Effects Of PM2 Research Articles

PM2.5 exposure aggravates kidney damage by facilitating the lipid metabolism disorder in diabetic mice.

Ambient fine particulate matter ≤ 2.5 µm (PM2.5) air pollution exposure has been identified as a global health threat, the epidemiological evidence suggests that PM2.5 increased the risk of chronic kidney disease (CKD) among the diabetes mellitus (DM) patients. Despite the growing body of research on PM2.5 exposure, there has been limited investigation into its impact on the kidneys and the underlying mechanisms. Past studies have demonstrated that PM2.5 exposure can lead to lipid metabolism disorder, which has been linked to the development and progression of diabetic kidney disease (DKD). In this study, db/db mice were exposed to different dosage PM2.5 for 8 weeks. The effect of PM2.5 exposure was analysis by assessment of renal function, pathological staining, immunohistochemical (IHC), quantitative real-time PCR (qPCR) and liquid chromatography with tandem mass spectrometry (LC-MS/MS) based metabolomic analyses. The increasing of Oil Red staining area and adipose differentiation related protein (ADRP) expression detected by IHC staining indicated more ectopic lipid accumulation in kidney after PM2.5 exposure, and the increasing of SREBP-1 and the declining of ATGL detected by IHC staining and qPCR indicated the disorder of lipid synthesisandlipolysis in DKD mice kidney after PM2.5 exposure. The expressions of high mobility group nucleosome binding protein 1 (HMGN1) and kidney injury molecule 1 (KIM-1) that are associated with kidney damage increased in kidney after PM2.5 exposure. Correlation analysis indicated that there was a relationship between HMGN1-KIM-1 and lipid metabolic markers. In addition, kidneys of mice were analyzed using LC-MS/MS based metabolomic analyses. PM2.5 exposure altered metabolic profiles in the mice kidney, including 50 metabolites. In conclusion the results of this study show that PM2.5 exposure lead to abnormal renal function and further promotes renal injury by disturbance of renal lipid metabolism and alter metabolic profiles.

Camera traps link population-level activity patterns with wildfire smoke events for mammals in Eastern Washington State

BackgroundDue to anthropogenic climate change and historic fire suppression, wildfire frequency and severity are increasing across the western United States. Whereas the indirect effects of fire on wildlife via habitat change are well studied, less is known about the impacts of wildfire smoke on animal health and behavior. In this study, we explore the effects of wildfire smoke on the behavior of eight medium- to large-bodied mammalian species in a heterogenous study area in Washington, USA. We linked population-level activity metrics derived from camera trap data to concentrations of fire-specific fine particulate matter (PM2.5). We hypothesized that mammalian activity would decline during smoke events, as animals attempt to reduce potential health impacts of smoke inhalation. We used occupancy models and Poisson regression models to test the effect of fire-specific PM2.5 levels on daily detection probability and the number of detections per day, respectively, for each study species.ResultsWhile we did not observe any significant responses to daily mean concentrations of PM2.5 in the occupancy models, we found three species with significant responses in their rates of detections per day in the Poisson regression. Specifically, for each standard deviation increase in the daily mean concentration of PM2.5, there was a 12.9% decrease in the number of bobcat detections per day, an 11.2% decrease in the number of moose detections per day, and a 5.8% increase in the number of mule deer detections per day. In general, the effects of PM2.5 were small compared to other relevant covariates.ConclusionsWe generally found little evidence to support our hypothesis that animals would reduce their activity in response to wildfire smoke. However, our study demonstrated that mammals exhibited species-specific behavioral responses to smoke, which are possibly adaptive responses to reduce health impacts from smoke inhalation. Though we found only a few immediate behavioral responses to smoke exposure, we note that longer-term health consequences of smoke exposure for wildlife are also likely and generally unknown. Our study shows how camera traps, which are already widely used to study wildlife, can also be used to investigate the impacts of wildfire smoke on animal behavior and provides a step towards developing methods to better understand this increasing source of environmental stress on wildlife.

Long-term exposure to ambient fine particulate components and leukocyte epigenome-wide DNA Methylation in older men: the Normative Aging Study

BackgroundEpigenome-wide association studies of ambient fine particulate matter (PM2.5) have been reported. However, few have examined PM2.5 components (PMCs) and sources or included repeated measures. The lack of high-resolution exposure measurements is the key limitation. We hypothesized that significant changes in DNA methylation might vary by PMCs and the sources.MethodsWe predicted the annual average of 14 PMCs using novel high-resolution exposure models across the contiguous U.S., between 2000–2018. The resolution was 50 m × 50 m in the Greater Boston Area. We also identified PM2.5 sources using positive matrix factorization. We repeatedly collected blood samples and measured leukocyte DNAm with the Illumina HumanMethylation450K BeadChip in the Normative Aging Study. We then used median regression with subject-specific intercepts to estimate the associations between long-term (one-year) exposure to PMCs / PM2.5 sources and DNA methylation at individual cytosine-phosphate-guanine CpG sites. Significant probes were identified by the number of independent degrees of freedom approach, using the number of principal components explaining > 95% of the variation of the DNA methylation data. We also performed regional and pathway analyses to identify significant regions and pathways.ResultsWe included 669 men with 1,178 visits between 2000–2013. The subjects had a mean age of 75 years. The identified probes, regions, and pathways varied by PMCs and their sources. For example, iron was associated with 6 probes and 6 regions, whereas nitrate was associated with 15 probes and 3 regions. The identified pathways from biomass burning, coal burning, and heavy fuel oil combustion sources were associated with cancer, inflammation, and cardiovascular diseases, whereas there were no pathways associated with all traffic.ConclusionsOur findings showed that the effects of PM2.5 on DNAm varied by its PMCs and sources.

Association of ambient PM10 and PM2.5 with coronary stenosis measured using selective coronary angiography

BackgroundLong-term ambient particulate matter (PM) exposure exerts detrimental effects on cardiovascular health. Evidence on the relation of chronically exposed ambient PM10 and PM2.5 with coronary stenosis remains lacking. Our aim was to investigate the association of PM10 and PM2.5 with coronary stenosis in patients undergoing coronary angiography. MethodsWe performed a retrospective cohort study consisting of 7513 individuals who underwent coronary angiography in Fujian Province, China, from January 2019 to December 2021. We calculated a modified Gensini score (GS) to represent the degree of stenosis in coronary arteries by selective coronary angiography. We fitted linear regressions and logistic models to assess the association of PM10 and PM2.5 with coronary stenosis. We employed restricted cubic splines to describe the exposure-response curves. We performed mediation analyses to assess the potential mediators. ResultsLong-term ambient PM10 and PM2.5 (prior three years average) exposure was significantly associated with the GS, with a breakpoint concentration of 47.5 μg/m3 and 25.8 μg/m3 for PM10 and PM2.5, respectively, above which we found a linear positive exposure-response relationship of ambient PM with GS. Each 10 µg /m3 increase in PM10 exposure (β: 4.81, 95 % CI: 0.44–9.19) and PM2.5 exposure [β: 10.50, 95 % CI: 3.14–17.86] were positively related to the GS. The adjusted odds ratio (OR) for each 10 µg/m3 increment in PM10 exposure on severe coronary stenosis was 1.33 (95 % CI: 1.04–1.76). Correspondingly, the adjusted OR for PM2.5 was 1.87 (95 % CI: 1.24–2.99). The mediation analysis indicated that the effect of PM10 on coronary stenosis may be partially mediated through total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, serum creatinine and blood urea nitrogen, and the effect of PM2.5 may be mediated in part by hemoglobin A1c. ConclusionOur study provides the first evidence that chronic ambient PM10 and PM2.5 exposure was associated with coronary stenosis assessed by GS in patients with suspected coronary artery disease and reveals its potential mediators.

Comprehensive and Understanding of PM2.5 among Thai High School Students

The majority of Thai people prefer to spend their time participating in outdoor activities. However, Thailand is considered a polluted country, and Bangkok is ranked as the most polluted city in the country. Younger generations faced an issue of lacking awareness about PM2.5. As a consequence of encountering particulate fine particles, individuals may be at high risk of developing respiratory and cardiovascular diseases. In addition, none of the researchers have ever conducted a survey researching the comprehensiveness and understanding of high school students in Thailand about PM2.5. Hence, this research aims to analyze and determine understanding among Thai high school students in Thailand. The research was conducted through an online survey consisting of 21-multiple choice questions. With 133 individuals participating in the survey, the mean score was rounded up to 13.65, illustrating the comprehension level of high school students to be on an average scale. From analyzing the correlation between the two variables, the F value was 0.27. According to mean value, the most prominent fundamental reasons for having average knowledge on fine particles may be a consequence of not including the topic into school’s syllabus and low promotion in the media, such as newspapers and social media. Thus, this research aims to raise awareness, concern, and comprehension among high school students about the effects of PM2.5.

Association between early preterm birth and maternal exposure to fine particular matter (PM10): A nation-wide population-based cohort study using machine learning.

Although preterm birth (PTB), a birth before 34 weeks of gestation accounts for only less than 3% of total births, it is a critical cause of various perinatal morbidity and mortality. Several studies have been conducted on the association between maternal exposure to PM and PTB, but the results were inconsistent. Moreover, no study has analyzed the risk of PM on PTB among women with cardiovascular diseases, even though those were thought to be highly susceptible to PM considering the cardiovascular effect of PM. Therefore, we aimed to evaluate the effect of PM10 on early PTB according to the period of exposure, using machine learning with data from Korea National Health Insurance Service (KNHI) claims. Furthermore, we conducted subgroup analysis to compare the risk of PM on early PTB among pregnant women with cardiovascular diseases and those without. A total of 149,643 primiparous singleton women aged 25 to 40 years who delivered babies in 2017 were included. Random forest feature importance and SHAP (Shapley additive explanations) value were used to identify the effect of PM10 on early PTB in comparison with other well-known contributing factors of PTB. AUC and accuracy of PTB prediction model using random forest were 0.9988 and 0.9984, respectively. Maternal exposure to PM10 was one of the major predictors of early PTB. PM10 concentration of 5 to 7 months before delivery, the first and early second trimester of pregnancy, ranked high in feature importance. SHAP value showed that higher PM10 concentrations before 5 to 7 months before delivery were associated with an increased risk of early PTB. The probability of early PTB was increased by 7.73%, 10.58%, or 11.11% if a variable PM10 concentration of 5, 6, or 7 months before delivery was included to the prediction model. Furthermore, women with cardiovascular diseases were more susceptible to PM10 concentration in terms of risk for early PTB than those without cardiovascular diseases. Maternal exposure to PM10 has a strong association with early PTB. In addition, in the context of PTB, pregnant women with cardiovascular diseases are a high-risk group of PM10 and the first and early second trimester is a high-risk period of PM10.

Effect of PM2.5 air pollution on the global burden of lower respiratory infections, 1990–2019: A systematic analysis from the Global Burden of Disease Study 2019

Particulate matter (PM) air pollution is closely related to lower respiratory infections (LRIs). However, the global LRI burden attributable to PM remains unclear. Here, we provide a comprehensive assessment of the PM2.5-attributable LRI burden using data from the Global Burden and Disease Study (GBD) 2019. We found that PM2.5 air pollution contributed to approximately 0.7 million deaths and 37.6 million disability-adjusted life years (DALYs) of LRIs in 2019. The LRI burden attributable to PM2.5 has decreased from 1990 to 2019, with a more pronounced decrease in household PM2.5 than in ambient PM2.5. Unlike the decreasing trend in LRI burden due to household PM2.5 worldwide, nearly one fifth of countries experienced an increase of LRI burden due to ambient PM2.5. The burden was unevenly distributed to less developed countries, mainly in Sub-Saharan Africa. All age groups experienced a decrease in the PM2.5-attributable burden, with the most significant decrease in children younger than 10 years. Notably, individuals aged 20–84 years experienced an increase in the LRI burden attributable to ambient PM2.5. Males had higher burden than females in the elder age and higher SDI regions. This study provided an evidence-based guidance for the prevention of LRIs and control of PM2.5 air pollution.

The relationship between PM2.5 and the onset and exacerbation of childhood asthma: a short communication.

Much is known about the link between air pollution and asthma in adults, particularly fine particulate matter (PM2.5). Studies have found that certain levels of fine PM2.5 can increase airway responsiveness and worsen asthma. PM2.5 may play a role in the onset and exacerbation of childhood asthma. However, there is little in the literature on how PM2.5 affects asthma attacks and exacerbations in children. Asthma is a common chronic disease in children, and air pollution can aggravate it. The effect of PM2.5 on childhood asthma needs further research. By evaluating, reviewing, and collating existing results in this area, this paper aims to explore the relationship between PM2.5 and asthma onset and exacerbation in children.

The mediating role of exhaled breath condensate metabolites in the effect of particulate matter on pulmonary function in schoolchildren: A crossover intervention study

The role played by metabolites in exhaled breath condensate (EBC) in the effect of PM on schoolchildren's pulmonary function has received little attention. Accordingly, we examined whether metabolites in EBC mediated the effect of PM10, PM2.5, and PM1 on the pulmonary function of schoolchildren at a residential primary school who had received an air-cleaner cross-over intervention. Samples of EBC were collected from a total of 60 schoolchildren and subjected to metabolomics analysis. We found that the effect of PM on six pulmonary function indicators was mediated by the following nine lipid peroxidation-related and energy metabolism-related metabolites present in EBC: 4-hydroxynonenal, arachidoyl ethanolamide, dl-pyroglutamic acid, 5-deoxy-d-glucose, myristic acid, lauric acid, linoleic acid, l-proline, and palmitic acid. However, while all nine of these metabolites mediated the effects of PM on boys' pulmonary function, only 4-hydroxynonenal, arachidoyl ethanolamide, and dl-pyroglutamic acid mediated the effects of PM on girls' pulmonary function. Overall, our results show that (1) short-term exposure to PM affected the schoolchildren's pulmonary function by causing an imbalance between lipid peroxidation and glutathione-based antioxidant activity and by perturbing energy metabolism in respiratory system and (2) there was a sex-dependent antioxidant response to PM exposure, with boys being less resistant than girls.

Body composition modify the association between ambient particulate matter and lung function among asthma patients.

The effect of ambient PM10 and PM2.5 on lung function modified by body muscle and adipose tissue is not fully understood at present. Our aims were to investigate the association between seasonal average air pollutants and lung function in asthmatic patients modified by body composition indicators. In this cross-sectional study, we recruited 914 doctor-diagnosed asthmatic patients, and performed interaction and stratified analysis using the median values of total body muscle (TBM), total body fat (TBF), and percentage body fat (PBF) as well as body mass index (BMI) =25 as the cutoff points of the high/low body composition groups. The adjusted R2 values of the developed LUR models of PM2.5 and PM10 were 91.4% and 90.5% and also verified by cross-validation, respectively. After adjusting for confounding factors, we found that TBM significantly modified the association between PM10 and lung function among asthma patients (interaction P value <0.05). In the low TBM group, seasonal average concentrations of PM10 estimated by the LUR model increased by 10 μg/m3, and negative associations with lung function indicators were observed. For obese patients with BMI>25 and high TBF, the increase in PM10 was associated with the decrease in lung function. The asthma patients with obesity and low total body muscle were more susceptible to adverse effects of PM10 on lung function.

In vitro toxicity and lung cancer risk: Atmospheric particulate matter from a city in southeastern Brazil impacted by biomass burning

The effects of PM10 on human health were investigated using samples collected in São Carlos city (São Paulo state), by the determination of the concentrations of PAHs and derivatives, together with evaluations of cytotoxicity and the formation of ROS in in vitro tests. In 2016, the mean concentrations of PM10, ΣPAHs, Σoxy-PAHs, Σnitro-PAHs, Σsaccharides, and Σions were 21.12 ± 9.90 μg m−3, 1.47 ± 1.70 ng m−3, 0.37 ± 0.31 ng m−3, 0.84 ng m−3, 119.91 ± 62.14 ng m−3, and 5.66 ± 4.52 μg m−3, respectively. The PM10 concentrations did not exceed the limit thresholds set by national legislation, however, the annual lung cancer risk calculated was 2.59 ± 1.22 cases per 100,000 people, in the dry season, which accounts for the annual risk (April to September). Moreover, the carcinogenic activities of the PAHs mixture were more than 1000-fold higher in the dry season (dry season: BaPeq = 0.30 ng m−3; wet season BaPeq = 0.02 ng m−3). The concentrations of most analytes were also higher during the dry season, as had already been demonstrated in the same city. This was due to reductions in precipitation, relative humidity and air temperature, and increased biomass burning, which was the main source of PM10 in the city in 2016 (contribution rate of more than 50%). Toxicological results also showed the negative impacts of PM10, exposure to PM10 extracts for 72 h reduced the viability of A549 and MRC5 cells, and the formation of ROS was observed. The cellular responses obtained using combined and individual extracts of PM10 differed and were sometimes associated with specific compounds. These demonstrate the importance of monitoring PM toxicity using different approaches and the main anthropogenic sources’ contribution. Therefore, to improve air quality and human health, existing legislation needs to be modified to incorporate these tests.

The association between ambient pollutants and influenza transmissibility: A nationwide study involving 30 provinces in China.

The impact of exposure to ambient pollutants on influenza transmissibility is poorly understood. We aim to examine the associations of six ambient pollutants with influenza transmissibility in China and assess the effect of the depletion of susceptibles. Provincial-level surveillance data on weekly influenza-like illness (ILI) incidence and viral activity were utilized to estimate the instantaneous reproduction number (Rt) using spline functions. Log-linear regression and the distributed lag non-linear model (DLNM) were employed to investigate the effects of ambient pollutants-ozone (O3), particulate matter ≤2.5μm (PM2.5), particulate matter ≤10μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO)-on influenza transmissibility across 30 Chinese provinces from 2014 to 2019. Additionally, the potential effects of the depletion of susceptibles and regional characteristics were explored. There is a significantly positive correlation between influenza transmissibility and five distinct ambient pollutants: PM2.5, PM10, SO2, CO, and NO2. On average, these ambient pollutants explained percentages of the variance in Rt: 0.8%, 0.8%, 1.9%, 1.3%, and 1.4%, respectively. Conversely, O3 was found to be negatively associated with Rt, explaining 1.5% of the variance in Rt. When controlling for the effect of susceptibles depletion, the effects of all pollutants were more pronounced. The effects of PM2.5, PM10, CO, and SO2 were higher in the eastern and southern regions. Most ambient pollutants may potentially contribute to the facilitation of human-to-human influenza virus transmission in China. This observed association was maintained even after adjusting for variation in the susceptible population.

Long-term effects of particulate matter on incident cardiovascular diseases in middle-aged and elder adults: The CHARLS cohort study

BackgroundAlthough there is evidence of long-term effects of particulate matter (PM) on cardiovascular diseases (CVD), researches about long-term effects of PM1 on CVD are limited. We aimed to examine the long-term effects and magnitude of PM, especially PM1, on incident CVD in China. MethodsWe included 6016 participants aged ≥ 45 years without CVD at baseline in 2011 from the China Health and Retirement Longitudinal Study. Personal PM (PM1, PM2.5, and PM10) concentrations were estimated using geocoded residential address. Generalized linear mixed models and SHapley Additive exPlanation were utilized to calculate the impacts and contributions of PM on CVD. Sensitivity analyses were used to check the robustness. ResultsAfter a follow up of 4-year, 481 (7.99 %) participants developed CVD. Per 10 μg/m3 uptick in 1-year average concentrations of PM1, PM2.5 and PM10 was associated with a 1.20 [95 % confidence interval (CI): 1.05–1.37], 1.13 (95 % CI: 1.11–1.15), and 1.10 (95 % CI: 1.06–1.13) fold risk of incident CVD, respectively. The 2-year average concentrations of PM1, PM2.5 and PM10 were associated with incident CVD, corresponding to a 1.03 (95 % CI: 0.96–1.10), 1.11 (95 % CI: 1.02–1.21), and 1.09 (95 % CI: 1.03–1.15) fold risk, respectively. The SHapley Additive exPlanation values of PM1, PM2.5, and PM10 were 0.170, 0.153, and 0.053, respectively, corresponding to the first, second, and fifth among all air pollutants. Effects of PM1, PM2.5 and PM10 on CVD remained statistically significant in two-pollutant models. The elderly, males, smokers and alcohol drinkers tended to have slightly higher effects, while the differences were not statistically significant (all P-values > 0.05) between subgroups. ConclusionLong-term exposure to PM1, PM2.5, and PM10 was associated with an increased incidence of CVD. The smaller the particle size, the more important it was for incident CVD indicating that emphasis should be placed on small size of PM.

Particulate matter 10 exposure affects intestinal functionality in both inflamed 2D intestinal epithelial cell and 3D intestinal organoid models.

A growing body of evidence suggests that particulate matter (PM10) enters the gastrointestinal (GI) tract directly, causing the GI epithelial cells to function less efficiently, leading to inflammation and an imbalance in the gut microbiome. PM10 may, however, act as an exacerbation factor in patients with inflamed intestinal epithelium, which is associated with inflammatory bowel disease. The purpose of this study was to dissect the pathology mechanism of PM10 exposure in inflamed intestines. In this study, we established chronically inflamed intestinal epithelium models utilizing two-dimensional (2D) human intestinal epithelial cells (hIECs) and 3D human intestinal organoids (hIOs), which mimic in vivo cellular diversity and function, in order to examine the deleterious effects of PM10 in human intestine-like in vitro models. Inflamed 2D hIECs and 3D hIOs exhibited pathological features, such as inflammation, decreased intestinal markers, and defective epithelial barrier function. In addition, we found that PM10 exposure induced a more severe disturbance of peptide uptake in inflamed 2D hIECs and 3D hIOs than in control cells. This was due to the fact that it interferes with calcium signaling, protein digestion, and absorption pathways. The findings demonstrate that PM10-induced epithelial alterations contribute to the exacerbation of inflammatory disorders caused by the intestine. According to our findings, 2D hIEC and 3D hIO models could be powerful in vitro platforms for the evaluation of the causal relationship between PM exposure and abnormal human intestinal functions.

Association between short-term exposure to PM2.5 and nasal microbiota dysbiosis, inflammation and oxidative stress: A panel study of healthy young adults

Fine particulate matter (PM2.5) is the primary environmental stressor and a significant threat to public health. However, the effect of PM2.5 exposure on human nasal microbiota and its pathophysiological implication remain less understood. This study aimed to explore the associations of PM2.5 exposure with indices of nasal microbiota and biomarkers of nasal inflammation and oxidative stress. We conducted a panel study with 75 students in Xinxiang, Henan Province, China, from September to December 2017. Biomarkers of nasal inflammation and oxidative stress including interleukin-6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α), 8-epi-prostaglandin F2 alpha (8-epi-PGF2α) and indices of nasal microbiota diversity and phenotypes were measured. Linear mixed-effect models and bioinformatic analyses were performed to assess the association of PM2.5 concentrations with the abovementioned biomarkers and indices. It was found that per 1 μg/m3 increase in PM2.5 was associated with increments of 13.15% (95 % CI: 5.53–20.76 %) and 78.98 % (95 % CI: 21.61–136.36 %) in TNF-α on lag2 and lag02. Indices of microbial diversity and phenotypes including equitability, Shannon index, biofilm forming, and oxidative stress tolerant decreased to different extent with the increment in PM2.5. Notably, thirteen differential microbes in Clostridia, Bacilli, and Gammaproteobacteria classes were recognized as keystone taxa and eight of them were associated with TNF-α, IL-6, or 8-epi-PGF2α. Moreover, environmental adaptation was the most critical functional pathway of nasal microbiota associated with PM2.5 exposure. In summary, short-term exposure to PM2.5 is associated with nasal inflammation, microbiota diversity reduction, and the microbiota phenotype alterations.

Urban environmental pollution in external and internal environments by PM2.5 particulate matter and the sick building syndrome: an overview

Abstract&#x0D; A healthy environment must have air free of pollution, but this issue has always existed and now affects the entire population. The PM2.5 particulate matter, which primarily originates from the car fleet, is one of the pollutants that has the biggest impact. With the energy crisis in the 1970s and the ensuing construction of closed buildings (without natural ventilation), primarily in developed countries, indoor air quality emerged as a science. It then gained importance when it was found that the declining ventilation levels in those nations were largely to blame for the rising concentrations of pollutants in indoor air. The occupants of buildings themselves make a considerable contribution to the pollution of these settings through their activities, and it is well acknowledged that poor ventilation is one of the most critical factors affecting indoor air quality. Sick building syndrome and poor indoor air quality are both connected to ailments like colds, allergies, and coughing. The application of special legislation must be integrated with research and education of building occupants to effectively provide a healthy environment. The goal of this review is to analyze various findings from investigations on the effects of PM2.5 particulate matter pollution on the internal and exterior urban environment, as well as the effects of these concentrations on human health. By comparing the findings with other studies, it is possible to compare the findings and identify some common behaviors of fine particles, determining the concentration differences in the environments and showing how different sources and conditions can produce different variations in concentrations.&#x0D;

Potential mechanisms mediating PM2.5-induced alterations of H3N2 influenza virus infection and cytokine production in human bronchial epithelial cells

Exposure to particulate matter (PM) has been associated with increased hospital admissions for influenza. Airway epithelial cells are a primary target for inhaled environmental insults including fine PM (PM2.5) and influenza viruses. The potentiation of PM2.5 exposure on the effects of influenza virus on airway epithelial cells has not been adequately elucidated. In this study, the effects of PM2.5 exposure on influenza virus (H3N2) infection and downstream modulation of inflammation and antiviral immune response were investigated using a human bronchial epithelial cell line, BEAS-2B. The results showed that PM2.5 exposure alone increased the production of pro-inflammatory cytokines including interleukin-6 (IL-6) and IL-8 but decreased the production of the antiviral cytokine interferon-β (IFN-β) in BEAS-2B cells while H3N2 exposure alone increased the production of IL-6, IL-8, and IFN-β. Importantly, prior exposure to PM2.5 enhanced subsequent H3N2 infectivity, expression of viral hemagglutinin protein, as well as upregulation of IL-6 and IL-8, but reduced H3N2-induced IFN-β production. Pre-treatment with a pharmacological inhibitor of nuclear factor-κB (NF-κB) suppressed pro-inflammatory cytokine production induced by PM2.5, H3N2, as well as PM2.5-primed H3N2 infection. Moreover, antibody-mediated neutralization of Toll-like receptor 4 (TLR4) blocked cytokine production triggered by PM2.5 or PM2.5-primed H3N2 infection, but not H3N2 alone. Taken together, exposure to PM2.5 alters H3N2-induced cytokine production and markers of replication in BEAS-2B cells, which in turn are regulated by NF-κB and TLR4.

Toxicological Effects of Fine Particulate Matter (PM2.5): Health Risks and Associated Systemic Injuries-Systematic Review.

Previous studies focused on investigating particulate matter with aerodynamic diameter ≤ 2.5µm (PM2.5) have shown therisk of disease development, and association with increased morbidity and mortality rates. The current review investigate epidemiological and experimental findings from 2016 to 2021, which enabled the systemic overview of PM2.5's toxic impacts on human health. The Web of Science database searchused descriptive terms to investigate theinteraction among PM2.5 exposure, systemic effects, and COVID-19 disease. Analyzed studies have indicated that cardiovascular and respiratory systems have been extensively investigated and indicated as the main air pollution targets. Nevertheless, PM2.5 reaches other organic systems and harms the renal, neurological, gastrointestinal, and reproductive systems. Pathologies onset and/or get worse due to toxicological effects associated with the exposure to this particle type, since it can trigger several reactions, such as inflammatory responses, oxidative stress generation and genotoxicity. These cellular dysfunctions lead to organ malfunctions, as shown in the current review. In addition, thecorrelation between COVID-19/Sars-CoV-2 and PM2.5 exposure was also assessed to help better understand the role ofatmospheric pollution in the pathophysiology of this disease. Despite the significant number of studies about PM2.5'seffects on organic functions, available in the literature, there are still gaps in knowledge about how this particulate matter can hinder human health. The current review aimed to approach the main findings about the effect of PM2.5 exposure on different systems, and demonstrate the likely interaction of COVID-19/Sars-CoV-2 and PM2.5.

The association between chemical constituents of ambient fine particulate matter and obesity in adults: A large population-based cohort study

ObjectivesCurrent evidence demonstrated that ambient fine particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5) and its constituents may be obesogenic in children, but evidence from adults is lacking. Our aim was to characterize the association between PM2.5 and its constituents and obesity in adults. MethodsWe included 68,914 participants from the China Multi-Ethnic Cohort (CMEC) baseline survey. Three-year average concentrations of PM2.5 and its constituents were evaluated by linking pollutant estimates to the geocoded residential addresses. Obesity was defined as body mass index (BMI) ≥ 28 kg/m2. Logistic regression was used to examine the relationship between PM2.5 and its constituents and obesity. We performed weighed quantile sum (WQS) regression to get the overall effect of PM2.5 and its constituents and the relative contribution of each constituent. ResultsPer-SD increase in PM2.5 (odds ratio [OR] = 1.43, 95% confidence interval [CI]: 1.37–1.49), black carbon (BC) (1.42, 1.36–1.48), ammonium (1.43, 1.37–1.49), nitrate (1.44, 1.38–1.50), organic matter (OM) (1.45, 1.39–1.51), sulfate (1.42, 1.35–1.48), and soil particles (SOIL) (1.31, 1.27–1.36) were positively associated with obesity, and SS (0.60, 0.55–0.65) was negatively associated with obesity. The overall effect (OR = 1.34, 95% CI: 1.29–1.41) of the PM2.5 and its constituents was positively associated with obesity, and ammonium made the most contribution to this relationship. Participants who were older, female, never smoked, lived in urban areas, had lower income or higher levels of physical activity were more significantly adversely affected by PM2.5, BC, ammonium, nitrate, OM, sulfate and SOIL compared to other individuals. ConclusionOur study revealed that PM2.5 constituents except SS were positively associated with obesity, and ammonium played the most important role. These findings provided new evidence for public health interventions, especially the precise prevention and control of obesity.

Association of multiple air pollutants with oxygen saturation during sleep in COPD patients: Effect modification by smoking status and airway inflammatory phenotypes

Air pollution contributes substantially to the development of chronic obstructive pulmonary disease (COPD). To date, the effect of air pollution on oxygen saturation (SpO2) during sleep and potential susceptibility factors remain unknown. In this longitudinal panel study, real-time SpO2 was monitored in 132 COPD patients, with 270 nights (1615 h) of sleep SpO2 recorded. Exhaled nitric oxide (NO), hydrogen sulfide (H2S) and carbon monoxide (CO) were measured to assess airway inflammatory characteristics. Exposure levels of air pollutants were estimated by infiltration factor method. Generalized estimating equation was used to investigate the effect of air pollutants on sleep SpO2. Ozone, even at low levels (<60 μg/m3), was significantly associated with decreased SpO2 and extended time of oxygen desaturation (SpO2 < 90%), especially in the warm season. The associations of other pollutants with SpO2 were weak, but significant adverse effects of PM10 and SO2 were observed in the cold season. Notably, stronger effects of ozone were observed in current smokers. Consistently, smoking-related airway inflammation, characterized by higher levels of exhaled CO and H2S but lower NO, significantly augmented the effect of ozone on SpO2 during sleep. This study highlights the importance of ozone control in protecting sleep health in COPD patients.