Autism spectrum disorder-like behaviors in developing zebrafish exposed to particulate matter.

A population exposure model for particulate matter (PM), called the Stochastic Human Exposure and Dose Simulation (SHEDS-PM) model, has been developed and applied in a case study of daily PM(2.5) exposures for the population living in Philadelphia, PA. SHEDS-PM is a probabilistic model that estimates the population distribution of total PM exposures by randomly sampling from various input distributions. A mass balance equation is used to calculate indoor PM concentrations for the residential microenvironment from ambient outdoor PM concentrations and physical factor data (e.g., air exchange, penetration, deposition), as well as emission strengths for indoor PM sources (e.g., smoking, cooking). PM concentrations in nonresidential microenvironments are calculated using equations developed from regression analysis of available indoor and outdoor measurement data for vehicles, offices, schools, stores, and restaurants/bars. Additional model inputs include demographic data for the population being modeled and human activity pattern data from EPA's Consolidated Human Activity Database (CHAD). Model outputs include distributions of daily total PM exposures in various microenvironments (indoors, in vehicles, outdoors), and the contribution from PM of ambient origin to daily total PM exposures in these microenvironments. SHEDS-PM has been applied to the population of Philadelphia using spatially and temporally interpolated ambient PM(2.5) measurements from 1992-1993 and 1990 US Census data for each census tract in Philadelphia. The resulting distributions showed substantial variability in daily total PM(2.5) exposures for the population of Philadelphia (median=20 microg/m(3); 90th percentile=59 microg/m(3)). Variability in human activities, and the presence of indoor-residential sources in particular, contributed to the observed variability in total PM(2.5) exposures. The uncertainty in the estimated population distribution for total PM(2.5) exposures was highest at the upper end of the distribution and revealed the importance of including estimates of input uncertainty in population exposure models. The distributions of daily microenvironmental PM(2.5) exposures (exposures due to time spent in various microenvironments) indicated that indoor-residential PM(2.5) exposures (median=13 microg/m(3)) had the greatest influence on total PM(2.5) exposures compared to the other microenvironments. The distribution of daily exposures to PM(2.5) of ambient origin was less variable across the population than the distribution of daily total PM(2.5) exposures (median=7 microg/m(3); 90th percentile=18 microg/m(3)) and similar to the distribution of ambient outdoor PM(2.5) concentrations. This result suggests that human activity patterns did not have as strong an influence on ambient PM(2.5) exposures as was observed for exposure to other PM(2.5) sources. For most of the simulated population, exposure to PM(2.5) of ambient origin contributed a significant percent of the daily total PM(2.5) exposures (median=37.5%), especially for the segment of the population without exposure to environmental tobacco smoke in the residence (median=46.4%). Development of the SHEDS-PM model using the Philadelphia PM(2.5) case study also provided useful insights into the limitations of currently available data for use in population exposure models. In addition, data needs for improving inputs to the SHEDS-PM model, reducing uncertainty and further refinement of the model structure, were identified.

Development of a high-throughput invivo screening platform for particulate matter exposures.

Polycyclic aromatic hydrocarbons (PAHs) are toxicants in particulate matter (PM). The vocal fold, part of the larynx and a key structure for voicing, is always in contact with air. In recent epidemic studies, PM was shown to cause laryngitis; however, the basic mechanism has not been evaluated. In the present study, intracellular reactive oxygen species (ROS) and proinflammatory cytokine levels were analyzed after exposing human vocal fold fibroblasts (hVFFs) to PM standard reference material (SRM 2786). Expression levels of the aryl hydrocarbon receptor (AhR) and Cytochrome P450 Family 1 Subfamily A Member 1 (CYP1A1) were also evaluated. PM induced ROS formation and proinflammatory cytokines via the AhR CYP1A1 pathway and caused lipid peroxidation and DNA damage. Blocking AhR or CYP1A1 production using siRNAs significantly decreased ROS production and IL-6 and IL-9 expression in PM-exposed hVFFs, thus protecting the cells against oxidative stress. These results confirm that PAHs in PM play an important role in cell damage and inflammation, confirming a basic pathophysiologic relationship between PM exposure and laryngitis.

Patients with asthma demonstrate airway inflammation after exposure to concentrated ambient particulate matter.

Combination effects of airborne particulate matter exposure and high-fat diet on hepatic fibrosis through regulating the ROS-endoplasmic reticulum stress-TGFβ/SMADs axis in mice

Objective: To assess the association between airborne particulate matter (PM) exposure and the development of asthma in children, a systematic review and meta-analysis that included nearly 10 years of related literature was conducted. Study Design: The study investigators conducted a systematic review of relevant research articles published between March 2013 and March 2023, which were accessible through several medical literature data bases of. Random-effects meta-analyses were used to analyze the effects of PM on childhood asthma. Subgroup analyses, including exposure period, type of PM, regional factors, and study type, were also used. Odds ratio (OR) and 95% confidence intervals (CI) were used to represent the estimated effect of the population. Publication bias was assessed by using the Egger test and funnel plot. Data analyses were performed using statistical analysis software and a systematic review management tool. Results: A total of 15,365 articles were identified, of which 19 studies were included in this meta-analysis. The results showed that PM exposure was positively correlated with asthma in children, with the overall random-effects risk estimates of OR 1.10 (95% CI, 1.07-1.13). In stratified analyses, PM exposure was found to be a risk factor for the development of childhood asthma. Both prenatal and postnatal PM exposure were associated with an increased risk of asthma in children, but prenatal exposure was associated with a greater increase in risk than postnatal exposure, with an effect estimate OR of 1.21 (95% CI, 1.02-1.43). In the analysis of different PM types, the OR of PM2.5 (PM < 2.5 μm in diameter) exposure was OR 1.10 (95% CI, 1.05-1.15), and no association was found between PM10 (PM < 10 μm in diameter), coarse PM (PM with an aerodynamic diameter between 2.5 and 10 μm), and black carbon BC (diameter of 0.01-0.05 μm) exposure. In different regional analyses, the effects of PM exposure on childhood asthma risk were OR 1.15 (95% CI, 1.13-1.17) in South America and OR 1.02 (95% CI, 1.01-1.03) in Asia, but no association was found in Europe and North America. In addition, the results of different study types only found that the literature that used the time-series research method had a significant association with OR 1.03 (95% CI, 1.02-1.04), whereas the literature that used the cohort study method had no statistical difference. Conclusion: Exposure to airborne PM increased the risk of asthma in children. Both prenatal and postnatal PM exposure was associated with an increased risk of childhood asthma, but prenatal PM exposure was associated with a greater increase than postnatal PM exposure.

Speciation of elements in NIST particulate matter SRMs 1648 and 1650

Oxidative stress and inflammation are considered an important mechanism for the development of cardiovascular diseases. Cytokines including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) play an important role in oxidative stress and inflammation. It is known that ambient fine particulate matter ( PM ) exposure is closely associated with cardiovascular diseases and oxidative stress. Caspase-recruitment domain 9 ( Card9 ) signaling is critically involvement in the function of macrophages, neutrophils and monocytes that are important for oxidative stress and inflammation. The present study was designed to evaluate the role of CARD9-mediated signaling in cytokines production in mice with PM exposure. Both male wild-type (WT) C57BL/6 mice (8-10 weeks) and age-matched CARD9 knockout (KO) mice (with C57BL/6 background) were exposed to PM2.5 for 6 weeks via intranasal approach with PBS as the control. Serum concentrations of the cytokines including IL-6, IL-1β, and TNF-α were measured with ELISA in the mice before and after PM exposure. There was no difference in the serum levels of IL-6, IL-1β, or TNF-α between WT mice and CARD9 KO mice exposed to PBS. As expected, PM exposure substantially increased the serum levels of IL-6, IL-1β, and TNF-α in the WT mice (by up to 6 times). However, no significant increase in the serum concentrations for IL-6, IL-1β, and TNF-α was observed in CARD9 KO mice exposed to PM. Increased inflammatory infiltrations in the lungs were observed in the WT mice as compared to the CARD9 KO mice with PM exposure. In conclusion, the present study demonstrated that increased cytokines were produced in WT mice, but not in CARD9 KO mice with PM exposure. The data suggested that CARD9 signaling played a critical role in the production of inflammatory cytokines in the mice in response to PM exposure, and might contribute to the development of cardiovascular diseases related to PM exposure.

Anemia is common among HIV/AIDS patients, impacting prognosis. Particulate matter (PM) exposure is an understudied, potentially modifiable risk factor in this group. We gathered 36,266 hemoglobin (Hb) measurements from 6808 HIV/AIDS patients from the HIV/AIDS Comprehensive Response Information Management System from 1 January 2004 to 31 December 2021. We evaluated the relationship between Hb levels and short-term PM exposure using linear mixed-effects models. We used logistic regression to estimate the association of long-term PM exposure with baseline anemia prevalence and time-varying Cox models to estimate the association of long-term PM exposure with follow-up incidence of anemia. Mediation analysis explored the role of chronic kidney disease (CKD) in the association between PM exposure and anemia. For every 5 µg/m³ increase in 28-day average PM 1 , Hb levels decreased by 0.43 g/l. For a 10 µg/m³ increase in PM 2.5 , Hb decreased by 0.55 g/l; for the same increase in PM 10, Hb decreased by 0.35 g/l. A 5 µg/m³ increase in 1-year average PM 1 corresponded to a 7% higher prevalence of anemia at baseline, a 10 µg/m³ increase in PM 2.5 to 8% higher prevalence, and a 10 µg/m³ increase in PM 10 to 6% higher prevalence. These rises in average PM concentrations during follow-up were associated with increased incident anemia by 54% (PM 1 ), 72% (PM 2.5 ), and 51% (PM 10 ). CKD partially mediated the positive associations between PM exposure and the incidence of anemia. PM exposure was associated with lower Hb levels and higher incidence of anemia in HIV/AIDS patients and CKD with mediating estimated effects in PM-induced anemia.

The Adjuvant Effect of Ambient Particulate Matter Is Closely Reflected by the Particulate Oxidant Potential

Gender difference is present in a variety of diseases especially cardiovascular diseases like coronary artery diseases ( CAD ). It is well known that males tend to suffer from CAD earlier than females for largely unknown reasons. Oxidative stress and inflammation are considered an important mechanism for the development of cardiovascular diseases. Cytokines including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) play an important role in oxidative stress and inflammation. Ambient fine particulate matter ( PM ) exposure is closely associated with cardiovascular diseases and oxidative stress. The present study was designed to determine if there was a gender difference in the production of cytokines in the mice with PM exposure. Both male and female wild-type C57BL/6 mice (8-10 weeks) were exposed to PM2.5 for 6 weeks via intranasal approach with PBS as the control. Serum concentrations of the cytokines including IL-6, IL-1β, and TNF-α were measured with ELISA in the mice before and after PM exposure. There was no difference between male and female mice in the serum levels of IL-6, IL-1β, or TNF-α at the baseline. As expected, PM exposure substantially increased the serum levels of IL-6, IL-1β, and TNF-α both in male and female mice (by up to 6 times). However, their serum concentrations were significantly higher in male mice than in the females by 64.2%, 26.5%, and 30.7% for IL-6, IL-1β, and TNF-α, respectively (p &lt; 0.05, n = 10). Similar changes in the inflammatory infiltrations in the lungs were observed in the male and female mice with PM exposure. The data from the present study demonstrated that more cytokines were produced in male mice than in the females with PM exposure. The clear gender difference in the serum levels of cytokines in response to PM exposure may partially contribute to the gender difference in the development of cardiovascular diseases. Further studies are needed to investigate the mechanisms related to the gender difference in the response to PM exposure.

Exposure to particulate matter may affect semen quality via trace metals: Evidence from a retrospective cohort study on fertile males

Systems level insights into the impact of airborne exposure on SARS-CoV-2 pathogenesis and COVID-19 outcome – A multi-omics big data study

LUAD, the most common subtype of lung cancer, particularly in non-smokers, is significantly influenced by air pollution from fine particulate matter (PM). One suspected method by which PM contributes to cancer progression is through angiogenesis, which promotes tumor growth and metastasis. This study was conducted to explore the impact of long-term PM exposure on the progression of LUAD, focusing on angiogenesis promotion. We conducted an integrative bioinformatics analysis incorporating epidemiological and transcriptomic datasets from public repositories (TCGA and GEO) to evaluate differential VEGFA expression in LUAD tissues and its relationship to regional PM exposure. In vitro and in vivo assays using PM-adapted NSCLC cell lines and murine xenograft models served as secondary confirmatory experiments supporting the computational results. Epidemiological analysis revealed a strong positive correlation between long-term PM exposure and lung adenocarcinoma mortality across U.S. states (r = 0.7638, p < 0.0001), underscoring a population-level impact. Bioinformatics analysis identified a significant upregulation of VEGFA in NSCLC tumors from regions with high PM levels, with VEGFA overexpression also associated with poorer patient survival. Gene ontology and pathway enrichment analyses implicated angiogenesis-related processes. These findings were supported by experimental models, in which long-term PM exposure on human and murine LUAD cell lines (A549, H1299, and LLC) induced VEGFA and p-ERK overexpression. Furthermore, PM-exposed cells enhanced angiogenesis processes, as evidenced by increased endothelial cell tube formation and migration in vitro, and promoted tumor vascularization in a xenograft model. These pro-angiogenesis effects were abrogated following inhibition of the MAPK signaling pathway or blockade of VEGFA. Our findings reveal a compelling molecular link between PM exposure and NSCLC progression, centered on VEGFA-driven angiogenesis and urging the need to reduce ambient PM exposure to mitigate its oncogenic impact.

Lung cancer is the leading cause of cancer death worldwide. Cigarette smoking is the well-known risk factor for lung cancer. Epidemiological studies suggest that air pollution, especially particulate matter (PM) exposure, is associated with increased lung cancer risk and mortality independent of cigarette smoking. English-language publications focusing on PM, epigenetic changes, and lung cancer were reviewed. The epigenome serves as an interface between the environment and the genome. PM is one of the environmental factors that can cause epigenetic changes. The epigenome serves as an interface between the environment and the genome. Some of the epigenetic changes lead to increased disease susceptibility and progression. In cardiovascular disease and asthma, the association between PM exposure and the disease specific epigenetic changes has been identified. In lung cancer, the epigenetic changes in DNA methylation, histone modification and microRNA expression are commonly found, but the specific link between PM exposure and lung cancer remains incompletely understood. The results of epidemiological studies indicate the important effects of PM exposure on lung cancer. PM2.5 is consistently associated with the increased lung cancer risk and mortality. Based on the epidemiological associations between PM exposure and lung cancer, PM-induced epigenetic changes may play important roles in the pathogenesis of lung cancer. In this review, we focus on the current knowledge of epigenetic changes associated with PM exposure and lung cancer. Better understanding of the link between PM exposure and lung cancer at the epigenomic level by comprehensive comparison approach may identify lung cancer early detection biomarkers and novel therapeutic targets.