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Respirable fine particulate matter (PM 2.5 ) has been one of the most widely publicized indicators of pollution in recent years. Epidemiological studies have established a strong association between PM 2.5 , lung disease, and cardiovascular disease. Recent studies have shown that PM 2.5 is also strongly associated with brain damage, mainly cerebrovascular damage (stroke) and neurological damage to the brain (changes in cognitive function, dementia, psychiatric disorders, etc.). PM 2.5 can pass through the lung–gas–blood barrier and the “gut–microbial–brain” axis to cause systemic oxidative stress and inflammation, or directly enter brain tissue via the olfactory nerve, eventually damaging the cerebral blood vessels and brain nerves. It is worth mentioning that there is a time window for PM 2.5 -induced brain damage to repair itself. However, the exact pathophysiological mechanisms of brain injury and brain repair are not yet fully understood. This article collects and discusses the mechanisms of PM 2.5 -induced brain injury and self-repair after injury, which may provide new ideas for the prevention and treatment of cerebrovascular and cerebral neurological diseases.

INTRODUCTION Growing evidence indicates that fine particulate matter (PM2.5) is a risk factor for Alzheimer's disease (AD), but the underlying mechanisms have been insufficiently investigated. We hypothesized differential DNA methylation (DNAm) in brain tissue as a potential mediator of this association. METHODS We assessed genome‐wide DNAm (Illumina EPIC BeadChips) in prefrontal cortex tissue and three AD‐related neuropathological markers (Braak stage, CERAD, ABC score) for 159 donors, and estimated donors’ residential traffic‐related PM2.5 exposure 1, 3, and 5 years prior to death. We used a combination of the Meet‐in‐the‐Middle approach, high‐dimensional mediation analysis, and causal mediation analysis to identify potential mediating CpGs. RESULTS PM2.5 was significantly associated with differential DNAm at cg25433380 and cg10495669. Twenty‐four CpG sites were identified as mediators of the association between PM2.5 exposure and neuropathology markers, several located in genes related to neuroinflammation. DISCUSSION Our findings suggest differential DNAm related to neuroinflammation mediates the association between traffic‐related PM2.5 and AD. Highlights First study to evaluate the potential mediation effect of DNA methylation for the association between PM2.5 exposure and neuropathological changes of Alzheimer's disease. Study was based on brain tissues rarely investigated in previous air pollution research. Cg10495669, assigned to RBCK1 gene playing a role in inflammation, was associated consistently with 1‐year, 3‐year, and 5‐year traffic‐related PM2.5 exposures prior to death. Meet‐in‐the‐middle approach and high‐dimensional mediation analysis were used simultaneously to increase the potential of identifying the differentially methylated CpGs. Differential DNAm related to neuroinflammation was found to mediate the association between traffic‐related PM2.5 and Alzheimer's disease.

Considerable financial resources are allocated for measuring ambient air pollution in the United States, yet the locations for these monitoring sites may not be optimized to capture the full extent of current pollution variability. Prior research on best sensor placement for monitoring fine particulate matter (PM2.5) pollution is scarce: most studies do not span areas larger than a medium-sized city or examine timescales longer than 1 week. Here we present a pilot study using multiresolution dynamic mode decomposition (mrDMD) to identify the optimal placement of PM2.5 sensors from 2000 to 2016 over the contiguous United States. This novel approach incorporates the variation of PM2.5 on timescales ranging from 1 d to over a decade to capture air pollution variability. We find that the mrDMD algorithm identifies more high-priority sensor locations in the western United States than those expected along the eastern coast, where a large number of Environmental Protection Agency (EPA) PM2.5 monitors currently reside. Specifically, 53% of mrDMD optimized sensor locations are west of the 100th meridian, compared to only 32% in the current EPA network. The mrDMD sensor locations can capture PM2.5 from wildfires and high pollution events, with particularly high skill in the west. These results suggest significant gaps in the current EPA monitoring network in the San Joaquin Valley in California, northern California, and in the Pacific Northwest (Idaho, and Eastern Washington and Oregon). Our framework diagnoses where to place air quality sensors so that they can best monitor smoke from wildfires. Our framework may also be applied to urban areas for equitable placement of PM2.5 monitors.

Air pollution is becoming a prominent social problem in fast-growing Asian economies. Taking the Bangkok Metropolitan Region (BMR) as a case, we conducted an observational study of fine particulate matter (PM2.5) and acid deposition, consisting of their continuous monitoring at two sites. To find the major contributing sources of PM2.5, the PM composition data were analyzed by a receptor modeling approach while the pollution load from BMR sources to the air was characterized by an emission inventory. Our data show generally alarming levels of PM2.5 in the region, of which transportation and biomass burning are two major sources. In this paper, we present a general overview of our observational findings, contrast the scientific information with the policy context of air quality management in BMR, and discuss policy implications. In BMR, where a set of conventional regulatory instruments on air quality management are already in place, a solution for the air pollution problem should lie in a combination of air quality regulation and other policies, such as energy and agricultural policies.

Air transportation has a deep impact on environmental degradation due to the higher fossil fuel consumption. On the other hand, this industry also embraces the highest innovation that may alter its environmental consequences. However, there is a dearth of empirical evidence that explores the impact of air transportation and eco-innovation on environmental quality. Therefore, this study is a pioneering attempt to examine the role of air-transportation and eco-innovation in reducing environmental degradation in G7 countries using annual data from 1990 to 2019. In doing so, we employed various advance econometric approaches to handle issues arises from panel data such as Pesaran ( 2007 ) and Bai and Carrion-I-Silvestre ( 2009 ) used to examine the presence of unit root, cross-sectional dependency checked through Pesaran ( 2015 ) test, and for parameters heterogeneity through Pesaran and Yamagata ( 2008 ). Moreover, the Westerlund and Edgerton ( 2008 ) test and Cross Sectional Augmented ARDL were employed to analyse the long run and short run association among variables. The overall results show that air transportation and eco-innovation play an important role in abating environmental deterioration. Air transportation is negatively correlated with carbon emission and PM 2.5 exposure (air quality) due to the improved technical structure of aircraft engines and the use of mixed ration or alternative aviation fuels. These results provide valuable suggestions for all stakeholders.

Ambient fine particulate matter (PM2.5) is one of the most concerning pollutants, characterized by its diverse chemical composition. Although various studies have revealed PM2.5 chemical components, there is limited knowledge on how to reduce PM2.5 concentrations through administrative policies focusing on source management. We compared PM2.5 compositional characteristics and performed source apportionment using the positive matrix factorization in four metropolitan cities (Seoul, Daejeon, Gwangju, and Ulsan) in South Korea from 2014 to 2018. The annual average of PM2.5 concentrations exceeded the annual national ambient air quality standard of 15 μg m−3 in all areas while secondary inorganic aerosols constituted the largest fraction of PM2.5. This implies that secondary formation from gaseous precursors in the atmosphere was the main factor contributing to ambient PM2.5. However, the concentrations of PM2.5 constituents varied significantly across cities, suggesting that PM2.5 is a heterogeneous pollutant considerably influenced by region-specific conditions. In line with the chemical composition, secondary nitrate, secondary sulfate, and mobile-related sources were found to be significant contributors of PM2.5. Additionally, the extent of contribution from each source varied across the study regions. We also evaluated the impacts of policy interventions by comparing the PM2.5 composition and source apportionment before and after the policies for improving air quality. Intensive programs focused on the vehicle sector in Seoul led to a considerable decrease in the concentrations of carbonaceous compounds and mobile-related sources. In addition, strengthened regulations on coal-fired power plants (CFPPs) since 2016 have influenced the contributions of coal combustion sources in two cities adjacent to the west coastal area, where approximately half of the CFPPs of the country are densely distributed. Overall, the study’s findings indicate that region-specific PM2.5 chemical constituents and source contributions should be considered for establishing PM2.5-related policies, considering the high heterogeneity of PM2.5.

Background Epidemiological studies have implicated exposure to PM₂.₅ in the development of pulmonary tuberculosis (PTB); however, the key constituents driving this effect have not been clearly identified. Methods A time-series analysis spanning 2019 to 2023 was performed across several centers in Beijing to assess the links between major PM 2.5 constituents and PTB risk. The effects of five specific components—namely organic matter, black carbon, nitrate, sulfate, and ammonium—were evaluated to pinpoint the most influential factors. Results All five examined components demonstrated significant relationships with an elevated risk of PTB. Associations were not statistically significant on the same day (lag 0) or the next day (lag 1) after exposure. A clear risk increase was detected starting at a 2-day lag, which was no longer observable by lag 3. Per interquartile range (IQR) rise in the 3-day moving average (lag 0–2) of black carbon and organic matter, the relative risks (RRs) for PTB were 1.11 [95% confidence interval (CI): 1.03, 1.19] and 1.11 (95% CI: 1.03, 1.21), correspondingly. Together, these two components were the dominant drivers of the overall PM₂.₅ effect, contributing 41% and 39% of the joint risk, respectively. Conclusions The results yield novel evidence that exposure to certain PM 2.5 constituents is demonstrated to elevate PTB risk, wherein black carbon and organic matter are established as the principal factors.

Studies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.BACKGROUNDStudies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.A total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β HSD), 17β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).METHODSA total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β HSD), 17β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).Exposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.RESULTSExposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.Concentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.CONCLUSIONConcentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.

Background As one of the environmental risk factors for human health, atmospheric fine particulate matter (PM 2.5 ) contributes to cognitive deterioration in addition to respiratory and cardiovascular injuries. Recently, increasing evidence implicates that PM 2.5 inhalation can affect neurological functions in offspring, but the sex-specific outcomes and the underlying biological processes are largely unknown. Objectives To observe the influence of prenatal PM 2.5 exposure on cognitive performance in offspring, to elucidate the neuronal morphological alterations and possible transcriptional regulation based on mRNA-sequencing (mRNA-Seq) data after birth, and to determine the key components of PM 2.5 contributing to the adverse effects. Methods Pregnant C57BL/6J mice were exposed to sterile saline or PM 2.5 suspension. Morris water maze test was used to assess the cognitive function in weanling offspring. Microscopic observation was applied to detect neuronal morphogenesis in vivo and in vitro. The cortex tissues from male offspring were collected on postnatal days (PNDs) 1, 7, and 21 for mRNA-Seq analysis. The organic and inorganic components of PM 2.5 were separated to assess their contributions using primary cultured neurons. Results Prenatal PM 2.5 exposure impaired spatial learning and memory in weanling male mice, but not female mice. The sex-specific outcomes were associated with mRNA expression profiles of the cortex during postnatal critical windows, and the annotations in Gene Ontology (GO) of differentially expressed genes (DEGs) revealed that the exposure persistently disrupted the expression of genes involved in neuronal features in male offspring. Consistently, axonal growth impairment and dendritic complexity reduction were observed. Importantly, Homeobox A5 (Hoxa5), a critical transcription factor regulating all of the neuronal morphogenesis-associated hub genes on PNDs 1, 7, and 21, significantly decreased in the cortex of male offspring following PM 2.5 exposure. In addition, both inorganic and organic components were harmful to axonal and dendritic growth, with organic components exhibiting stronger inhibition than inorganic ones. Conclusion Prenatal PM 2.5 exposure affected spatial learning and memory in male mice by disrupting Hoxa5-mediated neuronal morphogenesis, and the organic components, including polycyclic aromatic hydrocarbons (PAHs), posed more adverse effects than the inorganic components.

Air pollution has been classified as a human carcinogen based largely on findings for respiratory cancers. Emerging, but limited, evidence suggests that it increases the risk of breast cancer, particularly among younger women. We characterized associations between residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and breast cancer. Analyses were performed using data collected in the Ontario Environmental Health Study (OEHS). The OEHS, a population-based case-control study, identified incident cases of breast cancer in Ontario, Canada among women aged 18–45 between 2013 and 2015. A total of 465 pathologically confirmed primary breast cancer cases were identified from the Ontario Cancer Registry, while 242 population-based controls were recruited using random-digit dialing. Self-reported questionnaires were used to collect risk factor data and residential histories. Land-use regression and remote-sensing estimates of NO2 and PM2.5, respectively, were assigned to the residential addresses at interview, five years earlier, and at menarche. Logistic regression was used to estimate odds ratios (OR) and their 95 % confidence intervals (CI) in relation to an interquartile range (IQR) increase in air pollution, adjusting for possible confounders. PM2.5 and NO2 were positively correlated with each other (r = 0.57). An IQR increase of PM2.5 (1.9 µg/m3) and NO2 (6.6 ppb) at interview residence were associated with higher odds of breast cancer and the adjusted ORs and 95 % CIs were 1.37 (95 % CI = 0.98–1.91) and 2.33 (95 % CI = 1.53–3.53), respectively. An increased odds of breast cancer was observed with an IQR increase in NO2 at residence five years earlier (OR = 2.16, 95 % CI: 1.41–3.31), while no association was observed with PM2.5 (OR = 0.96, 95 % CI 0.64–1.42). Our findings support the hypothesis that exposure to ambient air pollution, especially those from traffic sources (i.e., NO2), increases the risk of breast cancer in young women. [Display omitted] •Study provides new data on ambient air pollution and early-onset breast cancer.•Residential PM2.5 and NO2 increased the risk of premenopausal breast cancer.•Stronger associations with NO2 highlight the role of traffic-related air pollution.