Long-term exposure to air pollution and incidence of gastric and the upper aerodigestive tract cancers in a pooled European cohort: The ELAPSE project.

Air pollution has been shown to significantly impact human health including cancer. Gastric and upper aerodigestive tract (UADT) cancers are common and increased risk has been associated with smoking and occupational exposures. However, the association with air pollution remains unclear. We pooled European subcohorts (N = 287,576 participants for gastric and N = 297,406 for UADT analyses) and investigated the association between residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone in the warm season (O3w) with gastric and UADT cancer. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,305,133 and 5,434,843 person-years, 872 gastric and 1139 UADT incident cancer cases were observed, respectively. For gastric cancer, we found no association with PM2.5, NO2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 µg/m3 increase in PM2.5, 1.19 (1.08-1.30) per 10 µg/m3 increase in NO2, 1.14 (1.04-1.26) per 0.5 × 10-5 m-1 increase in BC and 0.81 (0.72-0.92) per 10 µg/m3 increase in O3w. We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM2.5, NO2 and BC increased incidence of UADT cancer was observed.

Impact of air pollution on postoperative outcomes following organ transplantation: Evidence from clinical investigations.

INTRODUCTION: Air pollution is a worldwide problem affecting human health via various body systems, resulting in numerous significant adverse events. Air pollutants, including particulate matter < or = 2.5 microns (PM2.5), particulate matter < or = 10 microns (PM10), ozone (O3 ), nitrogen dioxide (NO2 ), and traffic-related air pollution (TRAP), have demonstrated the negative effects on human health (e.g., increased cerebrovascular, cardiovascular, and respiratory diseases, malignancy, and mortality). Organ transplant patients, who are taking immunosuppressive agents, are especially vulnerable to the adverse effects of air pollutants. The evidence from clinical investigation has shown that exposure to air pollution after organ transplantation is associated with organ rejection, cardiovascular disease, coronary heart disease, cerebrovascular disease, infection-related mortality, and vitamin D deficiency. OBJECTIVES AND METHOD: This review aims to summarize and discuss the association of exposure to air pollutants and serum 25-hydroxyvitamin D level and outcomes after transplantation. Controversial findings are also included and discussed. CONCLUSION: All of the findings suggest that air pollution results in a hazardous environment, which not only impacts human health worldwide but also affects post-transplant outcomes.

Association between ambient fine particular matter components and subsequent cognitive impairment in community-dwelling older people: a prospective cohort study from eastern China.

BACKGROUND: Fine particular matter (PM2.5) has been associated with dementia, but limited information is available regarding the association between PM2.5 components and dementia. AIMS: We aimed to identify the major components of PM2.5 that affect cognitive function to further investigate its mechanism of action, and develop a prevention strategy for dementia. METHODS: In this study, we included 7804 participants aged ≥ 60 years recruited from seven counties in Zhejiang province, eastern China. The participants completed the baseline survey between 2014 and 2015, and were followed up until the end of 2020. We adopted single-component robust Poisson regression models for analyses, and estimated relative risks and 95% confidence intervals describing associations between the chemical constituents of PM2.5 exposure and incident cognitive impairment in those who were free from cognitive impairment at baseline. RESULTS: Significantly positive associations were observed between sulfate, nitrate, ammonium, and organic matter in PM2.5 and incident cognitive impairment across different exposure periods; the relative risks of 10-year exposure before enrollment ranged from 1.01 to 1.02. However, we did not find a significant association between black carbon and cognitive impairment. The point estimates of the relative risk values did not change substantially after performing the sensitivity analyses. CONCLUSIONS: Our findings strengthen the idea that long-term exposure to PM2.5 mass and its chemical components is associated with an elevated risk of incident cognitive impairment among older adults.

Long-term effects of air pollutants on deaths in a semi-urban city in Northwestern Turkey: a time series analysis.

To examine the associations between daily variations of coarse Particulate Matter(PM10) and/or sulfur dioxide(SO2) and mortality. The Poisson Generalized Linear Model(GLM) was employed to analyze the relationship between ambient air pollutants such as PM10 and SO2 and mortality. For each 10 µg/m3 increase in PM10, the overall mortality risk was found to be 1.022-fold high on the previous-eighth-day(lag 7) (RR, 95%CI:1.002-1.042) in the unadjusted model; 1.031-fold high in men (RR, 95%CI:1.005-1.058); 1.024-fold high in those aged 65 and over (RR, 95%CI:1.001-1.048). Also, the risk of death in men was 1.028-fold high in the model adjusted on the previous- eighth-day(lag 7) (RR, 95%CI:1.002-1.055). Mortality risk was found to be 1.088-fold high in 10 µg/m3 increase in SO2 under 65 years in males in the previous-third-day(lag 2) in the unadjusted model, and the risk of death was found to be 1.086-fold (RR, 95%CI:1.007-1.164) high in males in the adjusted model. .

Long-term fine particular exposure and incidence of frailty in older adults: findings from the Chinese Longitudinal Healthy Longevity Survey.

BACKGROUND: The association between fine particular matter (PM2.5) and frailty is less studied, and the national burden of PM2.5-related frailty in China is unknown. OBJECTIVE: To explore the association between PM2.5 exposure and incident frailty in older adults, and estimate the corresponding disease burden. DESIGN: Chinese Longitudinal Healthy Longevity Survey from 1998 to 2014. SETTING: Twenty-three provinces in China. SUBJECTS: A total of 25,047 participants aged ≥65-year-old. METHODS: Cox proportional hazards models were performed to evaluate the association between PM2.5 and frailty in older adults. A method adapted from the Global Burden of Disease Study was used to calculate the PM2.5-related frailty disease burden. RESULTS: A total of 5,733 incidents of frailty were observed during 107,814.8 person-years follow-up. A 10 µg/m3 increment of PM2.5 was associated with a 5.0% increase in the risk of frailty (Hazard Ratio = 1.05, 95% confidence interval = [1.03-1.07]). Monotonic, but non-linear exposure-response, relationships of PM2.5 with risk of frailty were observed, and slopes were steeper at concentrations >50 µg/m³. Considering the interaction between population ageing and mitigation of PM2.5, the PM2.5-related frailty cases were almost unchanged in 2010, 2020 and 2030, with estimations of 664,097, 730,858 and 665,169, respectively. CONCLUSIONS: This nation-wide prospective cohort study showed a positive association between long-term PM2.5 exposure and frailty incidence. The estimated disease burden indicated that implementing clean air actions may prevent frailty and substantially offset the burden of population ageing worldwide.

Downregulation of TAZ elicits a mitochondrial redox imbalance and ferroptosis in lung epithelial cells exposed to diesel exhaust particles.

Mitochondrial dysfunction was reported to be involved in the development of lung diseases including chronic obstructive pulmonary disease (COPD). However, molecular regulation underlying metabolic disorders in the airway epithelia exposed to air pollution remains unclear. In the present study, lung bronchial epithelial BEAS-2B and alveolar epithelial A549 cells were treated with diesel exhaust particles (DEPs), the primary representative of ambient particle matter. This treatment elicited cell death accompanied by induction of lipid reactive oxygen species (ROS) production and ferroptosis. Lipidomics analyses revealed that DEPs increased glycerophospholipid contents. Accordingly, DEPs upregulated expression of the electron transport chain (ETC) complex and induced mitochondrial ROS production. Mechanistically, DEP exposure downregulated the Hippo transducer transcriptional co-activator with PDZ-binding motif (TAZ), which was further identified to be crucial for the ferroptosis-associated antioxidant system, including glutathione peroxidase 4 (GPX4), the glutamate-cysteine ligase catalytic subunit (GCLC), and glutathione-disulfide reductase (GSR). Moreover, immunohistochemistry confirmed downregulation of GPX4 and upregulation of lipid peroxidation in the bronchial epithelium of COPD patients and Sprague-Dawley rats exposed to air pollution. Finally, proteomics analyses confirmed alterations of ETC-related proteins in bronchoalveolar lavage from COPD patients compared to healthy subjects. Together, our study discovered that involvement of mitochondrial redox dysregulation plays a vital role in pulmonary epithelial cell destruction after exposure to air pollution.

Airborne bacterial community associated with fine particulate matter (PM2.5) under different air quality indices in Temuco city, southern Chile.

Temuco (Chile) is one of the most polluted cities in Chile and Latin America. Although the fine fraction of particulate matter (PM2.5) has been extensively studied and monitored due to its negative impact on public health, its microbiological components remain unknown. We explored, the airborne bacterial community in PM2.5 under good, moderate, alert, pre-emergency and emergency indices of air quality (AQIs) established by the Chilean government. Bacterial community relationship with environmental factors (PM2.5, PM10, carbon monoxide, among others), was also evaluated. Significant differences in PM2.5 bacterial community composition associated with AQIs were revealed, using 16S rRNA target sequences of denaturing gradient gel electrophoresis (DGGE) bands. Bacterial communities in PM2.5 were mainly clustered (80%) into emergency and pre-emergency samples. The dominant phylum was Proteobacteria and most abundant genus was Novosphingobium, traditionally related to opportunistic respiratory diseases. The main factors associated with community structure were PM2.5, PM10 and carbon monoxide concentrations. This study exposed that bacterial community composition in Temuco varies according to AQIs, with the occurrence of potential opportunistic bacteria on heavily polluted days.

TRP Channels as Cellular Targets of Particulate Matter.

Particulate matter (PM) is constituted by particles with sizes in the nanometer to micrometer scales. PM can be generated from natural sources such as sandstorms and wildfires, and from human activities, including combustion of fuels, manufacturing and construction or specially engineered for applications in biotechnology, food industry, cosmetics, electronics, etc. Due to their small size PM can penetrate biological tissues, interact with cellular components and induce noxious effects such as disruptions of the cytoskeleton and membranes and the generation of reactive oxygen species. Here, we provide an overview on the actions of PM on transient receptor potential (TRP) proteins, a superfamily of cation-permeable channels with crucial roles in cell signaling. Their expression in epithelial cells and sensory innervation and their high sensitivity to chemical, thermal and mechanical stimuli makes TRP channels prime targets in the major entry routes of noxious PM, which may result in respiratory, metabolic and cardiovascular disorders. On the other hand, the interactions between TRP channel and engineered nanoparticles may be used for targeted drug delivery. We emphasize in that much further research is required to fully characterize the mechanisms underlying PM-TRP channel interactions and their relevance for PM toxicology and biomedical applications.

Modeling of atmospheric particulate matters via artificial intelligence methods.

Nowadays, pollutants continue to be released into the atmosphere in increasing amounts with each passing day. Some of them may turn into more harmful forms by accumulating in different layers of the atmosphere at different times and can be transported to other regions with atmospheric events. Particulate matter (PM) is one of the most important air pollutants in the atmosphere, and it can be released into the atmosphere by natural and anthropogenic processes or can be formed in the atmosphere as a result of chemical reactions. In this study, it was aimed to predict PM10 and PM2.5 components measured in an industrial zone selected by adaptive neuro-fuzzy inference system (ANFIS), support vector regression (SVR), classification and regression trees (CART), random forest (RF), k-nearest neighbor (KNN), and extreme learning machine (ELM) methods. To this end, in the first stage of the study, the dataset consisting of air pollutants and meteorological data was created, the temporal and qualitative evaluation of these data was performed, and the PM (PM10 and PM2.5) components were modeled using the "R" software environment by artificial intelligence methods. The ANFIS model was more successful in predicting the PM10 (R2 = 0.95, RMSE = 5.87, MAE = 4.75) and PM2.5 (R2 = 0.97, RMSE = 3.05, MAE = 2.18) values in comparison with other methods. As a result of the study, it was clearly observed that the ANFIS model could be used in the prediction of air pollutants.

[Economic evaluation on the health hazards of residents caused by PM_(2.5) in Beijing, Tianjin and Hebei from 2013 to 2018].

OBJECTIVE: To learn the health hazards and health economic losses caused by PM_(2.5) pollution in Beijing, Tianjin and Hebei to the resident population. METHODS: Fine particular matter concentration and the basic demographic data of Beijing, Tianjin and Hebei from 2013 to 2018 were collected. Circulatory system disease hospitalization and other indexes were chosen as the end point of health effects, appropriate exposure-response relationship were selected, and the economic loss of health effect caused by PM_(2.5) was assessed by the combination of the cost of illness approach and human capital method. RESULTS: From 2013 to 2018, the economic loss of Beijing, Tianjin and Hebei caused by fine particular matter pollution showed a decreasing trend year by year. The health economic losses of Beijing from 2013 to 2018 were 3.815, 4.177, 4.090, 3.818, 2.567 and 2.031 billion yuan; The health economic losses of Tianjin were 3.046, 2.625, 1.882, 1.914, 1.448 and 1.000 billion yuan; The health economic losses of Hebei were 13.719, 11.850, 7.423, 7.216, 6.499 and 4.124 billion yuan, Hebei Province had the highest economic loss in 2013, accounting for 13.719 billion yuan, accounting for 0.51% of GDP in that year. Tianjin had the lowest economic loss in 2018, accounting for 10.0 billion yuan, accounting for 0.05% of GDP in that year. CONCLUSION: The health loss caused by PM_(2.5) pollution in Beijing, Tianjin and Hebei region shows a decreasing trend year by year, but the number is still very considerable, and the monitoring and control of PM_(2.5) pollution need to be further strengthened.

Particulate Matter, Asian Sand Dust Delays Cyclophosphamide-induced Type 1 Diabetes in NOD Mice.

Although it is known that desert dust exacerbates allergic diseases, how it affects the onset of autoimmune diseases is unclear. No epidemiological investigations or animal experiments have been conducted so far to elucidate the effects of desert dust on autoimmune diseases. Here, we focused on particulate matter, such Asian sand dust (ASD) that has been known to cause adverse health effects in East Asian countries, and conducted animal experiments to examine how ASD influences type 1 diabetes (T1D), an autoimmune disease. An ASD suspension was intratracheally administered into NOD mice, which spontaneously develop T1D, for 4 times at 2-week intervals. Subsequently, the incidence of cyclophosphamide (CY)-induced diabetes was examined, which was then quantified using adoptive splenocyte-transfer assays. Kaplan-Meier curves of the cumulative T1D incidence were compared using the log-rank test, and unpaired two-tailed t tests were used for comparing the other data. We observed that ASD administration delayed T1D, and adoptive splenocytes derived from ASD-administered donor NOD mice also delayed the onset of T1D in recipient NOD mice. We further found that ASD increases concanavalin A-induced IFN-γ production and decreases regulatory T cells. Consequently, ASD suppresses the onset of T1D, activates spleen cells, and affects T-cell differentiation.

Penalized local polynomial regression for spatial data.

When performing spatial regression analysis in environmental data applications, spatial heterogeneity in the regression coefficients is often observed. Spatially varying coefficient models, including geographically weighted regression and spline models, are standard tools for quantifying such heterogeneity. In this paper, we propose a spatially varying coefficient model that represents the spatially varying parameters as a mixture of local polynomials at selected locations. The local polynomial parameters have attractive interpretations, indicating various types of spatial heterogeneity. Instead of estimating the spatially varying regression coefficients directly, we develop a penalized least squares regression procedure for the local polynomial parameter estimation, which both shrinks the parameter estimation and penalizes the differences among parameters that are associated with neighboring locations. We develop confidence intervals for the varying regression coefficients and prediction intervals for the response. We apply the proposed method to characterize the spatially varying association between particulate matter concentrations ( PM2.5 ) and pollutant gases related to the secondary aerosol formulation in China. The identified regression coefficients show distinct spatial patterns for nitrogen dioxide, sulfur dioxide, and carbon monoxide during different seasons.

Association between ambient PM2.5 and emergency department visits for psychiatric emergency diseases.

BACKGROUND: Whether or not short-term exposure to particulate matter <2.5 µm in diameter (PM2.5) increases the risk of psychiatric emergency diseases is unclear. METHODS: The study was performed in a metropolis from January 2015 to December 2016. The exposure was PM2.5, and the confounders were weather (temperature and humidity) and other pollutants (PM10, SO2, CO, O3, and NO2). The outcomes were emergency department (ED) visits with psychiatric disease codes (F00-F99 in ICD10 codes). General additive models were used for the statistical analysis to calculate the adjusted relative risks (ARRs) and 95% confidence intervals (95% CIs) for the daily number of ED visits with a lag of 1 to 3 days following a 10 µg/m3 increase in PM2.5. RESULTS: During the study period, a total of 67,561 ED visits for psychiatric diseases were identified and tested for association with PM2.5. Daily ED visits for all psychiatric diseases were not associated with PM2.5 in the model that was not adjusted for other pollutants. The ARR (95% CI) in the model adjusted for SO2 was 1.011 (1.002-1.021) by 10 µg/m3 of PM2.5 on Lag 1 for all psychiatric diseases (F00-F99). The ARR (95% CI) in the model adjusted for O3 was 1.015 (1.003-1.029) by 10 µg/m3 of PM2.5 on Lag 1 for F40-F49 (Neurotic, stress-related and somatoform disorders). CONCLUSION: An increase in PM2.5 showed a significant association with an increase in ED visits for all psychiatric diseases (F00-F99) and for neurotic, stress-related and somatoform disorders (F40-F49) on lag day 1.

PM2.5 exposure impairs sperm quality through testicular damage dependent on NALP3 inflammasome and miR-183/96/182 cluster targeting FOXO1 in mouse.

Exposure to ambient fine particular matter (PM2.5) has been clearly associated with male reproductive disorders. However, very limited toxicological studies were carried out to investigate the potential mechanisms underlying the PM2.5-induced sperm quality decline. In the present study, we established a real time whole-body PM2.5 exposure mouse model to investigate the effects of PM2.5 on sperm quality and its potential mechanisms. Sixty male C57BL/6 mice were randomly subjected to three groups: filtered air group, unfiltered air group and concentrated air group. Half of the mice from each group were sacrificed for study when the exposure duration accumulated to 8 weeks and the rest of the mice were sacrificed when exposed for 16 weeks. Our results suggested that PM2.5 exposure could induce significant increases in circulating white blood cells and inflammation in lungs. PM2.5 exposure induced apparently DNA damages and histopathologic changes in testes. There were significantly decreased sperm densities of mice, which were paralleled with the down-regulated testosterone levels in testes tissue of mice after exposure to PM2.5 for 16 weeks. The numbers of motile sperms were decreased and sperms with abnormal morphology were increased after PM2.5 exposure in a time-depended and dose-depended manner. PM2.5 exposure significantly increased the expression of the major components of the NACHT, LRR and PYD domains-containing protein3 (NALP3) inflammasome, accompanied by the increased expression of miR-183/96/182 targeting FOXO1 in testes. The present data demonstrated that sperm quality decline induced by PM2.5 could be partly explained by the inflammatory reaction in testes which might be a consequence of systemic inflammation. The molecular mechanism was depended on the activation of NALP3 inflammasome accompanied by miR-183/96/182 targeting FOXO1 in testes.

Air pollution and short-term clinical outcomes of patients with acute myocardial infarction.

Ambient air pollution is well-known to be a serious risk factor for cardiovascular diseases, stroke, and death. However, the association between air pollutants (AP) exposure and short-term clinical outcomes in acute myocardial infarction (AMI) patients (pts) has not been elucidated well. In the present study, 37 880 AMI pts were enrolled from October 2005 to December 2013 in a nationwide large-scale, prospective, multicentre Korea AMI registry (KAMIR registry; http://www.kamir.or.kr). We obtained data on AP (e.g., NO2 , SO2 , CO, O3 and PM10 ) from the Korean National Institute of Environmental Research (NIER; http://www.nier.go.kr). Clinical endpoints included death, recurrent myocardial infarction (Re-MI), any revascularization and composite of all-cause death and Re-MI. Exposure to AP is defined as the average exposure to AP within 24 hours before AMI admission. We observed that a 0.01 part per million (ppm) increase in NO2 concentration, 0.001 ppm increase in SO2 concentration, and 0.1 ppm increase in CO concentration each increased the risk of total death by 9.7% (95% CI, 6.2%-13.4%), 1.9% (95% CI, 0.3%-3.6%), and 2.1% (95% CI, 0.5%-3.9%), respectively. Exceptionally, O3 decreased the risk of total death by 0.6% (95% CI -0.2% to -1.0%) per 0.01 ppm increase. PM10 was not related to any cardiovascular events. AP were each stratified into five quintiles according to ranges of AP levels. After adjusting analysis for risk variables, only high quintiles (Q4, Q5) of NO2 were positively associated with total death, cardiac death and MI, while SO2 , CO, O3 and PM10 were shown to be not related to any cardiovascular events at all levels. In AMI patients, each AP and its concentration has shown a different effect to short-term mortality and cardiovascular events.

Potential roles of air pollutants on the induction and aggravation of rheumatoid arthritis: From cell to bedside studies.

Rheumatoid arthritis (RA) is an involving chronic systemic inflammatory disease which mainly affects the joints. Several factors including genetic, environment and infections have been acknowledged as being involved in the pathogenesis and aggravation of RA. Air pollution, particularly particulate matter is widely recognized as a cause of health problems. This review is to summarize and discuss the association between air pollutants and the development or the aggravation of RA based on evidence from in vitro, in vivo and clinical studies. The results from the review found that air pollutants can stimulate immunological processes and stimulate inflammatory mediators and autoantibodies productions, both in intro and in vivo studies. In addition, air pollutants can induce RA and aggravate RA disease activity. Unfortunately, there also are some discrepancies in the results, which might be due to the type cell line and the concentration of air pollutants used in the in vitro and in vivo studies, as well as the concentration and duration of exposure in human studies. These findings suggest that future studies focused on elucidating these mechanisms using advanced techniques and identifying reliable biomarkers to assess individual susceptibility and disease activity should be carried out. Longitudinal studies, intervention strategies, and policy implications also should be explored. A comprehensive understanding on these association will facilitate targeted approaches for prevention and management of air pollutant-induced RA and improve health outcome.

An overview of atmospheric aerosol and their effects on human health.

Epidemiologic investigations have previously been published in more than 200 papers, and several studies have examined the impacts of particle air pollution on health. The main conclusions now being made about the epidemiological evidence of particle pollution-induced health impacts are discussed in this article. Although there is no universal agreement, most reviewers conclude that particulate air pollution, particularly excellent combustion-cause contamination prevalent in many municipal and manufacturing environments, is a significant risk for cardiopulmonary sickness and mortality. Most epidemiological research has concentrated on the impacts of acute exposure, although the total public health implications of chronic acquaintance's outcome may be more extraordinarily significant. According to some reviewers, prolonged, repeated exposure raises the risk of cardiorespiratory death and chronic respiratory illness. A more general (but still universal) agreement is that short-term particle pollution exposure has been shown to aggravate pre-existing pulmonary and cardiovascular diseases and increase the number of community members who become sick, require medical treatment, or die. Several in-depth studies conducted in the global and Indian regions are addressed.

Characteristics and Traceability Analysis of Microbial Assemblage in Fine Particulate Matter from a Pig House.

Fine particulate matter (PM2.5) can carry numerous substances and penetrate deep into the respiratory tract due to its small particle size; associated harmful microorganisms are suspected to increase health risks for humans and animals. To find out the microbial compositions of PM2.5 in piggeries, their interaction and traceability, we collected PM2.5 samples from a piggery while continuously monitoring the environmental indicators. We also identified pathogenic bacteria and allergens in the samples using high-throughput sequencing technology. We analyzed the microbial differences of PM2.5 samples at different heights and during different times of day and investigated the microbial dynamics among the PM2.5 samples. To better understand the interaction between microorganisms and environmental factors among different microbial communities, we applied the network analysis method to identify the correlation among various variables. Finally, SourceTracker, a commonly used microbial traceability tool, was used to predict the source of airborne microorganisms in the pig house. We identified 14 potential pathogenic bacteria and 5 allergens from PM2.5 in the pig houses, of which Acinetobacter was the dominant bacterium in all samples (relative abundance > 1%), which warrants attention. We found that bacteria and fungi directly affected the the microbial community. The bacterial community mainly played a positive role in the microbial community. Environmental variables mainly indirectly and positively affected microbial abundance. In the SourceTracker analysis using fecal matter and feed as sources and PM2.5 sample as sink, we found that fecal matter made the greatest contribution to both bacterial and fungal components of PM2.5. Our findings provide important insights into the potential risks of pathogens in PM2.5 to human and animal health and their main sources.

Tenascin C in Lung Diseases.

Tenascin C (TNC) is a multifunctional large extracellular matrix protein involved in numerous cellular processes in embryonic development and can be increased in disease, or under conditions of trauma or cell stress in adults. However, the role of TNC in lung diseases remains unclear. In this study, we investigated the expression of TNC during development, in offspring following maternal particulate matter (PM) exposure, asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. TNC expression is increased during lung development in biopsy cells, endothelial cells, mesenchymal cells, and epithelial cells. Maternal PM exposure increased TNC and collagen deposition, which was not affected by the removal of PM exposure after pregnancy. TNC expression was also increased in basal epithelial cells and fibroblasts in patients with asthma and AT2 and endothelial cells in patients with COPD. Furthermore, there was an increase in the expression of TNC in stage II compared to stage IA lung cancer; however, overall survival analysis showed no correlation between levels of TNC and survival. In conclusion, TNC is increased during lung development, in offspring following maternal PM exposure, and in asthma, COPD, and lung cancer tissues. Therefore, targeting TNC may provide a novel therapeutic target for lung diseases.

Global, regional, and national burden of preterm birth attributable to ambient and household PM2.5 from 1990 to 2019: Worsening or improving?

BACKGROUND: Maternal exposure to fine particular matter (PM2.5) during pregnancy, including ambient and household PM2.5, has been linked with increased risk of preterm birth (PTB). However, the global spatio-temporal distribution of PTB-related deaths and disability-adjusted life years (DALYs) attributable to PM2.5 is not well documented. We estimated the global, regional, and national patterns and trends of PTB burden attributable to both ambient and household PM2.5 from 1990 to 2019. METHODS: Based on the Global Burden of Disease Study (GBD) 2019 database, we obtained the numbers of deaths and DALYs as well as age-standardized mortality rate (ASMR) and age-standardized DALY rate (ASDR) of PTB attributable to total, ambient, and household PM2.5 by socio-demographic index (SDI) and sex during 1990-2019. The average annual percentage changes (AAPCs) were calculated to assess the temporal trends of attributable burdens. RESULTS: In 2019, 126,752 deaths and 11.3 million DALYs related to PTB worldwide (two-thirds in Western Sub-Saharan Africa and South Asia) could be caused by excess PM2.5 above the theoretical minimum-risk exposure level (TMREL), of which 39 % and 61 % were attributable to ambient PM2.5 and household PM2.5, respectively. From 1990 to 2019, the global ASMR due to ambient PM2.5 increased slightly by 7.08 % whereas that due to household PM2.5 decreased substantially by 58.81 %, although the latter still dominated the attributable PTB burden, especially in low and low-middle SDI regions. Similar results were also observed for ASDRs. In addition, PTB burden due to PM2.5 was higher in male infants and in lower SDI regions. CONCLUSIONS: Globally in 2019, PM2.5 remains a great concern on the PTB burden, especially in Western Sub-Saharan Africa and South Asia. Between 1990 and 2019, age-standardized burden of PTB due to ambient PM2.5 increased globally, while that due to household PM2.5 decreased markedly but still dominated in low and low-middle SDI regions.