Research on characteristics and influencing factors of road dust emission in a southern city in China.

One of the primary causes of urban atmospheric particulate matter, which is harmful to human health in addition to affecting air quality and atmospheric visibility, is road dust. This study used online monitoring equipment to examine the characteristics of road dust emissions, the effects of temperature, humidity, and wind speed on road dust, as well as the correlation between road and high-space particulate matter concentrations. A section of a real road in Jinhua City, South China, was chosen for the study. The findings demonstrate that the concentration of road dust particles has a very clear bimodal single-valley distribution throughout the day, peaking between 8:00 and 11:00 and 19:00 and 21:00 and troughing between 14:00 and 16:00. Throughout the year, there is a noticeable seasonal change in the concentration of road dust particles, with the highest concentration in the winter and the lowest in the summer. Simultaneously, it has been discovered that temperature and wind speed have the most effects on particle concentration. The concentration of road dust particles reduces with increasing temperature and wind speed. The particle concentrations of road particles and those from urban environmental monitoring stations have a strong correlation, although the trend in the former is not entirely consistent, and the changes in the former occur approximately 1 h after the changes in the latter.

Fine Particulate Matter and Osteoporosis: Evidence, Mechanisms, and Emerging Perspectives.

Air pollution, particularly fine particulate matter with an aerodynamic diameter of ≤ 2.5 µm (PM2.5), has been recognized for its adverse effects on multiple organs beyond the lungs. Among these, the bone began to garner significant attention. This review covers epidemiological, animal and cell studies on PM2.5 exposure and bone health as well as studies on PM2.5-induced diseases with skeletal complications. Emerging evidence from epidemiological studies indicates a positive association between PM2.5 exposure and the incidence of osteoporosis and fractures, along with a negative association with bone mineral density. Experimental studies have demonstrated that PM2.5 can disrupt the metabolic balance between osteoclasts and osteoblasts through inflammatory responses, oxidative stress, and endocrine disruption, thereby triggering bone loss and osteoporosis. Additionally, this review proposes a secondary mechanism by which PM2.5 may impair bone homeostasis via pathological alterations in other organs, offering new perspectives on the complex interactions between environmental pollutants and bone health. In conclusion, this contemporary review underscores the often-overlooked risk factors of PM2.5 in terms of its adverse effects on bone and elucidates the mechanisms of both primary and secondary toxicity. Further attention should be given to exploring the molecular mechanisms of PM2.5-induced bone impairment and developing effective intervention strategies. With global climate change, increasing ozone pollution, emerging pollutants, and multifactorial exposure to environmental factors, these issues are likely to become of greater concern in the near future.

Fine particulate matter potentiates Th17-cell pathogenicity in experimental autoimmune uveitis via ferroptosis.

The effect of fine particulate matter (PM2.5) on the development of uveitis remains unclear. Therefore, this study was designed to investigate the role of PM2.5 in experimental autoimmune uveitis (EAU) and its potential mechanism. Our results showed that PM2.5 could exacerbate the activity of EAU, as evidenced by severer clinical and pathological changes, correlated with elevated Th17 cells frequency and IL-17A expression. Proteomic analysis revealed ferroptosis was the most significant pathway. In vivo, the levels of Fe2+, ROS, lipid ROS, and malondialdehyde, as well as the expression of TFRC, HMOX1, FTH1, and FTL1 in CD4+ T cells were increased, while GSH/GSSG ratio and the expression of ACSL1 and GPX4 were decreased after PM2.5 exposure. In vitro, the expression of TFRC and HMOX1 were increased, while the expression FTH1, FTL1, ACSL1, and GPX4 were decreased after PM2.5 exposure. Ferrostatin-1 effectively alleviated PM2.5-induced intraocular inflammation and suppressed the frequency of Th17 cells. These results suggest that PM2.5 could aggravate intraocular inflammation and immune response in EAU mice through ferroptosis. Ferroptosis could be a potential marker for the prevention and treatment of uveitis.

Association between daily circulatory emergency ambulance dispatches and short-term PM2.5 exposure in a heavily polluted area.

Emergency ambulance dispatches (EAD) have been proven to be associated with ambient particulate matter with diameter < 2.5 µm (PM2.5) concentration, but the associations of circulatory EAD remained inconclusive, especially in heavily polluted areas. In this time series conducted in Shenyang City, Northeastern China, we explored the associations between circulatory EAD and ambient PM2.5 and its constituents. Data including 113,508 circulatory EAD records, five types of PM2.5 constituents, and meteorological information spanning from 2014 to 2019 were retrieved. Using generalized additive models (GAMs), we explored the association between circulatory EAD and calculated excess risks induced by a 10 µg/m3 increase (ERR10) in PM2.5 mass and its constituents. ERR by percentage change (ERRpc) to compare among the different constituents were also calculated. Positive associations between circulatory EAD and PM2.5 mass, sulfates, organic matters, and black carbon, were found particularly at lag0 and lag0-5, with the ERR10 of 3.8% (3.2%-4.4%), 6.5% (2.2%-10.8%), 4.2% (1.7%-6.6%), and 30.2% (17.2%-43.4%) at lag0-5, respectively. Similar associations were observed for cardiovascular EAD, while cerebrovascular EAD suggested a positive association with O3 rather than PM2.5 or its constituents. Notably, PM2.5 mass exhibited the largest ERRpc for circulatory and cardiovascular EAD, followed by sulfates and black carbon. Moreover, the risks were enhanced for circulatory and cardiovascular EAD in males compared to females and during warmer seasons compared to colder seasons. Our findings contribute new evidence on PM2.5 exposure and circulatory EAD in relatively polluted areas.

Geographic Variations in Urban-Rural Particulate Matter (PM2.5) Concentrations in the United States, 2010-2019.

Fine particulate matter 2.5 (PM2.5) is a widely studied pollutant with substantial health impacts, yet little is known about the urban-rural differences across the United States. Trends of PM2.5 in urban and rural census tracts between 2010 and 2019 were assessed alongside sociodemographic characteristics including race/ethnicity, poverty, and age. For 2010, we identified 13,474 rural tracts and 59,065 urban tracts. In 2019, 13,462 were rural and 59,055 urban. Urban tracts had significantly higher PM2.5 concentrations than rural tracts during this period. Levels of PM2.5 were lower in rural tracts compared to urban and fell more rapidly in rural than urban. Rural tract annual means for 2010 and 2019 were 8.51 [2.24] µg/m3 and 6.41 [1.29] µg/m3, respectively. Urban tract annual means for 2010 and 2019 were 9.56 [2.04] µg/m3 and 7.51 [1.40] µg/m3, respectively. Rural and urban majority Black communities had significantly higher PM2.5 pollution levels (10.19 [1.64] µg/m3 and 9.79 [1.10] µg/m3 respectively), in 2010. In 2019, they were: 7.75 [1.1] µg/m3 and 7.09 [0.78] µg/m3, respectively. Majority Hispanic communities had higher PM2.5 levels and were the highest urban concentration among all races/ethnicities (8.01 [1.73] µg/m3), however they were not the highest rural concentration among all races/ethnicities (6.22 [1.60] µg/m3) in 2019. Associations with higher levels of PM2.5 were found with communities in the poorest quartile and with higher proportions of residents age<15 years old. These findings suggest greater protections for those disproportionately exposed to PM2.5 are needed, such as, increasing the availability of low-cost air quality monitors.

Combined transcriptome and microbiome analysis reveals the thyrotoxic effects of PM2.5 in female rats.

Pervasive environmental pollutants, specifically particulate matter (PM2.5), possess the potential to disrupt homeostasis of female thyroid hormone (TH). However, the precise mechanism underlying this effect remains unclear. In this study, we established a model of PM2.5-induced thyroid damage in female rats through intratracheal instillation and employed histopathological and molecular biological methods to observe the toxic effects of PM2.5 on the thyroid gland. Transcriptome gene analysis and 16S rRNA sequencing were utilized to investigate the impact of PM2.5 exposure on the female rat thyroid gland. Furthermore, based on the PM2.5-induced toxic model in female rats, we evaluated its effects on intestinal microbiota, TH levels, and indicators of thyroid function. The findings revealed that PM2.5 exposure induced histopathological damage to thyroid tissue by disrupting thyroid hormone levels (total T3 [TT3], (P < 0.05); total T4 [TT4], (P < 0.05); and thyrotropin hormone [TSH], (P < 0.05)) and functional indices (urine iodine [UI], P > 0.05), thus further inducing histopathological injuries. Transcriptome analysis identified differentially expressed genes (DEGs), primarily concentrated in interleukin 17 (IL-17), forkhead box O (FOXO), and other signaling pathways. Furthermore, exposure to PM2.5 altered the composition and abundance of intestinal microbes. Transcriptome and microbiome analyses demonstrated a correlation between the DEGs within these pathways and the flora present in the intestines. Moreover, 16 S rRNA gene sequencing analysis or DEGs combined with thyroid function analysis revealed that exposure to PM2.5 significantly induced thyroid hormone imbalance. We further identified key DEGs involved in thyroid function-relevant pathways, which were validated using molecular biology methods for clinical applications. In conclusion, the homeostasis of the "gut-thyroid" axis may serve as the underlying mechanism for PM2.5-induced thyrotoxicity in female rats.

Associations between PM2.5, ambient heat exposure and congenital hydronephrosis in southeastern China.

Objectives: This research aims to analyze how exposure to fine particulate matter (PM2.5) and ambient heat during pregnancy increases the risk of congenital hydronephrosis (CH) in newborns. Methods: A case-control study was conducted to investigate the relationship between exposure to PM2.5 and ambient heat during pregnancy and the occurrence of CH in newborns. The study, which was conducted from 2015 to 2020, included 409 infants with CH as the case group and 409 infants without any abnormalities as the control group. Using spatial remote sensing technology, the exposure of each pregnant mother to PM2.5 concentration was meticulously mapped. Additionally, data on the ambient temperature of exposure for each participant were also collected. A logistics regression model was used to calculate the influence of exposure to PM2.5 and ambient heat on the occurrence of CH. Stratified analysis and interaction analysis were used to study the interaction between ambient heat exposure and PM2.5 on the occurrence of CH. Results: At the 6th week of gestation, exposure to PM2.5 may increase the risk of CH. For every 10 µg/m3 increase in PM2.5 exposure, the risk of CH increased by 2% (95%CI = 0.98, 1.05) at a p-value of >0.05, indicating that there was no significant relationship between the results. Exposure to intense heat at 6th and 7th weeks of gestation increased the risk of CH. Specifically, for every 1°C increase in heat exposure, the risk of CH in offspring increased by 21% (95%CI = 1.04, 1.41) during the 6th week and 13% during the 7th week (95%CI = 1.02, 1.24). At 5th and 6th weeks of gestation, the relative excess risk due to interaction (RERI) was greater than 0 at the 50th percentile (22.58°C), 75th percentile (27.25°C), and 90th percentile (29.13°C) of daily maximum temperature (Tmax) distribution, indicating that the risk of CH was higher when exposed to both ambient heat and PM2.5 at the same time compared to exposure to a single risk factor. Conclusion: Exposure to higher levels of PM2.5 and ambient heat during pregnancy increases the risk of CH in infants. There was a positive interaction between exposure to intense heat and high concentration of PM2.5 on the occurrence of CH.

Ambient PM2.5 Chemical Composition and Cardiovascular Disease Hospitalizations in China.

Little is known about the impacts of specific chemical components on cardiovascular hospitalizations. We examined the relationships of PM2.5 chemical composition and daily hospitalizations for cardiovascular disease in 184 Chinese cities. Acute PM2.5 chemical composition exposures were linked to higher cardiovascular disease hospitalizations on the same day and the percentage change of cardiovascular admission was the highest at 1.76% (95% CI, 1.36-2.16%) per interquartile range increase in BC, followed by 1.07% (0.72-1.43%) for SO42-, 1.04% (0.63-1.46%) for NH4+, 0.99% (0.55-1.43%) for NO3-, 0.83% (0.50-1.17%) for OM, and 0.80% (0.34%-1.26%) for Cl-. Similar findings were observed for all cause-specific major cardiovascular diseases, except for heart rhythm disturbances. Short-term exposures to PM2.5 chemical composition were related to higher admissions and showed diverse impacts on major cardiovascular diseases.

Long-term exposure to air pollution and the risks of venous thromboembolism: a nationwide population-based retrospective cohort study.

OBJECTIVES: To delineate the effects of exposure to air pollution on the risk of venous thromboembolism (VTE). BACKGROUND: The association between air pollution and arterial occlusive diseases has been well reported in the literature. VTE is the third most common acute cardiovascular syndrome; however, its relationship with exposure to air pollution has been controversial. METHODS: This study linked data from the Taiwan National Health Insurance Research Database with that from the Taiwan Environmental Protection Administration. Patients who were first admitted for VTE between January 1, 2001, and December 31, 2013, were analyzed. A time-stratified, case-crossover design was employed. Three different exposure periods were defined: exposure for 1 month, one quarter, and 1 year. Four control periods were designated for each exposure period. The association between exposure to air pollutants and the risk of VTE was tested using logistic regression analysis. Subgroup analyses were also performed, stratified by age, sex, type of VTE, the use of hormone therapy, and level of urbanization at the site of residence. RESULTS: Exposures to particulate matter (PM) smaller than 2.5 µm (PM2.5) and those smaller than 10 µm (PM10) were associated with higher risks of VTE, with longer exposures associated with higher risk. The concentration of PM2.5 exposure for 1 month was linearly associated with a greater risk of VTE up to 28.0 µg/m3, beyond which there was no association. PM2.5 exposure for one quarter or 1 year remained significantly associated with higher risks of VTE at higher concentrations. The increased risk in VTE associated with exposure to PM2.5 was more prominent in older patients and in patients not under hormone therapy. Similar results were observed for PM10 exposures. CONCLUSIONS: Exposure to PM, particularly PM2.5, leads to an increased risk of VTE, with possible accumulative effects. With increased PM production in industrializing countries, the effects of PM on VTE occurrence warrant further attention.

Ventilation heterogeneity is increased in adults exposed to coal mine fire-related PM2.5.

BACKGROUND AND OBJECTIVES: The Hazelwood Health Study was set up to study long-term health effects of a mine fire that blanketed residents of the Latrobe Valley with smoke for 45 days in 2014. The Respiratory Stream specifically assessed the impact of fine particulate matter <2.5 µm diameter (PM2.5) exposure from mine fire smoke on lung health. The multiple breath nitrogen washout (MBW) test assesses ventilation heterogeneity, which may detect sub-clinical airways dysfunction not identified using standard tests such as spirometry. This analysis assessed the association of PM2.5 exposure with measures of ventilation heterogeneity. METHODS: Exposed (Morwell) and unexposed (Sale) participants were recruited 3.5-4 years after the fire from those who had participated in an Adult Survey. MBW was performed to measure lung clearance index (LCI), functional residual capacity (FRC), acinar (Sacin) and conductive (Scond) ventilation heterogeneity. PM2.5 exposure was estimated with emission and chemical transport models. Multivariable linear regression models were fitted controlling for confounders. RESULTS: We recruited 519 participants. MBW tests were conducted on 504 participants with 479 acceptable test results (40% male; 313 exposed, 166 unexposed). Exposure to mine fire-related PM2.5 was associated with increasing Scond (ß = 1.57/kL, 95%CI: 0.20-2.95, p = 0.025), which was comparable to the estimated effect on Scond of 4.7 years of aging. No other MBW outcomes were statistically different. CONCLUSION: Increasing exposure to PM2.5 was associated with increased ventilation heterogeneity in the conductive region of the lungs 4 years after the event.

Semi-diurnal distribution of polycyclic aromatic hydrocarbons bound to PM2.5 and PM0.1 during pollution episode in the urban area of Hanoi.

Every year, Hanoi suffers from several episodes (periods with daily concentration of PM2.5 higher than 50 µg m-3 during at least two consecutive days). These episodes are of health concern because of the high concentration of PM2.5 and/or PM0.1 and the presence of PM-bound toxic components, such as, PAHs. In this study, the concentrations of PAHs bound to PM2.5 and PM0.1 in night-time and day-time samples during episode and non-episode periods in December 2021 were determined. The concentrations of PAHs bound to PM2.5 were found to increase significantly from day-time samples of 3.24 ± 0.83 ng m-3 to night-time samples of 10.8 ± 4.45 ng m-3 in episode periods. However, PAHs bound to PM0.1 increased slightly from day-time samples of 0.58 ± 0.12 ng m-3 to night-time samples of 0.89 ± 0.30 ng m-3 in episode periods. Diagnostic ratios of PAHs indicate that biomass/coal combustion and vehicular emission are the primary sources of PAHs. The incremental lifetime cancer risk was estimated to vary from 8.7E-09 to 2.5E-08 for children and 6.7E-08 to 2.2E-07 for adults, respectively. Accordingly, loss of life expectancy was estimated at 0.11 min and 0.82 min for children and adults, respectively. These findings imply that the carcinogenic impact induced by PAHs via inhalation is negligible during the episode period.

The inhibitory effect of chlorogenic acid on oxidative stress and apoptosis induced by PM2.5 in HaCaT keratinocytes.

Exposure to fine particulate matter with an aerodynamic diameter of less than 2.5 µm (PM2.5) can cause oxidative damage and apoptosis in the human skin. Chlorogenic acid (CGA) is a bioactive polyphenolic compound with antioxidant, antifungal, and antiviral properties. The objective of this study was to identify the ameliorating impact of CGA that might protect human HaCaT cells against PM2.5. CGA significantly scavenged the reactive oxygen species (ROS) generated by PM2.5, attenuated oxidative cellular/organelle damage, mitochondrial membrane depolarization, and suppressed cytochrome c release into the cytosol. The application of CGA led to a reduction in the expression levels of Bcl-2-associated X protein, caspase-9, and caspase-3, while simultaneously increasing the expression of B-cell lymphoma 2. In addition, CGA was able to reverse the decrease in cell viability caused by PM2.5 via the inhibition of extracellular signal-regulated kinase (ERK). This effect was further confirmed by the use of the mitogen-activated protein kinase kinase inhibitor, which acted upstream of ERK. In conclusion, CGA protected keratinocytes from mitochondrial damage and apoptosis via ameliorating PM2.5-induced oxidative stress and ERK activation.

Relationship between exposure to fine particulate matter and cardiovascular risk factors and the modifying effect of socioeconomic status: a cross-sectional study in Beijing, China.

Accumulating research suggested that long-term exposure to fine particulate matter (PM2.5) is related to cardiovascular disease (CVD). However, evidence regarding the relationship between PM2.5 and CVD risk factors remains inconsistent. We hypothesized that this association may be partially modified by socioeconomic status (SES). To investigate the relationships and to test the modifying effect of SES, we included baseline data for 21,018 adults from September 2017 to May 2018. PM2.5 concentrations were determined by employing an amalgamation of linear measurements obtained from monitoring stations located near the participants' residential and workplace addresses. We assessed SES across several domains, including income, education, and occupation levels, as well as through a composite SES index. The results indicated that for every 10 µg/m3 increase in PM2.5 exposure, the risk of hypercholesterolemia, hyperbetalipoproteinemia, diabetes, and hyperhomocysteinemia (HHcy) increased by 7.7% [Odds ratio (OR) = 1.077, 95% Confidence Interval (CI) = 1.011, 1.146], 19.6% (OR = 1.196, 95% CI = 1.091, 1.312), 4.2% (OR = 1.042, 95% CI = 1.002, 1.084), and 17.1% (OR = 1.171, 95% CI = 1.133, 1.209), respectively. Compared to the high SES group, those with low SES are more prone to hypercholesterolemia, hyperbetalipoproteinemia, diabetes, and HHcy. Notably, the disparities in SES appear significant in the relationship between PM2.5 exposure and hypercholesterolemia as well as hyperbetalipoproteinemia. But for diabetes and HHcy, the modification effect of SES on PM2.5 shows an inconsistent pattern. In conclusion, the results confirm the association between PM2.5 and cardiovascular risk factors and low SES significantly amplified the adverse PM2.5 effect on dyslipidemia. It is crucial to emphasize a need to improve the socioeconomic inequality among adults in Beijing and contribute to the understanding of the urgency in protecting the health of vulnerable groups.

Ambient air pollution and survival in childhood cancer: A nationwide survival analysis.

BACKGROUND: Particulate matter consisting of fine particles measuring 2.5 microns or less in diameter (PM2.5), a component of air pollution, has been linked to adverse health outcomes. The objective of this study was to assess the association between ambient PM2.5 exposure and survival in children with cancer in the United States. METHODS: Individuals aged birth to 19 years who were diagnosed with cancer between January 1, 2004, and December 31, 2019, were selected from the National Cancer Database. The association between the annual PM2.5 level at the patient's zip code of residence at the time of diagnosis and overall survival was evaluated using time-varying Cox proportional hazards models (crude and adjusted for diagnosis year and age). To address concerns that exposure to air pollution is correlated with other social determinants of health, the authors tested the association between PM2.5 levels and survival among sociodemographic subgroups. RESULTS: Of the 172,550 patients included, 27,456 (15.9%) resided in areas with annual PM2.5 concentrations above the US Environmental Protection Agency (EPA) annual PM2.5 standard of 12 µg/m3. Residing in these high-pollution areas was associated with worse overall survival (adjusted hazard ratio [aHR], 1.06; 95% confidence interval [CI], 1.012-1.10). Similarly, when PM2.5 was evaluated as a linear measure, each unit increase in PM2.5 exposure was associated with worse survival (aHR, 1.011; CI, 1.005-1.017). Exposure to PM2.5 at levels above the EPA standards was also significantly associated with worse overall survival among sociodemographic subgroups. CONCLUSIONS: Exposure to PM2.5 was significantly associated with worse overall survival among children with cancer, even at levels below EPA air quality standards. These results underscore the importance of setting appropriate air quality standards to protect the health of this sensitive population. PLAIN LANGUAGE SUMMARY: The authors investigated how living in areas with high air pollution (defined as particulate matter consisting of fine particles measuring 2.5 microns or less in diameter; PM2.5) affects the overall survival of children with cancer in the United States. The results indicated that children living in areas with higher PM2.5 levels, and even at levels below prior and current US Environmental Protection Agency standards, had lower survival rates than children living in areas with lower levels of PM2.5. This finding emphasizes the need for stricter air quality standards to better protect children, particularly those with serious health conditions like childhood cancer.

Association Between Particulate Matter Exposure and Preterm Birth in Women With Abnormal Preconception Thyrotropin Levels: Large Cohort Study.

Background: Prior research has linked exposure to particulate matter with an aerodynamic diameter of ≤2.5 µm (PM2.5) with preterm birth (PTB). However, the modulating effect of preconception thyroid stimulating hormone (TSH) levels on the relationship between PM2.5 exposure and PTB has not been investigated. Objective: This study aimed to assess whether preconception TSH levels modulate the impact of PM2.5 exposure on PTB. Methods: This cohort study was conducted in Guangdong, China, as a part of the National Free Pre-Pregnancy Checkups Project. PM2.5 exposure was estimated by using the inverse distance weighting method. To investigate the moderating effects of TSH levels on trimester-specific PM2.5 exposure and PTB, we used the Cox proportional hazards model. Additionally, to identify the susceptible exposure windows for weekly specific PM2.5 exposure and PTB, we built distributed lag models incorporating Cox proportional hazards models. Results: A total of 633,516 women who delivered between January 1, 2014, to December 31, 2019, were included. In total, 34,081 (5.4%) of them had abnormal preconception TSH levels. During the entire pregnancy, each 10-µg/m3 increase in PM2.5 was linked to elevated risks of PTB (hazard ratio [HR] 1.559, 95% CI 1.390-1.748), early PTB (HR 1.559, 95% CI 1.227-1.980), and late PTB (HR 1.571, 95% CI 1.379-1.791) among women with abnormal TSH levels. For women with normal preconception TSH levels, PM2.5 exposure during the entire pregnancy was positively associated with the risk of PTB (HR 1.345, 95% CI 1.307-1.385), early PTB (HR 1.203, 95% CI 1.126-1.285), and late PTB (HR 1.386, 95% CI 1.342-1432). The critical susceptible exposure windows were the 3rd-13th and 28th-35th gestational weeks for women with abnormal preconception TSH levels, compared to the 1st-13th and 21st-35th gestational weeks for those with normal preconception TSH levels. Conclusions: PM2.5 exposure was linked with a higher PTB risk, particularly in women with abnormal preconception TSH levels. PM2.5 exposure appears to have a greater effect on pregnant women who are in the early or late stages of pregnancy.

Assessing the effectiveness of PM2.5 pollution control from the perspective of interprovincial transport and PM2.5 mitigation costs across China.

Due to the transboundary nature of air pollutants, a province's efforts to improve air quality can reduce PM2.5 concentration in the surrounding area. The inter-provincial PM2.5 pollution transport could bring great challenges to related environmental management work, such as financial fund allocation and subsidy policy formulation. Herein, we examined the transport characteristics of PM2.5 pollution across provinces in 2013 and 2020 via chemical transport modeling and then monetized inter-provincial contributions of PM2.5 improvement based on pollutant emission control costs. We found that approximately 60% of the PM2.5 pollution was from local sources, while the remaining 40% originated from outside provinces. Furthermore, about 1011 billion RMB of provincial air pollutant abatement costs contributed to the PM2.5 concentration decline in other provinces during 2013-2020, accounting for 41.2% of the total abatement costs. Provinces with lower unit improvement costs for PM2.5, such as Jiangsu, Hebei, and Shandong, were major contributors, while Guangdong, Guangxi, and Fujian, bearing higher unit costs, were among the main beneficiaries. Our study identifies provinces that contribute to air quality improvement in other provinces, have high economic efficiency, and provide a quantitative framework for determining inter-provincial compensations. This study also reveals the uneven distribution of pollution abatement costs (PM2.5 improvement/abatement costs) due to transboundary PM2.5 transport, calling for adopting inter-provincial economic compensation policies. Such mechanisms ensure equitable cost-sharing and effective regional air quality management.

Involvement of M2 macrophages polarization in PM2.5-induced COPD by upregulating MMP12 via IL4/STAT6 pathway.

Biomass-related airborne fine particulate matter (PM2.5) is an important risk factor for chronic obstructive pulmonary disease (COPD). Macrophage polarization has been reported to be involved in PM2.5-induced COPD, but the dynamic characteristics and underlying mechanism of this process remain unclear. Our study established a PM2.5-induced COPD mouse model and revealed that M2 macrophages predominantly presented after 4 and 6 months of PM2.5 exposure, during which a notable increase in MMP12 was observed. Single cell analysis of lung tissues from COPD patients and mice further revealed that M2 macrophages were the dominant macrophage subpopulation in COPD, with MMP12 being involved as a hub gene. In vitro experiments further demonstrated that PM2.5 induced M2 polarization and increased MMP12 expression. Moreover, we found that PM2.5 increased IL-4 expression, STAT6 phosphorylation and nuclear translocation. Nuclear pSTAT6 then bound to the MMP12 promoter region. Furthermore, the inhibition of STAT6 phosphorylation effectively abrogated the PM2.5-induced increase in MMP12. Using a coculture system, we observed a significantly reduced level of E-cadherin in alveolar epithelial cells cocultured with PM2.5-exposed macrophages, while the decrease in E-cadherin was reversed by the addition of an MMP12 inhibitor to the co-culture system. Taken together, these findings indicated that PM2.5 induced M2 macrophage polarization and MMP12 upregulation via the IL-4/STAT6 pathway, which resulted in alveolar epithelial barrier dysfunction and excessive extracellular matrix (ECM) degradation, and ultimately led to COPD progression. These findings may help to elucidate the role of macrophages in COPD, and suggest promising directions for potential therapeutic strategies.

Associations between indoor fine particulate matter (PM2.5) and sleep-disordered breathing in an urban sample of school-aged children.

OBJECTIVES: Environmental risk factors may contribute to sleep-disordered breathing. We investigated the association between indoor particulate matter ≤2.5µm in aerodynamic diameter (PM2.5) and sleep-disordered breathing in children in an urban US community. METHODS: The sample consisted of children aged 6-12years living in predominantly low-income neighborhoods in Boston, Massachusetts. Indoor PM2.5 was measured in participants' main living areas for 7days using the Environmental Multipollutant Monitoring Assembly device. High indoor PM2.5 exposure was defined as greater than the sample weekly average 80th percentile level (≥15.6 µg/m3). Sleep-disordered breathing was defined as an Apnea-Hypopnea-Index (AHI) or Oxygen-Desaturation-Index (ODI) (≥3% desaturation) of ≥5 events/hour. Habitual loud snoring was defined as caregiver-report of loud snoring (most or all the time each week) over the past 4weeks. We examined the associations of PM2.5 with sleep-disordered breathing or snoring using logistic regression adjusting for potential confounders. RESULTS: The sample included 260 children (mean age 9.6years; 41% female), with 32% (n = 76) classified as having sleep-disordered breathing. In a logistic regression model adjusted for socioeconomics and seasonality, children exposed to high indoor PM2.5 levels (n = 53) had a 3.53-fold increased odds for sleep-disordered breathing (95%CI: 1.57, 8.11, p = .002) compared to those with lower indoor PM2.5. This association persisted after additional adjustments for physical activity, outdoor PM2.5, environmental tobacco smoke, and health characteristics. Similar associations were observed for snoring and indoor PM2.5. CONCLUSIONS: Children with higher indoor PM2.5 exposure had greater odds of sleep-disordered breathing and habitual loud snoring, suggesting that indoor air quality contributes to sleep disparities.

Incidence of cardiovascular disease in a cohort of mine workers exposed to ultrafine aluminum powder in Ontario, Canada.

BACKGROUND: A retrospective cohort study was conducted to estimate associations between an ultrafine aluminum powder, McIntyre Powder (MP), and cardiovascular disease incidence in a cohort of mine workers from Ontario, Canada. Disease outcomes included ischemic heart disease (IHD), acute myocardial infarction (AMI), congestive heart failure (CHF), and strokes and transient ischemic attacks (STIA). METHODS: Using work history records from the Ontario Mining Master File (MMF) mine workers were followed for disease incidence in administrative health records. The analysis included 25,813 mine workers who were exposed to MP between 1943 and 1979 and followed for cardiovascular disease (CVD) diagnoses between 2006 and 2018. Cardiovascular disease cases were ascertained using physician, hospital, and ambulatory care records. Poisson regression models were used to estimate age and birth-year adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) for associations between MP exposure and CVD outcomes. RESULTS: Ever-exposure to MP was positively associated with modest increases in the incidence rate of IHD, AMI, and CHF, but not STIA, using both assessment approaches. Duration of self-reported MP exposure was positively associated with monotonically increasing rates of IHD and AMI compared to never-exposed miners, with the greatest association observed among miners with >20 years of exposure (for IHD: RR 1.24, 95% CI: 0.91-1.68; and for AMI: RR 1.52, 95% CI 1.01-2.28). CONCLUSION: Mine workers ever-exposed to MP had modestly elevated rates of CVD. The rate of CVD diagnoses appeared to increase with longer duration of exposure when assessed by both self-reported exposure and through historical records.

Spatial and Temporal Distribution Characteristics and Cytotoxicity of Atmospheric PM2.5 in the Main Urban Area of Lanzhou City.

PM2.5, as one of the most harmful pollutant in the atmospheric environment and population health, has received much attention. We monitored PM2.5 levels at five sampling sites in the Lanzhou City and collected PM2.5 particles from two representative sites for cytotoxicity experiment. The cytotoxicity of PM2.5 samples on A549 cells and migration ability of the cells were respectively detected by Cell Counting kit-8 (CCK-8) assay and scratch assay. We detected the levels of cellular inflammatory factors and oxidative damage-related biochemical indexes. RT-qPCR was used to detect the mRNA levels of NF-κB and epithelial-mesenchymal transition (EMT)-related genes. We found that the Lanlian Hotel station had the highest PM2.5 annual average concentration. The annual average concentration change curve of PM2.5 showed a roughly "U"-shaped distribution during the whole sampling period. The cytotoxicity experiment showed the viability of A549 cells decreased and the scratch healing rate increased in the 200 and 400 µg/mL PM2.5-treated groups. We also found 400 µg/mL PM2.5 induced changes in the mRNA levels of NF-κB and EMT-related genes, the mRNA levels of IKK-α, NIK, and NF-κB in the 400 µg/mL PM2.5 group were higher than those in the control group. The mRNA levels of E-cadherin decreased and α-SMA increased in the 400 µg/mL PM2.5 groups, and the mRNA levels of Fibronectin increased in the 400 µg/mL PM2.5 groups. Moreover, we found hydroxyl radical scavenging ability and T-AOC levels were lower, and LPO levels were higher in the 200 and 400 µg/mL PM2.5 groups, and the SOD activity of cells in the 400 µg/mL PM2.5 group decreased. And compared with the control group, the levels of TNF-α were higher in the 200 and 400 µg/mL PM2.5 groups and the levels of IL-1 were higher in the 400 µg/mL PM2.5 group. The results indicated that the cytotoxicity of atmospheric PM2.5 was related to oxidative damage, inflammatory response, NF-κB activity and EMT.