Smoke Pollution Research Articles

Associations of Fire Smoke and Other Pollutants With Incident Rheumatoid Arthritis and Rheumatoid Arthritis-Associated Interstitial Lung Disease.

The aim of this study was to determine whether pollutants such as fire smoke-related particulate matter <2.5 μm (PM2.5) are associated with incident rheumatoid arthritis (RA) and RA-associated interstitial lung disease (RA-ILD). This patient-control study used Veterans Affairs (VA) data from October 1, 2009, to December 31, 2018. We identified patients with incident RA and RA-ILD using validated algorithms, matching each patient to ≤10 controls on age, sex, and VA enrollment year. We obtained pollutants including fire smoke PM2.5, carbon monoxide, nitrogen oxides (NOx), ozone, overall PM2.5, PM10, and sulfur dioxide (SO2) at least one year before the index date. We fit conditional logistic regression models to estimate adjusted odds ratios (aORs) with 95% confidence intervals (CIs) for incident RA and RA-ILD, adjusted for confounders. We identified 9,701 patients with incident RA (mean age 65 years, 86% male), including 531 patients with RA-ILD (mean age 69 years, 91% male), and 68,852 matched controls. Fire smoke PM2.5 was not associated with RA (aOR 1.07, 95% CI 0.92-1.23) but was associated with RA-ILD (aOR 1.98, 95% CI 1.08-3.62, per 1 μg/m3). Increased levels of NOx were associated with RA (aOR 1.16, 95% CI 1.06-1.27, highest vs lowest quartile). The highest quartiles of ozone (aOR 1.19, 95% CI 1.06-1.34) and PM10 (aOR 1.25, 95% CI 1.10-1.43) were associated with seronegative RA. Carbon monoxide, overall PM2.5, and SO2 were not, or negatively, associated with RA and RA-ILD. Increased fire smoke PM2.5 was associated with RA-ILD, whereas NOx, ozone, and PM10 were associated with RA risk. Thus, air pollution may increase the risk of RA and RA-ILD.

Impact of gaseous smoke pollutants from modelled fires on air and soil quality

Forest fires produce large volumes of pollutants in the atmospheric air. Fires contribute significantly to greenhouse gas emissions worldwide apart from industrial and traffic pollutants. The study reports the results of research on the effect of gaseous substances from burning forest combustibles on air quality and deposition of emissions on soil. It was determined a significant excess in smoke of such substances as carbon monoxide (3570 mg/m3), nitrogen oxide and dioxide (40 mg/m3 and 60 mg/m3) saturated hydrocarbons – methane, ethane, propane, butane, pentane, hexane, heptane, octane, nonane, decane, dodecane, tridecane, tetradecane, pentadecane, hexadecane, heptadecane, octadecane nonadecane. The obtained results evidence the increased concentrations of pollutants, including climate-active substances in the air. They can affect negatively both the climate and ecological state of soils. A negative effect of gaseous products of combustion on soil (Haplic Chernozem) by deposition was determined, which caused changes in soil properties. It was reliably established that the enzymatic activity of soil (Haplic Chernozem) significantly decreased under the influence from smoke of fire during 60 min. Catalase appeared to be the most sensitive indicator. The catalase activity decreased by 25% compared to control values. Peroxidase activity decreased by 15%, urease by 20% and phosphatase by 16%. The pH changed from 7.8 to 6.3 after exposure of the soil to smoke. Soil microbiota was also adversely affected by smoke. High sensitivity was recorded for microscopic fungi. Their abundances decreased by 26%–87% after 10–60 min of smoke exposure. Bacteria were found to be more resistant to toxic smoke (28%–33% decrease in abundance). Therefore, smoke from fires can be considered as one of the factors that can affect soil.Graphical

DOP039 Dietary methyl group donor intake alleviates the susceptibility to inflammatory bowel disease influenced by environmental pollution in a prospective cohort study

Abstract Background Both genetic and environmental factors play crucial roles in individual susceptibility to inflammatory bowel disease (IBD) [1], though its exact etiology remains unclear. Multiple studies have identified environmental pollutants, such as cigarette smoke and fine particulate matter, as significant risk factors for IBD [2, 3]. Chronic exposure to air pollution alters DNA methylation patterns, with a typically long-term hypomethylated status. Our previous study also found that smoking can lead to susceptibility to IBD by affecting the methylation levels of key genes [2]. Moreover, DNA methylation, as an epigenetic mechanism, has been implicated in the pathogenesis of IBD. The intake and quality of dietary methyl group donors (MGDs) directly affects the methylation process in vivo, potentially modulating the risk of developing IBD. Therefore, the present study explored the effect of dietary MGDs on the development of IBD and whether dietary MGDs intake is beneficial in modulating the susceptibility to IBD influenced by environmental pollution. Methods We included 186,195 IBD-free participants at baseline with available dietary information from UK Biobank. Dietary MGDs intake was aggerated by the z-score of methionine, folate, choline, betaine intake by 24h dietary recalls. Smoking behavior and intensity were ascertained via self-report questionnaires. Susceptibility to air pollution was estimated by summing up the exposure to four air pollutant (PM2.5, PM10, NOx, NO2) weighted by effect size on liability to IBD [3, 4]. Diagnosis of IBD were determined by at least two health-related records in national registries. Cox proportional hazard models were applied to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs). Results During a mean follow-up of 10.8 years, we identified 139 and 285 incident cases of CD and UC. We found that individuals with the highest quintiles of dietary MGDs have a significant reduction in risk of CD (HR 0.50, 95% CI 0.28-0.90, P=0.021; P-trend=0.018) and UC (HR 0.62, 95% CI 0.40-0.96, P=0.034; P-trend=0.022) compared to those in the lowest quintile (Figure 1). The associations between dietary MGD and CD were more pronounced in individuals with smoking history (HR 0.66, 95% CI 0.51-0.86), who smoke more than 20 pack-years (HR 0.63, 95% CI 0.45-0.86), who were exposed to high air pollution (HR 0.58, 95% CI 0.37-0.91) than individuals without smoking history, who smoke less than 20 pack-years, who exposed to lower air pollution (all P-interaction&amp;lt;0.05, Figure 4). Conclusion This study demonstrates the potential of dietary methyl donors for the prevention of IBD and provides more precise nutritional intervention strategies for populations affected by smoking and air pollution problems.

Allergy and immunotoxicology in preventive and clinical medicine from theory to practice: Environmental factors in bronchial asthma

According to the gene-environment interactions concept, the mechanism of health impairment can be explained by genetic factors, environmental factors, or their interaction. Physical and mental health effects resulting from environmental exposure may be classified either as toxicity, immune response, and allergic reaction. Moreover, despite the already established therapeutic approaches to bronchial asthma and decreasing mortality due to bronchial asthma, patients with difficult and severe asthma are increasing in number. This review outlines recent topics in the field of allergies, focusing on asthma. Living environment-derived pollutants and their involvement in the pathogenesis of asthma and its exacerbation, referred to here as an exposome concept, comprises the three domains of internal, specific external, and general external. Living environment-derived pollutants include exposure to pollutants in workplaces, climate change, air pollution, microplastics, tobacco smoke, biodiversity change and loss, changing dietary habits, and the microbiome. These are associated with the modernization, urbanization, and globalization of human society. Although many novel compounds are currently available, their harmful health effects, such as allergy, are not thoroughly understood. Hence, the means to mitigate these are unknown. Dietary changes from a traditional diet rich in fish to a Western-style diet are considered critical environmental factors and therefore, associated with an increased prevalence of allergies. Cytokines, including thymic stromal lymphopoietin, IL-25, and IL-33, released from the airway epithelium in response to various triggers (exposure to diverse environmental factors) are known as alarmins. Anti-alarmin antibodies are a promising therapeutic approach against severe and difficult allergic disorders. Collaboration between hospitals and clinics and occupational and clinical medicine is imperative for treating and managing severe asthma. In addition to avoiding environmental exposure, understanding the pathogenesis and exacerbation of asthma is essential for future research in the field of allergy and immunotoxicology.

Lung cancer screening in India: Preparing for the future using smart tools &amp; biomarkers to identify highest risk individuals

There is a growing burden of lung cancer cases in India, incidence projected to increase from 63,708 cases (2015) to 81,219 cases (2025). The increasing numbers are attributed to smoking (India currently has nearly 100 million adult smokers) and environmental pollution. Most patients present with advanced disease (80-85% are incurable), causing nearly 60,000 annual deaths from lung cancer. Early detection through lung cancer screening (LCS) can result in curative therapies for earlier stages of lung cancer and improved survival. Annual low-dose computerized tomography (LDCT) is the standard method for LCS. Usually, high-risk populations (age&gt;50 yr and &gt;20 pack-years of smoking) are considered for LCS, but even such focused screening may be challenging in resource-limited countries like India. However, developing a smart LCS programme with high yield may be possible by leveraging demographic and genomic data, use of smart tools, and judicious use of blood-based biomarkers. Developing this model over the next several years will facilitate a structured cancer screening programme for populations at the highest risk of lung cancer. In this paper, we discuss the demographics of lung cancer in India and its relation to smoking patterns. Further, we elaborate on the potential applications and challenges of bringing a smart approach to LCS in high-risk populations in India.

Mitochondrial quality control: a pathophysiological mechanism and potential therapeutic target for chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a prevalent chronic respiratory disease worldwide. Mitochondrial quality control mechanisms encompass processes such as mitochondrial biogenesis, fusion, fission, and autophagy, which collectively maintain the quantity, morphology, and function of mitochondria, ensuring cellular energy supply and the progression of normal physiological activities. However, in COPD, due to the persistent stimulation of harmful factors such as smoking and air pollution, mitochondrial quality control mechanisms often become deregulated, leading to mitochondrial dysfunction. Mitochondrial dysfunction plays a pivotal role in the pathogenesis of COPD, contributing toinflammatory response, oxidative stress, cellular senescence. However, therapeutic strategies targeting mitochondria remain underexplored. This review highlights recent advances in mitochondrial dysfunction in COPD, focusing on the role of mitochondrial quality control mechanisms and their dysregulation in disease progression. We emphasize the significance of mitochondria in the pathophysiological processes of COPD and explore potential strategies to regulate mitochondrial quality and improve mitochondrial function through mitochondrial interventions, aiming to treat COPD effectively. Additionally, we analyze the limitations and challenges of existing therapeutic strategies, aiming to provide new insights and methods for COPD treatment.

Decoding the disproportionate risk factor landscape of global type 2 diabetes burden in adults: An attribution analysis from 1990 to 2050.

Limited systematic assessments of risk factor contributions to the global burden of type 2 diabetes (T2D) across subpopulations hinder targeted policies and resource allocation. Utilizing the Global Burden of Disease study (GBD) 2019, we analyzed the disability-adjusted life-years (DALYs) for T2D attributable to 15 risk factors in adults (aged 25+ years) globally and by sex, age, Socio-demographic Index (SDI), and GBD region, from 1990 to 2019. Additionally, we assessed future trends of these risk factors through 2050. High body-mass index (BMI) emerged as the predominant risk factor in all subpopulations in 2019, with its impact projected to double by 2050. During 1990-2019, males were more affected by smoking, while females by secondhand smoke and household air pollution. The related DALYs increased with age, except for high BMI and smoking peaking at 60-74 years. In 2019, diet high in processed meat ranked second in high SDI regions, contrasting with household air pollution in low SDI regions. National disparities were observed, with Fiji recording the highest rates of DALYs related to both high BMI and dietary risks in 2019, which were approximately 50 and 15 times higher than those observed in Japan, respectively. Tailored interventions targeting major contributing risk factors specific to each subpopulation are key to the success of the global combat against T2D.

Burdens of Tracheal, Bronchus, and Lung Cancer From 1990 to 2021 in China Compared to the Global Projection of 2036: Findings From the 2021 Global Burden of Disease Study.

Tracheal, bronchial, and lung cancers (TBL cancers) pose a significant global health challenge, with rising incidence and mortality rates, particularly in China. Studies from the Global Burden of Disease (GBD), 2021, can guide screening and prevention strategies for TBL cancer. This study aims to provide a comprehensive analysis of the burden of TBL cancers in China compared to global data. We conducted an analysis of incidence, prevalence, mortality, and disability-adjusted life years (DALYs) from 1990 to 2021. We also performed Joinpoint regression analysis and Bayesian age-period-cohort (BAPC) modeling to project future trends. From 1990 to 2021, there was a substantial increase in TBL cancer indicators for all sexes in China, with the most significant rise observed in females. The female population showed alarming increases in age-standardized incidence rate (ASIR) and age-standardized prevalence rate (ASPR). While global efforts have managed to stabilize these rates, China's figures remain high, suggesting the impact of persistent risk factors such as smoking and air pollution, coupled with an aging population. Furthermore, we utilized the projection model in China to estimate that these indicators of TBL cancers in females will likely follow continuous and rapid upward trends, while the burden of TBL cancers among males is expected to have a steady trend. Although global efforts have been effective in reducing the burden of TBL cancers over the past three decades, there still remains strong regional and gender heterogeneity. TBL cancers need more screening strategies and medical attention in China and in the female population.

Risk Factors for Adults with Chronic Obstructive Pulmonary Disease in the United States, Utilizing State-Based Surveillance

Chronic Obstructive Pulmonary Disease (COPD) is a complex and heterogeneous condition. Exposure to tobacco smoke and air pollutants are key risk factors for COPD development; however, other risk factors include race/ethnicity, sex of adults, a history of asthma, occupational exposures, and chronic respiratory infections. Data for the current study were from the 2022 Behavioral Risk Factor Surveillance Survey. Chi-squares and multinomial logistic regression analyses, adjusted with the survey’s sampling weight, were used to examine how critical health indicators impacted a COPD diagnosis. Participants (N = 311,175) were adults aged 45 years and older. Adjusted multinomial regression analyses showed adults who reported asthma, current and former smoking, poor physical health, depression, less physical activity, and fatigue were more likely to report COPD. Those with COPD were more likely to be male than female. Moreover, those with COPD reported higher rates of health insurance coverage, and yet had lower income and more financial difficulty affording a doctor for health services. In a follow up regression analysis, examining racial differences in COPD for participants, American Indian adults had a higher odds of reporting COPD than the “other” race groups. Because COPD remains a leading cause of death and disability in the U.S., and racial disparities persist in respiratory outcomes, continuing to identify risk factors for vulnerable groups could assist health program planners with development of successful health messaging.

Chronic obstructive pulmonary disease (COPD): New treatment and management approaches

COPD is the third leading cause of morbidity and mortality from chronic diseases worldwide, and exposure to toxic particles, such as tobacco smoke and air pollution, is the first risk factor. The management of symptoms advances with the prevention of acute relapse rather than the loss of preciosity in the early stages of the disease. Current therapies focus mainly on the alleviation of symptoms and lack intervention in the underlying inflammatory mechanisms responsible for tissue destruction in the lungs and airway obstruction. In this context, there has been an explosion of advances in omics and imaging technologies that will shed light on the pathobiology of COPD, leading to better methods for its diagnosis, treatment, and prevention. In addition, novel biomarker-based approaches also allowed for better patient stratification, which led to the reappropriation of existing drugs for more personalized care in specific patient populations. The coronavirus pandemic has further aggravated the situation of COPD patients. This is because, by nature, COPD patients are more prone to severe forms of respiratory illness. They added the burdens of social isolation and disrupted healthcare services, further complicating disease management. Components of a strategy for COPD burden reduction are early diagnosis, proper management of comorbidities, promotion of regular physical activity, vaccine interventions, and other smoking cessation programs. It is crucial to fight tobacco use, minimize exposure to environmental risk factors at all levels and increase access to healthcare. Another way to reduce COPD is also important in areas where there are alternatives to biomass fuels, thus reducing the burden on COPD rates. This can otherwise minimize the long-term impact.

Temporal trend and attributable risk factors of cardiovascular diseases burden for adults 55 years and older in 204 countries/territories from 1990 to 2021: an analysis for the Global Burden of Disease Study 2021.

The aging global population and overall population growth have significantly increased the burden of cardiovascular diseases (CVDs). This study aims to examine global temporal trends in the incidence, disability-adjusted life years (DALY), and mortality rates of both overall and type-specific CVDs among adults aged 55 and older from 1990 to 2021, with a focus on identifying changes over time, regional disparities, and the key risk factors contributing to this burden. We analyzed data from the Global Burden of Disease (GBD) Study 2021, covering 204 countries and territories. Trends in age-standardized rates of incidence, DALY, and mortality for both overall and specific types of CVDs were assessed, alongside the impact of key risk factors. Between 1990 and 2021, global age-standardized incidence, DALY, and mortality rates showed a declining trend, with estimated annual percentage changes (EAPCs) of -0.39, -1.30, and -1.11, respectively. However, due to overall population growth and aging, the absolute number of CVD cases continued to rise. Regions with high-middle Socio-demographic Index (SDI) exhibited the highest incidence and mortality rates, while high SDI regions saw the greatest declines. Men had higher age-standardized rates of CVDs incidence, DALY, and mortality compared to women. The burden increased with age, with the oldest age groups (80+ years) showing the highest rates. High systolic blood pressure was the leading modifiable risk factor, contributing to more than half of the CVD-related DALY globally. Other major risk factors included high low-density lipoprotein cholesterol, smoking, and ambient particulate matter pollution. While age-standardized rates of CVD incidence, DALY, and mortality have declined over the past three decades, the total burden of CVDs continues to rise due to population aging and growth. These findings highlight the need for targeted prevention strategies in regions with high CVD burden, particularly those with lower socioeconomic status.

Neuroticism and asthma: Mendelian randomization analysis reveals causal link with mood swings and BMI mediation

Background Neuroticism has been associated with asthma, but the nature of this relationship remains unclear due to limited understanding of the impact of psychological factors on asthma risk. While Neuroticism is known to affect various health outcomes, its specific role in respiratory conditions like asthma is not fully understood. Methods We conducted Mendelian randomization (MR) analyses using genome-wide association studies (GWAS) to explore the causal link between 12 Neuroticism traits and asthma. Various MR approaches, including MR-PRESSO, were employed, with validation through independent GWAS and the FinnGen dataset. Results MR-PRESSO revealed a significant causal relationship between mood swings and asthma (OR: 1.927, 95% CI: 1.641–2.263), surpassing the Bonferroni-corrected threshold (p < 4.167 × 10−³). Mood swings emerged as the only significant trait associated with asthma, with reverse MR analyses showing no causal links for other traits. Secondary analyses supported these findings. Multivariate analysis showed mood swings increased asthma risk, independent of smoking, BMI, and air pollution. Mediation analysis indicated that BMI partially mediates the mood swing-asthma relationship, accounting for 9.87% of the effect (95% CI: 4.54%–15.2%, p = 2.850 × 10−4). Conclusion Mood swings elevate asthma risk, with BMI partially mediating this effect, highlighting a potentially significant pathway through which psychological traits influence asthma.

Variation of Modified Combustion Efficiency and Its Impact on Biomass Burning Emission Estimation in Africa

AbstractBiomass burning (BB) is one of the largest sources of trace gases and primary carbonaceous particles in the global troposphere, posing great impacts on air quality and regional climate. Accurate quantification of BB emissions is vital for assessing its environmental and climate impacts. However, there are still large uncertainties in current BB emission inventories due to poorly characterized emission rates under different combustion states. The fixed emission factor (EF) instead of varying EF associated with different combustion efficiencies may be the reason for the bias. Here, based on satellite‐retrieved carbon dioxide (CO2) and carbon monoxide (CO), the modified combustion efficiency (MCE) is derived for fire‐prone regions in Africa. The monthly and inter‐annual variability of MCE shows a good correlation with meteorological variables such as relative humidity. Therefore, variable EF was established based on its statistical relationship with MCE for different fire‐emitted species. Application of such MCE‐dependent EF in the global climate‐chemistry model can greatly improve the performance of wildfire smoke pollution during the fire season, indicated by an increase of 31% in aerosol optical depth (AOD) and a 50% reduction in normalized mean bias compared with AOD observations. The study elucidates the critical role of meteorology in BB emission estimates and highlights the importance of implementing a dynamic fire emission inventory in response to meteorological conditions.

Berberine and Lung Cancer: From Pure Form to Its Nanoformulations.

Lung cancer is the most fatal cancer worldwide. The etiology of lung cancer has yet to be fully characterized. Smoking and air pollution are several risk factors for lung cancer. Berberine, an isoquinoline alkaloid, is an antihyperglycemic, antidepressant, antioxidative, anti-inflammatory, and anticancer compound. Evidence substantiates that berberine has antitumor effects, exerting its effects by targeting a variety of cellular and molecular processes, such as apoptosis, autophagy, cell cycle arrest, migration, and metastasis. Although the beneficial effects of berberine have been reported, some limitations including low bioavailability and absorption as well as poor aqueous solubility have hindered its clinical application. Nanotechnology and nanodelivery bioformulation approaches may bypass these limitations. In addition, the combination of berberine with other therapies has been shown to result in greater treatment efficacy for lung cancer. Herein, we summarize cellular and molecular pathways that are affected by berberine, its clinical efficacy upon various combinations, and the potential for nanotechnology in lung cancer therapy.

Levels of OH-PAHs and markers of oxidative stress in urine of taxi drivers and controls

Polycyclic aromatic hydrocarbons are pervasive in the atmosphere, originating from sources like vehicle emissions and incomplete combustion. Exposure to PAHs occurs through diet, tobacco smoke, and air pollutants, and they are recognized as carcinogens. This study, conducted from July to October 2021 in Seoul, Gyeonggi, and Ulsan regions, focused on taxi drivers, a group with elevated PAH exposure due to prolonged vehicle use. The study involved 19 male taxi drivers and 46 control participants (18 male, 28 female). LC-MS/MS analysis was employed to quantify urinary levels of 18 hydroxy-PAHs, oxidative damage markers (MDA, 8-OHdG), and cotinine. The detection rates of OH-PAHs were 1-naphthol (96.9 %), 2-naphthol (90.8 %), 2-hydroxyfluorene (86.2 %), and 1-hydroxypyrene (80.0 %). Compared to the male controls, taxi drivers showed higher median concentrations of 2-OH-Na (1.698 ng/mL), 1-OH-Na (0.666 ng/mL), 2-OH-Flu (0.067 ng/mL), and 1-OHP (0.045 ng/mL). Similarly, significant differences were observed between taxi drivers and female controls for 1-OH-Na, 2-OH-Na, 2-OH-Flu, 3-OH-Phe, and 1-OHP. MDA and 8-OHdG were detected in over 90% of all groups, with significant differences between taxi drivers. Strong positive correlations were revealed between urinary OH-PAHs, MDA, and 8-OHdG (r ranging from 0.589 to 0.770, p&lt;0.01). The findings suggest that taxi drivers, due to prolonged exposure to traffic-related air pollutants, have elevated levels of PAH metabolites and oxidative stress, especially among smokers. Further studies with larger sample sizes are recommended to validate these results and explore the long-term health implications of occupational PAH exposure in urban transportation workers..

The impact of wildfire smoke exposure on excess mortality and later-life socioeconomic outcomes: the Great Fire of 1910

AbstractThe Great Fire of 1910 in the northwestern United States burnt more than 1.2 million hectares in just two days and stands as one of the largest wildfires ever recorded. While it is known for having led to the introduction of a rigorous fire suppression regime that lasted for much of the twentieth century, it also generated a considerable amount of smoke far beyond the burnt areas that is likely to have impacted the health of those exposed. This paper examines the short- and long-term impact of this fire-sourced smoke pollution on children, combining historical data with smoke emission and dispersion modelling. The econometric results indicate a 119% increase in excess mortality during the week of the fire and a decrease of 4–14% in later-life socioeconomic status scores 20 and 30 years after the event. This research offers novel insights into wildfire smoke repercussions on health and long-run human capital formation in a setting where avoidance behaviour was minimal.

Aryl-hydrocarbon receptor in smooth muscle cells protect against dioxin induced adverse remodeling of atherosclerosis.

Environmental exposure to dioxin has been linked to increased myocardial infarction. Smooth muscle cells (SMC) in the coronary vasculature play a critical role in atherosclerotic plaque remodeling due to their phenotypic plasticity, however, the detailed mechanism linking dioxin exposure to adverse SMC modulation is not well understood. Single-cell RNA and ATAC sequencing and histological analyses were performed on the aorta from mouse models of atherosclerosis exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) or control. Primary human coronary artery SMC (HCASMC) treated in culture with TCDD were used to perform RNA-Seq, ATAC-Seq, and functional phenotypic assays. ChIP-Seq was performed with antibodies against Aryl-hydrocarbon receptor (AHR) and TCF21, two of known SMC modulating transcription factors. Modulated SMC were the most transcriptionally responsive cell type to dioxin in the atherosclerotic aorta. Dioxin accelerated disease phenotype by promoting a modulated SMC phenotype early, resulting in increased lesion size, migration of SMC, and macrophage recruitment to the lesion. We found C3 expressing modulated SMCs to be likely contributing to the increased macrophage recruitment and inflammation. Analysis of the RNA-Seq data from HCASMC treated with TCDD showed differential enrichment of biological pathways related to cell migration, localization, and inflammation. Furthermore, ATAC-Seq data showed a significant activation for pathways regulating vascular development, cell migration, inflammation, and apoptosis. With TCDD treatment, there was also enrichment of AHR ChIP-Seq peaks, while the TCF21 enrichment decreased significantly. The SMC-specific Ahr knockout resulted in increased oxidative stress in SMC, increased lesion size and macrophage content, and loss of SMC lineage cells in the lesion cap when exposed to TCDD, consistent with a more vulnerable plaque phenotype. Dioxin adversely remodels atherosclerotic plaque by accelerating the SMC- phenotypic modulation, and increasing inflammation and oxidative stress resulting in increased macrophage recruitment and lesion size. Dioxin may adversely affect the SMC phenotype and disease state by affecting the TCF21 occupancy in the open chromatin regions. Furthermore, we observed that SMC-specific deletion of Ahr in mice resulted in worsening of dioxin mediated SMC modulation and atherosclerosis, suggesting that Ahr in SMC confers protection against dioxin by promoting a stable plaque phenotype and reducing dioxin induced oxidative stress. Exposure to dioxin, an environmental pollutant present in tobacco smoke and air pollution, accelerates smooth muscle cell modulation, and atherosclerosis.Dioxin exposure leads to inflammatory smooth muscle cell phenotype characterized by complement pathway activation and increased macrophage recruitment to plaqueAryl-hydrocarbon receptor in SMC protects against oxidative stress, and promotes a stable plaque phenotype.

Global, Regional, and National Burden of Intracerebral Hemorrhage in Young Adults From 1990 to 2021: A Population-Based Study.

Intracerebral hemorrhage (ICH) in young adults demands greater attention, given its poor prognosis; however, there has been a paucity of epidemiological data. The objective of this study is to estimate the temporal trends and distribution characteristics of the disease burden in 204 countries or territories between 1990 and 2021. The data, including incidence, mortality, prevalence, and disability-adjusted life year (DALY) rates were sourced from the Global Burden of Diseases Study 2021. From 1990 to 2021, there was a significant decline in the global incidence (estimated annual percentage change=-1.05), mortality (estimated annual percentage change=-0.92), and DALY (estimated annual percentage change=-1.00) rates of ICH in young adults. In 2021, the highest incidence, mortality, and DALY rates were observed in Southeast Asia, East Asia, and Oceania. Globally, high systolic blood pressure, smoking, and ambient particulate matter pollution were identified as the primary contributors to the largest proportion of DALYs associated with ICH in young adults. The health inequality of ICH in young adults has been reduced over the past 3 decades. There is a considerable degree of heterogeneity in the global burden of ICH in young adults. A decline in the incidence, mortality, prevalence, and DALY rates has been observed from 1990 to 2021, however, the number of absolute cases has increased. These results will enable health care professionals, policymakers, and researchers to refine the implementation of cost-effective policies, the allocation of health care resources, and the management of patients to further mitigate the burden of ICH in young adults.

Wildfire Seasons, Prenatal PM2.5 Exposure, and Respiratory Infections by Age 1 Year: A Population-Based Case-Control Analysis of Critical Developmental Windows.

The 2017 and 2018 wildfire seasons in British Columbia (BC), Canada were unprecedented. Among all the pollutants in wildfire smoke, fine particulate matter (PM2.5) poses the most significant risk to human health. There is limited research on prenatal wildfire smoke exposure and its impacts on infant health. We used a population-based nested case-control design to assess the association between daily PM2.5 exposures during specific developmental windows and the occurrence of otitis media or lower respiratory infections by age 1 year, including infections associated with dispensations of the antibiotic amoxicillin. We observed the strongest association between per 10 μg/m3 increase in PM2.5 exposure and otitis media during the fourth window of eustachian tube development (weeks 19-28) with an OR [95% confidence interval] of 1.31 [1.22, 1.41]. Similarly, the canalicular stage of lower respiratory tract development (weeks 18-27) was associated with the highest odds of lower respiratory infections, with an OR of 1.21 [1.15, 1.28]. Measures to reduce wildfire smoke exposure during pregnancy are warranted.

Epigenetics and Asthma: A Systematic Review.

Asthma is a chronic respiratory condition characterized by the narrowing of the airways, causing difficulty in breathing. Its heritability has long been an area of research, and the study of genetics alone has not been sufficient in the explanation of both its heritability and susceptibility. The study of epigenetics, which is defined as "the study of heritable changes in gene expression that do not involve changes to the underlying DNA sequence," can be used to explain the heritability and susceptibility of asthma. These epigenetic alterations to our DNA are influenced by environmental factors which are already known as risk factors for asthma; these include factors such as diet, smoking, and air pollution. The epigenetic mechanisms work by altering gene transcription and therefore determine whether specific genes are expressed, such mechanisms include DNA methylation and histone acetylation.