5 cut-off value of 13.40 μg/m3, the sensitivity and specificity for MØI were 81% and 66%, respectively. Conclusions We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is a risk factor for vulnerable plaque features and for plaque rupture as mechanism of coronary instability mediated by systemic and local plaque inflammation. Of importance, the thresholds of air pollutants that predicted the presence of vulnerable plaque features are far lower than commonly accepted safety thresholds used to start preventive measures for public health, suggesting that further efforts are needed in order to reduce the adverse effects on the cardiovascular system. Funding Acknowledgement Type of funding sources: None. Air pollutants exposure and OCT featuresROC curve analysis

Joint effect of multiple air pollutants on lipid profiles in obese and normal-weight young adults: The key role of ozone

Dyslipidemia may be a potential mechanism linking air pollution to adverse cardiovascular outcomes and this may differ among obese and normal-weight populations. However, the joint effect of multiple air pollutants on lipid profiles and the role of each pollutant are still unclear. This panel study aims to investigate and compare the overall associations of major air pollutants with lipid parameters in obese and normal-weight adults, and assess the relative importance of each pollutant for lipid parameters. Forty-four obese and 53 normal-weight young adults were recruited from December 2017 to June 2018 in Beijing, China. Their fasting blood was collected and serum lipid levels were measured in three visits. Six major air pollutants were included in this study, which were PM2.5, PM10, NO2, SO2, O3 and CO. Bayesian kernel machine regression (BKMR) was implemented to estimate the joint effect of the six air pollutants on various lipid parameters. We found that decreased high-density lipoprotein cholesterol (HDL-C) in the obese group and increased low-density lipoprotein cholesterol (LDL-C) and non-HDL-C in the normal-weight group were associated with the exposure to the mixture of six air pollutants above. Significant increases in total cholesterol (TC)/HDL-C and non-HDL-C/HDL-C were observed in both groups, and the effect was stronger in obese group. Of the six air pollutants above, O3 had the largest posterior inclusion probability in above lipid indices, ranging from 0.75 to 1.00. In the obese group, approximately linear exposure-response relationships were observed over the whole range of logarithmic O3-8 h max concentration, while in the normal-weight group, these relationships existed when the logarithmic concentration exceeded about 2.8. Therefore, lipid profiles of obese adults may be more sensitive to air pollution and this study highlights the importance of strengthening emissions control efforts for O3 in the future.

Ambient Air Pollution (PM2.5 & O3) in Relation to ADHD in NYC Children Age 3-13 Years

BACKGROUND AND AIM: Recent studies have investigated the relationship between air pollution and Attention Deficit/Hyperactivity Disorder (ADHD) with inconsistent results. The specific causes of ADHD remain unknown; however, there is biologic plausibility for etiologic mechanisms linking air pollution exposure and neurodevelopmental outcomes, such as ADHD. METHODS: We included 5,032 children ages 3-13 years from the 2017 New York City KIDS survey on children’s health provided by New York City Department of Health & Mental Hygiene, of which 303 had a parent report of ADHD diagnosed by a mental health professional. Using the child’s date of birth and residential neighborhood (sub-borough) during the survey, we linked to daily air pollution data from U.S. Environmental Protection Agency fused air quality using surface downscaling (FAQSD) model, focusing on particulate matter 2.5 micrometers in diameter (PM2.5) and ozone (O3). We estimated odds ratios (aOR) adjusting for child’s sex, child’s race/ethnicity, highest parental education, household income, and indoor tobacco use. RESULTS:One-year postnatal PM2.5 and O3 mean, standard deviations and correlation: 11.1±1.5 (ug/m3); 66.3±4.4 (ppb); -0.67 correlation. ADHD was associated with PM2.5, with aOR and 95% confidence interval (CI) per ug/m3 increase in PM2.5: prenatal=1.13(1.01,1.27); postnatal=1.19(1.07,1.31); combined prenatal and postnatal=1.18(1.07,1.31). In contrast, ozone exhibited inverse associations, with aOR and 95%CI per ppb increase in O3 exposures for prenatal=0.92 (0.87,0.98), postnatal=0.85(0.78,0.94), and combined prenatal and postnatal=0.87(0.79,0.94). CONCLUSIONS:Despite air pollution measurement error resulting from geographic aggregation at the neighborhood-level, we observed links between PM2.5 and ADHD that align with prior studies. Our observed inverse associations between O3 and ADHD are unlikely to reflect beneficial effects of ozone given its known harmful impacts and may be artifacts of the negative correlation between ozone and PM2.5. These results provide further support for the adverse impact of air pollutants such as PM2.5 during pregnancy and infancy on the risk for development of ADHD. KEYWORDS: ADHD, Air Pollution, Children's Environmental Health, Neurodevelopmental Outcomes, Ozone, Particulate Matter

Air pollution and neurological development in children.

Pregnancy and early childhood are periods with high plasticity in neurological development. Environmental perturbations during these sensitive windows can have lifelong developmental consequences. This review summarizes key findings relevant to the effects of air pollution on neurological development. Mounting evidence suggests that exposure to air pollution, both during pregnancy and childhood, is associated with childhood developmental outcomes ranging from changes in brain structures to subclinical deficits in developmental test scores, and, ultimately, developmental disorders such as attention-deficit/hyperactivity disorders or autism spectrum disorders. Although the biological mechanisms of effects remain to be elucidated, multiple pathways are probably involved and include oxidative stress, inflammation, and/or endocrine disruption. Given the alarming global increase in developmental disorders in recent years, and increased human exposures to pollution, it is critical to reduce personal and community-level exposures through tight collaboration of interdisciplinary and multi-level bodies including community partners, physicians, industry partners, policy makers, public health practitioners, and researchers. WHAT THIS PAPER ADDS: Exposure to air pollution is associated with a range of childhood developmental complications. Biological mechanisms may include oxidative stress, inflammation, and endocrine disruption.

Air Pollution and Adverse Pregnancy and Birth Outcomes: Mediation Analysis Using Metabolomic Profiles.

Review how to use metabolomic profiling in causal mediation analysis to assess epidemiological evidence for air pollution impacts on birth outcomes. Maternal exposures to air pollutants have been associated with pregnancy complications and adverse pregnancy and birth outcomes. Causal mediation analysis enables us to estimate direct and indirect effects on outcomes (i.e., effect decomposition), elucidating causal mechanisms or effect pathways. Maternal metabolites and metabolic pathways are perturbed by air pollution exposures may lead to adverse pregnancy and birth outcomes, thus they can be considered mediators in the causal pathways. Metabolomic markers have been used to explain the biological mechanisms linking air pollution and respiratory function, and of arsenic exposure and birth weight. However, mediation analysis of metabolomic markers has not been used to assess air pollution effects on adverse birth outcomes. In this article, we describe the assumptions and applications of mediation analysis using metabolomic markers that elucidate the potential mechanisms of the effects of air pollution on adverse pregnancy and birth outcomes. The hypothesis of mediation along specified pathways can be assessed within the structural causal modeling framework. For causal inferences, several assumptions that go beyond the data-including no uncontrolled confounding-need to be made to justify the effect decomposition. Nevertheless, studies that integrate metabolomic information in causal mediation analysis may greatly improve our understanding of the effects of ambient air pollution on adverse pregnancy and birth outcomes as they allow us to suggest and test hypotheses about underlying biological mechanisms in studies of pregnant women.

Short-term Effect of Air Pollution on Tuberculosis Based on Kriged Data: A Time-series Analysis.

Tuberculosis (TB) has a very high mortality rate worldwide. However, only a few studies have examined the associations between short-term exposure to air pollution and TB incidence. Our objectives were to estimate associations between short-term exposure to air pollutants and TB incidence in Wuhan city, China, during the 2015–2016 period. We applied a generalized additive model to access the short-term association of air pollution with TB. Daily exposure to each air pollutant in Wuhan was determined using ordinary kriging. The air pollutants included in the analysis were particulate matter (PM) with an aerodynamic diameter less than or equal to 2.5 micrometers (PM2.5), PM with an aerodynamic diameter less than or equal to 10 micrometers (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ground-level ozone (O3). Daily incident cases of TB were obtained from the Hubei Provincial Center for Disease Control and Prevention (Hubei CDC). Both single- and multiple-pollutant models were used to examine the associations between air pollution and TB. Seasonal variation was assessed by splitting the all-year data into warm (May–October) and cold (November–April) seasons. In the single-pollutant model, for a 10 μg/m3 increase in PM2.5, PM10, and O3 at lag 7, the associated TB risk increased by 17.03% (95% CI: 6.39, 28.74), 11.08% (95% CI: 6.39, 28.74), and 16.15% (95% CI: 1.88, 32.42), respectively. In the multi-pollutant model, the effect of PM2.5 on TB remained statistically significant, while the effects of other pollutants were attenuated. The seasonal analysis showed that there was not much difference regarding the impact of air pollution on TB between the warm season and the cold season. Our study reveals that the mechanism linking air pollution and TB is still complex. Further research is warranted to explore the interaction of air pollution and TB.

Particulate air pollution exposure during pregnancy and postpartum depression symptoms in women in Mexico City

BackgroundPostpartum depression (PPD), which affects up to 1 in 5 mothers globally, negatively impacts the health of both mothers and children. Exposure to ambient air pollution has been linked to depressive symptoms in animal models and human studies, but the relationship between air pollution and PPD has not been widely studied. MethodsIn a birth cohort in Mexico City (509 mothers with available data), we examined the association between exposure to particulate matter ≤2.5 μm in diameter (PM2.5) with symptoms of psychological dysfunction at 1 and 6 months postpartum. Daily PM2.5 estimates were derived from a hybrid satellite-based spatio-temporally resolved model and averaged over pregnancy and the first year postpartum. Edinburgh Postnatal Depression Scale (EPDS) scores at 1 and 6 months were used to assess the relationship between PM2.5 exposure and probable PPD (EPDS score ≥13) using relative risk regression and symptoms of anhedonia, depression, and anxiety (derived from EPDS subscales) using negative binomial regression. ResultsA 5-μg/m3 increase in average PM2.5 exposure during pregnancy was associated with an increased risk of PPD at 6 months (RR = 1.59; 95% CI: 1.11 to 2.28) and of late-onset PPD (no PPD at 1 month, PPD at 6 months) (RR = 2.58; 95% CI: 1.40 to 4.73) in covariate-adjusted models. No association was observed between PM2.5 exposure in the first year postpartum and PPD. Average PM2.5 exposure during pregnancy was also associated with increased 6-month EPDS subscale symptom scores for anhedonia (p = 0.03) and depression (p = 0.04). ConclusionOur results suggest that in women in Mexico City, particulate matter exposure during pregnancy is positively associated with PPD and symptoms of anhedonia and depression at 6 months postpartum. Future studies should examine mechanisms linking air pollution and other environmental exposures during pregnancy with postpartum psychological functioning.

Emerging role of air pollution in autoimmune diseases.

Autoimmune diseases (ADs) are a broad spectrum of disorders featured by the body's immune responses being directed against its own tissues, resulting in prolonged inflammation and subsequent tissue damage. Recently, the exposure to ambient air pollution has been implicated in the occurrence and development of ADs. Mechanisms linking air pollution exposures and ADs mainly include systemic inflammation, increased oxidative stress, epigenetic modifications induced by exposures and immune response caused by airway damage. The lung may be an autoimmunity initiation site in autoimmune diseases (ADs). Air pollutants can bind to the Aryl hydrocarbon receptor (AHR) to regulate Th17 and Treg cells. Oxidative stress and inducible bronchus associated lymphoid tissue caused by the pollutants can influence T, B cells, resulting in the production of proinflammatory cytokines. These cytokines stimulate B cell and dendritic cells, resulting in a lot of antibodies and self-reactive T lymphocytes. Moreover, air pollutants may induce epigenetic changes to contribute to ADs. In this review, we will concern the associations between air pollution and immune-inflammatory responses, as well as mechanisms linking air pollution exposure and autoimmunity. In addition, we focus on the potential roles of air pollution in major autoimmune diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), and type 1 diabetes mellitus (T1DM).

Regional and traffic-related air pollutants are associated with higher consumption of fast food and trans fat among adolescents

Air pollution exposures are novel contributors to the growing childhood obesity epidemic. One possible mechanism linking air pollution exposures and obesity is through changes in food consumption patterns. The aim of this study was to examine the longitudinal association between childhood exposure to air pollutants and changes in diet among adolescents. School-age children were enrolled in the Southern California Children's Health Study during 1993-1994 (n=3100) and were followed for 4-8 y. Community-level regional air pollutants [e.g., nitrogen dioxide (NO2), elemental carbon (EC), and fine particles with aerodynamic diameter <2.5 µm (PM2.5)] were measured at central monitoring stations. Line dispersion modeling was used to estimate concentrations of traffic-related air pollutants based on nitrogen oxides (NOx) at participants' residential addresses. In addition, self-reported diet information was collected annually using a structured youth/adolescent food-frequency questionnaire during 1997-2001. Generalized linear mixed-effects models were used in the association analyses. Higher exposures to regional and traffic-related air pollutants were associated with intake of a high-trans-fat diet, after adjusting for confounders including socioeconomic status and access to fast food in the community. A 2-SD (12.2 parts per billion) increase in regional NO2 exposure was associated with a 34% increased risk of consuming a high-trans-fat diet compared with a low-trans-fat diet (OR: 1.34; 95% CI:1.05, 1.72). In addition, higher exposures to acid vapor, EC, PM2.5, and non-freeway NOx were all associated with higher consumption of dietary trans fat (all P<0.04). Notably, higher exposures to regional NO2, acid vapor, and EC were also associated with a higher consumption of fast food (all P<0.05). Childhood exposures to regional and traffic-related air pollutants were associated with increased consumption by adolescents of trans fat and fast foods. Our results indicate that air pollution exposures may contribute to obesogenic behaviors. This study was registered at clinicaltrials.gov as NCT03379298.

Establishment and evaluation of chronic obstructive pulmonary disease model by chronic exposure to motor vehicle exhaust combined with lipopolysaccharide instillation.

What is the central question of this study? In this study, by using motor vehicle exhaust (MVE) exposure with or without lipopolysaccharide (LPS) instillation, we established, evaluated and compared MVE, LPS and MVE+LPS treatment-induced chronic obstructive pulmonary disease (COPD) models in mice. What is the main finding and its importance? Our study demonstrated that the combination of chronic exposure to MVE with early LPS instillation can establish a mouse model with some features of COPD, which will allow researchers to investigate the underlying molecular mechanisms linking air pollution and COPD pathogenesis. Although it is well established that motor vehicle exhaust (MVE) has a close association with the occurrence and exacerbation of chronic obstructive pulmonary disease (COPD), very little is known about the combined effects of MVE and intermittent or chronic subclinical inflammation on COPD pathogenesis. Therefore, given the crucial role of inflammation in the development of COPD, we wanted to establish an animal model of COPD using both MVE exposure and airway inflammation, which could mimic the clinical pathological changes observed in COPD patients and greatly benefit the study of the molecular mechanisms of COPD. In the present study, we report that mice undergoing chronic exposure to MVE and intratracheal instillation of lipopolysaccharide (LPS) successfully established COPD, as characterized by persistent air flow limitation, airway inflammation, inflammatory cytokine production, emphysema and small airway remodelling. Moreover, the mice showed significant changes in ventricular and vascular pathology, including an increase in right ventricular pressure, right ventricular hypertrophy and remodelling of pulmonary arterial walls. We have thus established a new mouse COPD model by combining chronic MVE exposure with early intratracheal instillation of LPS, which will allow us to study the relationship between air pollution and the development of COPD and to investigate the underlying molecular mechanisms.

Acute changes in DNA methylation in relation to 24 h personal air pollution exposure measurements: A panel study in four European countries

BackgroundOne of the potential mechanisms linking air pollution to health effects is through changes in DNA-methylation, which so far has mainly been analyzed globally or at candidate sites. ObjectiveWe investigated the association of personal and ambient air pollution exposure measures with genome-wide DNA-methylation changes. MethodsWe collected repeated 24-hour personal and ambient exposure measurements of particulate matter (PM2.5), PM2.5 absorbance, and ultrafine particles (UFP) and peripheral blood samples from a panel of 157 healthy non-smoking adults living in four European countries. We applied univariate mixed-effects models to investigate the association between air pollution and genome-wide DNA-methylation perturbations at single CpG (cytosine-guanine dinucleotide) sites and in Differentially Methylated Regions (DMRs). Subsequently, we explored the association of air pollution-induced methylation alterations with gene expression and serum immune marker levels measured in the same subjects. ResultsPersonal exposure to PM2.5 was associated with methylation changes at 13 CpG sites and 69 DMRs. Two of the 13 identified CpG sites (mapped to genes KNDC1 and FAM50B) were located within these DMRs. In addition, 42 DMRs were associated with personal PM2.5 absorbance exposure, 16 DMRs with personal exposure to UFP, 4 DMRs with ambient exposure to PM2.5, 16 DMRs with ambient PM2.5 absorbance exposure, and 15 DMRs with ambient UFP exposure. Correlation between methylation levels at identified CpG sites and gene expression and immune markers was generally moderate. ConclusionThis study provides evidence for an association between 24-hour exposure to air pollution and DNA-methylation at single sites and regional clusters of CpGs. Analysis of differentially methylated regions provides a promising avenue to further explore the subtle impact of environmental exposures on DNA-methylation.