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Background: Previous studies have primarily focused on the links between fine particulate matter (PM2.5) and bone health among the general population instead of PM2.5 components and the specific population. We aimed to investigate the associations between PM2.5 components and bone health among middle-aged and elderly women. Methods: A total of 748 middle-aged and elderly women were randomly sampled from 32 streets/villages in Hubei Province. The concentrations of ambient PM2.5 and its components were extracted across various residential areas from the Tracking Air Pollution in China (TAP) dataset. Bone mineral density measurements were obtained from dual-energy X-ray absorptiometry scans of study participants. Multivariable logistic and linear models were employed to assess the relationship between PM2.5 and its components and bone loss. Results: Per interquartile range (IQR) increase in nitrate (NO3−) and ammonium (NH4+) concentrations were associated with 1.65 [95% confidence intervals (CI): 1.13, 2.30] and 1.77 (95% CI: 1.26, 2.49) times higher odds of osteoporosis, respectively. Long-term exposure to sulfate (SO42−), NO3−, and NH4+ was negatively associated with T-scores and bone mineral density in L1-L4 lumbar vertebrae. In addition, the elderly, women who have experienced menarche after the age of 14, and postmenopausal women were more susceptible to the water-soluble inorganic salts of PM2.5. Conclusion: The study emphasizes the need for comprehensive policies addressing air quality, with a specific focus on vulnerable populations such as middle-aged and elderly women. Public health interventions aimed at reducing ambient PM2.5 concentrations and minimizing exposure to its harmful components are crucial in mitigating the adverse impact on skeletal health and improving the overall well-being of communities. [ABSTRACT FROM AUTHOR]

There is a growing need in public health to conduct large-scale epidemiological studies to investigate the health effects of fine particulate matter (PM2.5) exposure levels. In response to this need, we developed a real-time personal PM2.5 exposure monitoring system (PEPS: Personal Exposure PM2.5 System), which is capable of monitoring personal exposure concentration and uploading data in real time. The air quality self-labelling device, specifically customized for the PEPS, can be worn on the body and features functions for real-time data automatic upload, data storage, data export, and localization. This system enables researchers to obtain the big data of personal PM2.5 exposure concentration at low cost, with minimal manpower and technical requirements. It has been utilized to investigate the personal exposure levels of PM2.5 among college students in Beijing, China, providing a substantial volume of valuable data for indoor air quality and related epidemiological study. The maximum difference between the monitored daily average exposure concentration and the outdoor concentration was 265 µg/m3, corresponding to a relative error of 1579.5%. The correlation analysis of 11 factors showed that the correlation between exposure concentration and outdoor concentration was as high as 0.66 (p < 0.001), and the correlation between exposure concentration and other certain factors was in the range of [−0.11, −0.03]. [ABSTRACT FROM AUTHOR]

PM2.5 exposure is a challenging environmental issue that is closely related to cognitive development impairment; however, currently, relevant means for prevention and treatment remain lacking. Herein, we determined the preventive effect of docosahexaenoic acid (DHA) supplementation on the neurodevelopmental toxicity induced by PM2.5 exposure. Neonatal rats were divided randomly into three groups: control, PM2.5, and DHA + PM2.5 groups. DHA could ameliorate PM2.5-induced learning and memory dysfunction, as well as reverse the impairment of hippocampal synaptic plasticity, evidenced by enhanced long-term potentiation, recovered synaptic ultrastructure, and increased expression of synaptic proteins. Moreover, DHA increased CREB phosphorylation and BDNF levels and attenuated neuroinflammation and oxidative stress, reflected by lower levels of IBA-1, IL-1β, and IL-6 and increased levels of SOD1 and Nrf2. In summary, our findings demonstrated that supplementation of DHA effectively mitigated the cognitive dysfunction and synaptic plasticity impairment induced by early postnatal exposure to PM2.5. These beneficial effects may be attributed to the upregulation of the CREB/BDNF signaling pathway, as well as the reduction of neuroinflammation and oxidative stress. [ABSTRACT FROM AUTHOR]

Accumulating animal studies have demonstrated associations between ambient air pollution (AP) and metabolic dysfunction-associated fatty liver disease (MAFLD), but relevant epidemiological evidence is limited. We evaluated the association of long-term exposure to AP with the risk of incident MAFLD in Northwest China. The average AP concentration between baseline and follow-up was used to assess individual exposure levels. Cox proportional hazard models and restricted cubic spline functions (RCS) were used to estimate the association of PM2.5 and its constituents with the risk of MAFLD and the dose–response relationship. Quantile g-computation was used to assess the joint effects of mixed exposure to air pollutants on MAFLD and the weights of the various pollutants. We observed 1516 cases of new-onset MAFLD, with an incidence of 10.89%. Increased exposure to pollutants was significantly associated with increased odds of MAFLD, with hazard ratios (HRs) of 2.93 (95% CI: 1.22, 7.00), 2.86 (1.44, 5.66), 7.55 (3.39, 16.84), 4.83 (1.89, 12.38), 3.35 (1.35, 8.34), 1.89 (1.02, 1.62) for each interquartile range increase in PM2.5, SO42−, NO3−, NH4+, OM, and BC, respectively. Stratified analyses suggested that females, frequent exercisers and never-drinkers were more susceptible to MAFLD associated with ambient PM2.5 and its constituents. Mixed exposure to SO42−, NO3−, NH4+, OM and BC was associated with an increased risk of MAFLD, and the weight of BC had the strongest effect on MAFLD. Exposure to ambient PM2.5 and its constituents increased the risk of MAFLD. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) is a risk factor of cardiovascular disease. Associations between PM2.5 compositions and cardiovascular disease are a point of special interest but inconsistent. This study aimed to explore the cardiovascular effects of heavy metal(loid) compositions in PM2.5. Data for mortality, air pollutants and meteorological factors in Anyang, China from 2017 to 2021 were collected. Heavy metal(loid) in PM2.5 were monitored and examined monthly. A Case-crossover design was applied to the estimated data set. The interquartile range increase in cadmium (Cd), antimony (Sb) and arsenic (As) at lag 1 was associated with increment of 8.1% (95% CI: 3.3, 13.2), 4.8% (95% CI: 0.2, 9.5) and 3.5% (95% CI: 1.1, 6.0) cardiovascular mortality. Selenium in lag 2 was inversely associated with cerebrovascular mortality (RR = 0.920 95% CI: 0.862, 0.983). Current-day exposure of aluminum was positively associated with mortality from ischemic heart disease (RR = 1.083 95% CI: 1.001, 1.172). Stratified analysis indicated sex, age and season modified the cardiovascular effects of As (P < 0.05). Our study reveals that heavy metal(loid) play key roles in adverse effects of PM2.5. Cd, Sb and As were significant risk factors of cardiovascular mortality. These findings have potential implications for accurate air pollutants control and management to improve public health benefits. [ABSTRACT FROM AUTHOR]

In order to study the characteristics and transport path of PM2.5 in the subway station office, three different types of typical subway station were selected for sampling and analysis. The PM2.5 of mechanical air duct and VAC (ventilation and air conditioning system) were tested simultaneously. Both the particulate matter in the station office and VAC exhibit highly enriched characteristics of metal elements. The mass balance equation with elemental Fe as the tracer element is established firstly in subway station, and the transport path of PM2.5 in the work area is revealed: if the work area is obviously under positive pressure compared to the station hall, metal-enriched fine particles come from the VAC system; otherwise, the particles come both from the VAC system and air infiltration from the station hall. The contribution of air infiltration to metal-enriched fine particles can reach 50%. Finally, following an investigation into the source of fine particles in the office, the measures to improve air quality are proposed and validated. [ABSTRACT FROM AUTHOR]

In Bangladesh, particularly in Dhaka, gridlock in the transportation network is such a typical occurrence that it is critical to have a thorough understanding of the magnitude of carcinogenic airborne toxins like polycyclic aromatic hydrocarbons (PAHs) along the city's busy streets. In this study, we investigated the airway deposition of PM2.5- and PM10-bound 16 USEPA (United States Environmental Protection Agency) designated priority PAHs, their potential sources, and associated health risk. The samples were collected over seven high-traffic congestion areas in Dhaka during the monsoon (June–September 2021) and winter (December–February 2022) seasons and analyzed by gas chromatography–mass spectrometry (GC-MS). The winter season exhibited 2.7 and 2.3 times more PM2.5- and PM10-bound PAHs than the monsoon. The positive matrix factorization (PMF) identified vehicular emissions as the primary PAHs source, followed by biomass and coal combustion. The transboundary incursion of pollutants was predominant during winter, as almost 91% of the trajectories for air mass came from the neighboring country. An adult inhaled 9.70 μg of PAHs per day during winter, of which 1.22 μg entered the alveolar region of the pulmonary tract via PM2.5 inhalation. The total B[a]Peq values ranged from 31.0 to 145.1 ng/m3, substantially exceeding the WHO recommended limit (1 ng/m3). Lifetime lung cancer risk (LLRC) and incremental lifetime cancer risk (ILCR) for different age groups revealed that adults had a higher potential cancer risk due to long-term exposure. Overall, prolonged traffic emission increased the risk of lung cancer due to the deposition of carcinogenic B[a]P in the alveolar region (0.72–3.48 ng/h). [ABSTRACT FROM AUTHOR]

Emerging pollutants, nitro-polycyclic aromatic hydrocarbons (NPAHs), and halogenated PAHs (HPAHs), in atmospheric fine particulate matter (PM2.5) in four cities (Taiyuan, Yangquan, Changzhi, and Jincheng) during the non-heating and heating periods of Shanxi province, China, in 2020, were monitored to investigate their pollution characteristics and potential health risk. The exposure levels of PM2.5-bound ∑16PAHs, ∑13NPAHs, ∑6ClPAHs, and ∑7BrPAHs during the heating period ascended compared to the non-heating period. 2N-Nap, 1N-Nap, 2N-Fle, and 9N-Phe were primary monomers in NPAHs with higher concentrations, while higher levels of 2Br-Fle, 2Cl-Ant, and 9Cl-Phe were in HPAHs. Toxic equivalency quotients (TEQs), incremental lifetime cancer risk (ILCR), and loss of life expectancy (LLE) results suggested that PM2.5-bound PAHs during the heating periods posed a potential carcinogenic risk. The ILCR and loss of life expectancy (LLE) values of PM2.5-bound PAHs showed a similar decreasing trend with an order: adults (age 30–70) > toddler >adults (age 18–30) > teenagers > children >baby. The TEQ and ILCR values of ∑13NPAHs and ∑13HPAHs in PM2.5 were far below the safety threshold, indicating no obvious cancer risks. The pollution of PM2.5-bound PAHs, NPAHs, and HPAHs and potential health risks in Yangquan and Changzhi was more serious compared to Taiyuan and Jincheng. [ABSTRACT FROM AUTHOR]

Maternal exposure to fine particulate matter (PM2.5) is associated with adverse pregnancy and neonatal health outcomes. To explore the mechanism, we performed mRNA sequencing of neonatal cord blood. From an ongoing prospective cohort, Air Pollution on Pregnancy Outcome (APPO) study, 454 pregnant women from six centers between January 2021 and June 2022 were recruited. Individual PM2.5 exposure was calculated using a time-weighted average model. In the APPO study, age-matched cord blood samples from the High PM2.5 (˃15 ug/m3; n = 10) and Low PM2.5 (≤ 15 ug/m3; n = 30) groups were randomly selected for mRNA sequencing. After selecting genes with differential expression in the two groups (p-value < 0.05 and log2 fold change > 1.5), pathway enrichment analysis was performed, and the mitochondrial pathway was analyzed using MitoCarta3.0. The risk of preterm birth (PTB) increased with every 5 µg/m3 increase of PM2.5 in the second trimester (odds ratio 1.391, p = 0.019) after adjusting for confounding variables. The risk of gestational diabetes mellitus (GDM) increased in the second (odds ratio 1.238, p = 0.041) and third trimester (odds ratio 1.290, p = 0.029), and entire pregnancy (odds ratio 1.295, p = 0.029). The mRNA-sequencing of cord blood showed that genes related to mitochondrial activity (FAM210B, KRT1, FOXO4, TRIM58, and FBXO7) and PTB-related genes (ADIPOR1, YBX1, OPTN, NFkB1, HBG2) were upregulated in the High PM2.5 group. In addition, exposure to high PM2.5 affected mitochondrial oxidative phosphorylation (OXPHOS) and proteins in the electron transport chain, a subunit of OXPHOS. These results suggest that exposure to high PM2.5 during pregnancy may increase the risk of PTB and GDM, and dysregulate PTB-related genes. Alterations in mitochondrial OXPHOS by high PM2.5 exposure may occur not only in preterm infants but also in normal newborns. Further studies with larger sample sizes are required. [ABSTRACT FROM AUTHOR]

While studies on the reduction and management of PM2.5 are currently underway, there is a limitation in not considering the types and effects of the toxic chemicals deposited on PM2.5 based on regional sources' variations. Therefore, this study was conducted to confirm the necessity of health effects research considering the toxic chemicals deposited on PM2.5 exposure in the study of health effects related to PM2.5 exposure. Over approximately 2 years, we measured the concentrations of PM2.5 and heavy metals in the air during both spring and winter. The study focused on the Ansan/Siheung industrial complex and the Ulsan industrial complex. Based on the measured concentrations, we calculated and compared the health risks with PM2.5 and heavy metal exposure for each industrial complex. The concentration analysis results revealed differences in the concentrations of PM2.5, Ni, Mn, As, and Cr between the two regions. Furthermore, the calculated health risks associated with PM2.5 and heavy metals also showed differences between the regions. In this study, differences in the concentrations of PM2.5 and its chemical components were observed based on the industrial sources and regional characteristics of each industrial complex. These variations were shown to lead to differences in the levels of health impacts. The results emphasize the importance of considering not only PM2.5 but also its chemical components for accurate and efficient health effect assessments. [ABSTRACT FROM AUTHOR]

The objective of this study was to investigate the effects of anthracene (Ant) with 3 rings, benzo[a]anthracene (BaA) with 4 rings and benzo[b]fluoranthene (BbF) with 5 rings in fine particulate matter (PM2.5) at different exposure times (4 h and 24 h) and low exposure levels (0 pg/mL, 0.1 pg/mL, 1 pg/mL, 100 pg/mL and 10,000 pg/mL) on RAW264.7 cells. The changes of interleukin-6 (IL-6) and oxidative stress levels in RAW264.7 cells were investigated by methyl-thiazolyl-tetrazolium (MTT) and enzyme-linked immunosorbent assay (ELISA). Pearson correlation analysis was used to analyze the correlation between variables. Ant, BaA and BbF induced the secretion of IL-6 and the occurrence of oxidative stress in RAW264.7 cells. The inflammatory effect and oxidative damage were exacerbated with prolonged exposure time, increasing exposure concentration and increasing number of PAH rings. At the same time, IL-6 was found to have a certain correlation with the levels of ROS, MDA and SOD. Exposure to atmospheric PAHs at low concentrations can also produce toxic effects on cells, IL-6 and oxidative stress work together in cell damage. The study is expected to provide a theoretical and experimental basis for air pollution control and human health promotion. [ABSTRACT FROM AUTHOR]

Unabated emissions of precursor gases from coal-fired power stations in South Africa greatly contribute to ambient PM2.5 concentration in the region, but estimates of the number of associated premature mortalities vary vastly. The application of the exposure-response function is one of the reasons for the differences in estimates of premature mortalities; since the relationship between mortality and PM2.5 exposure flattens out at higher PM2.5 concentrations, a smaller number of premature mortalities is calculated if a reduction in PM2.5 concentration occurs at the actual ambient concentration ("avoidable deaths"), while a greater number of mortalities is calculated if other sources are not considered (at low ambient concentrations) ("single-source deaths"). It is more appropriate to attribute deaths to a source in proportion to the contribution made by the source to ambient PM2.5 levels ("attributable deaths"). Total ambient PM2.5 concentrations are extrapolated from 38 ambient monitoring stations in the north-eastern region of South Africa using a regression model based on household socio-economic factors, and PM2.5 concentrations derived from power station emissions are estimated using a reduced-form intake fraction model. It is estimated that there are around 800 attributable premature mortalities per year due to PM2.5 from coal-fired power station emissions in South Africa. The number of premature mortalities is 44% higher when calculating single-source deaths and 53% lower when calculating avoidable deaths. Using the attributable death approach is particularly important in highly polluted areas such as low-income residential areas where households use solid and liquid fuels. [ABSTRACT FROM AUTHOR]

Rapidly urbanizing cities in Latin America experience high levels of air pollution which are known risk factors for population health. However, the estimates of long-term exposure to air pollution are scarce in the region. We developed intraurban land use regression (LUR) models to map long-term exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) in the five largest cities in Colombia. We conducted air pollution measurement campaigns using gravimetric PM2.5 and passive NO2 sensors for 2 weeks during both the dry and rainy seasons in 2021 in the cities of Barranquilla, Bucaramanga, Bogotá, Cali, and Medellín, and combined these data with geospatial and meteorological variables. Annual models were developed using multivariable spatial regression models. The city annual PM2.5 mean concentrations measured ranged between 12.32 and 15.99 µg/m3 while NO2 concentrations ranged between 24.92 and 49.15 µg/m3. The PM2.5 annual models explained 82% of the variance (R2) in Medellín, 77% in Bucaramanga, 73% in Barranquilla, 70% in Cali, and 44% in Bogotá. The NO2 models explained 65% of the variance in Bucaramanga, 57% in Medellín, 44% in Cali, 40% in Bogotá, and 30% in Barranquilla. Most of the predictor variables included in the models were a combination of specific land use characteristics and roadway variables. Cross-validation suggests that PM2.5 outperformed NO2 models. The developed models can be used as exposure estimate in epidemiological studies, as input in hybrid models to improve personal exposure assessment, and for policy evaluation. [ABSTRACT FROM AUTHOR]

This study assessed the regional differences of PM2.5 (fine particulate matter) concentration and secondary components in China. Through chemical analysis (Thermal/Optical Carbon Analyzer and ion chromatography) and statistical tools (SPSS and Origin software), PM2.5 samples' concentration and main components were estimated and compared in Tianjin and Guangzhou in December 2016. The average PM2.5 mass concentration was 148 μg/m3 in Tianjin and 62 μg/m3 in Guangzhou, indicating heavy air pollution in both cities. Organic carbon constituted 15% of PM2.5 in Tianjin, while that accounted for 25% in Guangzhou. The concentration of the secondary organic carbon accounted for 40% and 33% of organic carbon in Tianjin and Guangzhou, respectively. The ionic components in Tianjin made up 49% of PM2.5, while those of Guangzhou were responsible for 36% locally. The sulfate oxidation ratio reached 0.41 in Tianjin and 0.53 in Guangzhou while the nitrate oxidation ratio was 0.23 and 0.14 in the two cities, respectively. These results indicated high secondary conversion rate in PM2.5 pollution in both cities and suggested that PM2.5 mass concentration could not fully reflect its environmental and health effects, and so more attentions should be paid to the effects of its components, especially secondary components. In addition, the results could provide a scientific basis for making policies concerning air pollution control and developing strategies of air quality improvement. [ABSTRACT FROM AUTHOR]

Black carbon (BC) in ambient fine particulate matter (PM2.5) was measured for 15 months (Sept 2013–Dec 2014) at six locations throughout the state of Mississippi, USA, to investigate the distribution, temporal variations, potential sources, and health risks of BC. Sampling sites were divided into two groups based on population: large cities (Gulfport, Hattiesburg, and Jackson) and small cities (Grenada, Hernando, and Pascagoula). The mean concentration of BC was higher in large cities compared to small (mean ranges of 1.55 to 2.04 µg m−3 in large cities and 1.01 to 1.73 µg m−3 in small cities) and across locations BC was impacted by season and meteorological variables, particularly wind and precipitation. The results of potential source contribution function (PSCF) and concentration weighted trajectory (CWT) and trajectory cluster analysis confirmed that the long-range transport impacted BC concentration and air masses from the north-west were a major distant source of BC at all study sites. The accumulation of pollutants was enhanced by short trajectories connected to air masses coming from the continental areas of the USA and Canada, while low BC concentrations in fast moving air masses originated in both the ocean and continental areas with lower emissions. Following BC environmental analyses, cancer and non-cancer risk assessments were conducted for BC exposure in adults and children, with cancer risks for adults being higher than the Environmental Protection Agency (EPA) recommended limits, while non-cancer risks were below the threshold values. BC is poorly understood in rural states, like Mississippi, and this research identifies patterns and potential health risks associated with BC. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) is a major air pollutant in most cities of China, and poses great health risks to local residents. In this study, the health effects of PM2.5 in Nanjing and Yangzhou were compared using computational and experimental methods. The global exposure mortality model (GEMM), including the results of a cohort study in China, was used to estimate the disease-related risks. Premature mortality attributable to PM2.5 exposure were markedly higher in Nanjing than that in Yangzhou at comparable levels of PM2.5 (8191 95% CI, 6975–9994 vs. 6548 95% CI, 5599–8049 in 2015). However, the baseline mortality rate was on a country-level and the age distribution was on a province-level, traditional estimation method could not accurately represent the health burdens of PM2.5 on a city-level. We proposed a refined calculation method which based on the actual deaths of each city and the disease death rates. Conversely, similar concentrations of PM2.5 exposure resulted in higher actual deaths per million population in Yangzhou (1466 95% CI, 1266–1746) than that in Nanjing (1271 95% CI, 1098–1514). Health risks of PM2.5 are associated with the generation of reactive oxygen species, among which hydroxyl radial (·OH) is the most reactive one. We then collected these PM2.5 samples and quantified the induced ·OH. Consistently, average ·OH concentration in 2015 was higher in Yangzhou than that in Nanjing, again indicating that PM2.5 in Yangzhou was more toxic. The combination of computational and experimental methods demonstrated the complex relationship between health risks and PM2.5 concentrations. The refined estimation method could help us better estimate and interpret the risks caused by PM2.5 exposure on a city-level. [ABSTRACT FROM AUTHOR]

Outdoor air pollution has been considered as a severe environmental health issue that almost affecting everyone in the world, and intensive actions were launched. However, little is known about the association between dynamic changes in ambient fine particulate matter (PM2.5) exposure and body mass index (BMI) among old adults. To investigate the dynamic changes in ambient PM2.5 and body mass index among the elderly, we included a total of 7204 participants from 28 provinces of China during 2011–2015 in the China Health and Retirement Longitudinal Study (CHARLS). Ambient fine particle matter (PM2.5) was estimated using a well-validated space–time extremely randomized trees model. Change in PM2.5 and BMI (ΔPM2.5 and ΔBMI) were calculated as the value at a follow-up visit minus value at baseline. Linear mixed-effects models were applied to quantify the associations, controlling for sociodemographic factors. We found that per 1 μg/m3 increase in PM2.5 exposure was associated with a 0.031–0.044 kg/m2 increase in BMI among the elderly. We observed an approximate linear concentration-response relationship of PM2.5 and BMI in each visit. Each 1 μg/m3 increase in ΔPM2.5 exposure was associated with an increase in ΔBMI (β = 0.040, 95% CI 0.030, 0.049), while per 1 μg/m3 decrease in the ΔPM2.5 exposure level was associated with a decrease in ΔBMI (β = −0.016, 95% CI −0.027, −0.004). Our findings suggest that dynamic changes in ambient PM2.5 was positively associated with changes in BMI among old Chinese population. [ABSTRACT FROM AUTHOR]

Liquid desiccant systems are promising methods to recover water and waste heat simultaneously from flue gas. Prior research found that the reduction of particulate matter could occur during the absorption processes. In the present paper, experiments were carried out to explore the effect of removing fine particulate matter (PM2.5) in a liquid desiccant dehumidifier. Aqueous calcium chloride (CaCl2) was used as the desiccant in the experiments. The discrepancies in mass and energy conservation were within ±10% and ±15%, respectively, which showed the good reliability of the experimental results. Additionally, 23.5%–46.0% of the PM2.5 and 23.9%–45.1% of the moisture in the flue gas were removed. By comparing the desiccant solution and water, it was found that they could minimally remove PM2.5 through washing the flue gas. Regardless of whether the flue gas was dehumidified by water or the solution, the removal fractions of PM2.5 of these two methods could be very close if they achieve the same fraction of moisture removal. From the results of a parameter analysis, it was found that the removal fraction of PM2.5 was nearly proportional to the removal fraction of moisture within the experimental range. [ABSTRACT FROM AUTHOR]

Trace metals (TRs) and polycyclic aromatic hydrocarbons (PAHs) are major toxic components of fine particulate matter (PM2.5) and related to various health adverse outcomes. The study aims to get a better understanding of the contents, sources and risks of PM2.5-bounded TRs and PAHs in Hefei, China, during the period of 2019–2021. We collected 504 samples and measured twelve TRs and sixteen priority PAHs by inductively coupled plasma mass spectrometry and high-performance liquid chromatography. The annual mass concentrations of PM2.5 was fluctuated in the year of 2019–2021 at 50.95, 47.48 and 59.38 μg/m3, with seasonal variations in rank order of winter > spring > autumn > summer. The median concentrations of PM2.5-bounded ƩTRs and ƩPAHs were also fluctuated, 132.85, 80.93 and 120.27 ng/m3 for ƩTRs, 2.57, 5.85 and 2.97 ng/m3 for ƩPAHs, in the year of 2019, 2020 and 2021, respectively. Seasonal variations of ƩTRs and ƩPAHs show the highest concentration in winter. Positive matrix factorization was used for identified pollution emission sources, and TRs mainly originated from coal combustion, traffic emission and fugitive dust, while PAHs stemmed from biomass, diesel, gasoline and coal combustion. Health risk assessment indicated that adults were more vulnerable than children, the carcinogenic risk assessment of As and Cr manifested a certain degree of cancer risk (1.0 × 10–6 < CR < 1.0 × 10–4) in adults group, and health risks of TRs were higher than PAHs in Hefei. These findings suggest that PM2.5-bounded TRs and PAHs should be considered when making emission control strategies for air pollution, and winter, combustion sources and adults should achieve more policy attention to decrease exposure risks in Hefei. [ABSTRACT FROM AUTHOR]

This study explores the relationship between air pollution and judicial rulings. Although environmental factors should not affect judicial decisions, realists contend that there is substantial room for external factors to transpire into sentencing and sway human reasoning. We hypothesize that air pollution is one of these factors. Using Poisson panel models and instrumental variable techniques, we show that exposure leads to more convictions. We posit that this effect occurs because the impact of exposure on the central nervous system changes the cognitive performance and empathy of judges. Back-of-the-envelope calculations suggest that decreasing average air pollution in India by one standard deviation would lead to up to 145,000 fewer convictions regarding currently active cases. [ABSTRACT FROM AUTHOR]

Purpose: The incidence of thyroid cancer has increased substantially over the past few decades and is partially explained by overdiagnosis. Geographical variations in incidence rates were reported to be related to national development status. This study aimed to gain deeper insights into global thyroid cancer burden by incorporating additional social and economic factors to account for cross-national disparities. Methods: We performed a multivariate analysis of age-standardized incidence and mortality data from the GLOBOCAN 2020 database for 126 countries that had more than 100 incident cases of thyroid cancer. The human development index (HDI), current health expenditure, and additional Global Health Observatory indicators were extracted from multiple sources. Results: Age-standardized incidence was highly correlated with HDI (standardized coefficient beta = 0.523, 95% confidence interval [CI] = 0.275–0.771) among the countries studied. The prevalence of raised fasting blood glucose was associated with age-standardized mortality (beta = 0.277, 95% CI = 0.038–0.517). Generally, the mortality-to-incidence ratio was higher in males than in females. In multivariate analysis, HDI (beta = − 0.767, 95% CI = − 0.902 to − 0.633), current health expenditure (beta = 0.265, 95% CI = 0.137–0.394), and fine particulate matter (PM2.5) concentrations (beta = 0.192, 95% CI = 0.086–0.298) were associated with mortality-to-incidence ratios. Conclusions: National developments gauged by HDI explain the majority of the variation in incidence rates of thyroid cancer but play a smaller role in disparities in mortality rates. The association between air pollution and thyroid cancer outcomes warrants further investigation. [ABSTRACT FROM AUTHOR]

Oxidative stress and inflammation are mechanisms underlying toxicity induced by fine particulate matter (PM2.5). The antioxidant baseline of the human body modulates the intensity of oxidative stress in vivo. This present study aimed to evaluate the role of endogenous antioxidants in alleviating PM2.5-induced pulmonary injury using a novel mouse model (LiasH/H) with an endogenous antioxidant capacity of approximately 150% of its wild-type counterpart (Lias+/+). LiasH/H and wild-type (Lias+/+) mice were randomly divided into control and PM2.5 exposure groups (n = 10), respectively. Mice in the PM2.5 group and the control group were intratracheally instilled with PM2.5 suspension and saline, respectively, once a day for 7 consecutive days. The metal content, major pathological changes in the lung, and levels of oxidative stress and inflammation biomarkers were examined. The results showed that PM2.5 exposure induced oxidative stress in mice. Overexpression of the Lias gene significantly increased the antioxidant levels and decreased inflammatory responses induced by PM2.5. Further study found that LiasH/H mice exerted their antioxidant function by activating the ROS-p38MAPK-Nrf2 pathway. Therefore, the novel mouse model is useful for the elucidation of the mechanisms of pulmonary injury induced by PM2.5. [ABSTRACT FROM AUTHOR]

Globally, air pollution is the fourth leading risk factor for death, while lung cancer (LC) is the leading cause of cancer-related death. The aim of this study was to explore the prognostic factors of LC and the influence of high fine particulate matter (PM2.5) on LC survival. Data on LC patients were collected from 133 hospitals across 11 cities in Hebei Province from 2010 to 2015, and survival status was followed up until 2019. The personal PM2.5 exposure concentration (μg/m3) was matched according to the patient's registered address, calculated from a 5-year average for every patient, and stratified into quartiles. The Kaplan–Meier method was used to estimate overall survival (OS), and Cox's proportional hazard regression model was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). The 1-, 3-, and 5-year OS rates of the 6429 patients were 62.9%, 33.2%, and 15.2%, respectively. Advanced age (75 years or older: HR = 2.34, 95% CI: 1.25–4.38), subsite at overlapping (HR = 4.35, 95% CI: 1.70–11.1), poor/undifferentiated differentiation (HR = 1.71, 95% CI: 1.13–2.58), and advanced stages (stage III: HR = 2.53, 95% CI: 1.60–4.00; stage IV: HR = 4.00, 95% CI: 2.63–6.09) were risk factors for survival, while receiving surgical treatment was a protective factor (HR = 0.60, 95% CI: 0.44–0.83). Patients exposed to light pollution had the lowest risk of death with a 26-month median survival time. The risk of death in LC patients was greatest at PM2.5 concentrations of 98.7–108.9 μg/m3, especially for patients at advanced stage (HR = 1.43, 95% CI: 1.29–1.60). Our study indicates that the survival of LC is severely affected by relatively high levels of PM2.5 pollution, especially in those with advanced-stage cancer. [ABSTRACT FROM AUTHOR]

Many studies have examined the associations between exposure to indoor and outdoor atmospheric particulate matter and health outcomes in humans. There is increasing evidence that the oxidative characteristics of such particulate matter have a role in determining the adverse health effects of fine particulates. Moreover, since people spend more time in indoors (office and home), indoor air quality and its impact on human health have increased in importance. However, to date, studies examining the oxidative characteristics of indoor particulates are few, and there has been a limited examination of the impact on physiological conditions of indoor fine particulates exposure on microorganisms. Therefore, this study aimed to investigate the oxidative characteristics of fine particulates in an indoor environment on the -3rd floor. The chemical characteristics of indoor PM2.5 samples were determined through their elemental composition, particle oxidation state, and organic and inorganic functional groups using EDX and FTIR spectrometry. Oxidative characteristics were also examined in terms of the cellular response of opportunistic bacteria (Staphylococcus aureus and Escherichia coli) by oxidative stress indicators (e.g., antioxidant, catalase, superoxide dismutase, glutathione (reduced), lipid peroxidation, and hydrogen peroxide), applied to artificial lung fluid and TRIS soluble fractions of aerosol that was extracted from the fine mode (PM2.5) of 120-h filter samples. Bacterial activity and protein content of S. aureus and E. coli were also studied in order to understand the main biochemical response of opportunistic bacteria. The chemical analysis results showed that elements in the indoor PM2.5 filters were both crustal origin (e.g., Al, Si, K, and Ca) and anthropogenic (e.g., Ba, Zn, and Ce). The identified functional groups were S = O, N–H, N = O, C = O, C-H, and O–H, which can cause oxidative stress. Bacteria-based oxidative indicators showed that both PM2.5 and physicological fluids induced the oxidative stress. However, oxidative responses were changed by the type of bacteria and physicological fluid, and PM2.5 was disturbed by the natural protection of physicological fluids. [ABSTRACT FROM AUTHOR]

This paper investigates the impact of air pollution on students' cognitive performance in a high-stakes exam: China's College English Test (CET). We match exams taken from 2013 to 2017 at 22 universities across China with hourly air pollution measures from the nearest monitoring stations. Identification leverages a student fixed effects model, which alleviates the concern of omitted variables, such as students' ability. Our estimates indicate a statistically significant negative impact of fine particulate matters (PM 2.5 ) exposure during exam windows on cognitive performance. By focusing on a single language exam, instead of comparing performance across different test subjects, we are able to paint a more accurate picture of the cognitive impact of air pollution. We highlight the importance of short-term air pollution exposure for high-stakes cognitive performance. Our results suggest that temporary defensive measures could be important in mitigating the negative consequences of air pollution. [ABSTRACT FROM AUTHOR]

Short-term or long-term exposure to fine particulate matter (PM2.5) is related to increased incidences of respiratory diseases. This study aimed to investigate the influences of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) supplementation on oxidative stress, inflammation, lung metabolic profile, and gut microbiota in PM2.5-induced lung injury mice. Mice were divided into four groups (n = 15, per group): two unsupplemented groups, control group and PM2.5 group, and two supplemented groups with ω-3 PUFAs, ω-3 PUFAs group, and ω-3 PUFAs + PM2.5 group. Mice in the supplemented groups were placed on an ω-3 PUFAs-enriched diet (ω-3 PUFAs, 21 g/kg). During the 5th to 6th week of dietary supplementation, mice were exposed to PM2.5 by intra-tracheal instillation. ω-3 PUFAs ameliorate lung histopathological injury, reduce inflammatory responses and oxidative stress, affect lung metabolite profile, and modulate gut microbiota in PM2.5-induced lung injury mice. Thus, supplementary ω-3 PUFAs showed effectiveness in attenuation of PM2.5-induced lung injury, indicating that the interventions exhibited preventive and therapeutic potential. [ABSTRACT FROM AUTHOR]

Long-term exposure to fine particulate matter (PM2.5) may increase the risk of neonatal encephalopathy due to birth asphyxia and trauma. However, little is known about the trends of PM2.5-related neonatal encephalopathy burden under different levels of social and economic development. We studied the burden of PM2.5-related neonatal encephalopathy due to birth asphyxia and trauma measured by the age-standardized mortality rate (ASMR) and the age-standardized disability-adjusted life years rate (ASDR), and its trends with the socio-demographic index (SDI) in 192 countries and regions from 1990 to 2019. This is a retrospective study using the Global Burden of Disease Study 2019 (GBD2019) database. The age-standardized mortality rate (ASMR) and age-standardized disability-adjusted life years rate (ASDR) are used to measure the burden of PM2.5-related neonatal encephalopathy in different countries and regions. The mortality rate (per 100 thousand) is used to evaluate the differences of PM2.5-related neonatal encephalopathy burden in sex and age. The annual percentage changes (APCs) and the average annual percentage changes (AAPCs) are used to reflect the trends of PM2.5-related neonatal encephalopathy burden over years (1990–2019) and are calculated using a Joinpoint model. The relationship of the socio-demographic index with the ASMR and ASDR is calculated using Gaussian process regression. In summary, the global burden of PM2.5-related neonatal encephalopathy increased since 1990, especially in boys, early neonates, and regions with low-middle SDI. Globally, the ASMR and ASDR of PM2.5-related neonatal encephalopathy burden in 2019 were 0.59 (95% CI: 0.40, 0.83) per 100,000 people and 52.59 (95% CI: 35.33, 73.67) per 100,000 people, respectively. From 1990 to 2019, the ASMR and ASDR of PM2.5-related neonatal encephalopathy increased by 44.39% and 44.19%, respectively. The global average annual percentage changes of ASMR and ASDR were 1.3 (95% CI: 1.0, 1.6). The relationship between the socio-demographic index and the burden of PM2.5-related neonatal encephalopathy presented negative correlation when the socio-demographic index was more than 0.60. Middle, high-middle, and high SDI regions had decreasing trends of PM2.5-related neonatal encephalopathy, of which the AAPCs for both ASMR and ASDR ranged from − 0.3 to − 3.1. Besides improving the progress in national policy and the coverage rate of maternal and neonatal health care and facility-based delivery, air pollution control may also be a better way for countries with large and increasing amounts of exposure to PM2.5 pollution to reduce neonatal encephalopathy. And our results also suggest that low and low-middle SDI countries should appropriately pay more attention to early newborns and boys. [ABSTRACT FROM AUTHOR]

Air pollution, especially in urban regions, is receiving increasing attention in Vietnam. Consequently, this work aimed to study and analyze the air quality in several provinces and cities in the country focusing on PM2.5. Moreover, the impacts of COVID-19 social distancing on the PM2.5 level were investigated. For this purpose, descriptive statistic, Box and Whisker plot, correlation matrix, temporal variation, and trend analysis were conducted. R-based program and the R package "openair" were employed for the calculations. Hourly PM2.5 data were obtained from 8 national air quality monitoring sites. The study results indicated that provinces and cities in the North experienced more PM2.5 pollution compared to the Central and South. PM2.5 concentrations at each monitoring site varied significantly. Among monitoring sites, the northern sites showed high PM2.5 correlations with each other than the other sites. Seasonal variation was observed with high PM2.5 concentration in the dry season and low PM2.5 concentration in the wet season. PM2.5 concentration variation during the week was not so different. Diurnal variation showed that PM2.5 concentration rose at peak traffic hours and dropped in the afternoon. There was mainly a decreasing trend in PM2.5 concentration over the studied period. The COVID-19 pandemic has contributed to PM2.5 reduction. In the months implemented social distancing for preventing the epidemic, PM2.5 concentration declined but it would mostly increase in the following months. This study provided updated and valuable assessments of recent PM2.5 air quality in Vietnam. [ABSTRACT FROM AUTHOR]

The association between fine particulate matter (PM2.5) and rheumatoid arthritis (RA) is currently unclear, especially in Beijing, a city with severe air pollution. Our study aimed to explore the relationship between short-term outdoor exposure to PM2.5 and RA outpatient visits using a time-series analysis in Beijing. We used the Beijing's Medical Claims for Employees database to identify patients with RA in 2010–2012. A generalized additive model with a Poisson link was used to estimate the percentage change in RA outpatient visits after the PM2.5 concentration increased by 10 μg/m3. From January 1, 2010, to June 30, 2012, a total of 541,061 RA outpatient visits were identified. During the study period, the average daily (standard deviation) concentration of PM2.5 was 99.5 (75.3) µg/m3. A 10 µg/m3 increase in PM2.5 concentration was correlated with a 0.21% (95% CI, 0.18–0.23%) increase in outpatient visits for RA on the same day. A significant association for the cumulative effect of PM2.5 was found, and the largest significant association was observed for a lag of 0–3 days (0.26%; 95% CI, 0.23–0.29%). Stratified analyses revealed that females (0.29%, 95% CI: 0.26–0.33%) and 18–65 years old patients (0.29%, 95% CI: 0.25–0.32%) were most susceptible to the effects of PM2.5 exposure. The current findings showed that short-term exposure to PM2.5 was followed by an increase in the number of outpatient visits for RA in Beijing. Future studies should investigate the mechanisms underlying this association. [ABSTRACT FROM AUTHOR]

Obesity and exposure to fine particulate matter (PM2.5) are risk factors for insulin resistance, to which physical exercise is the most powerful non-pharmacological strategy. However, public concern over whether exercise could be protective in a polluted environment exists. Therefore, evaluating the possible benefits of exercise in polluted conditions in different contexts (age, gender, and cardiometabolic health) is imperative. In this sense, muscle plays a major role in maintaining glucose homeostasis, and its oxidative status is closely affected during exercise. This study tested whether moderate aerobic training could alleviate the metabolic and oxidative impairment in the gastrocnemius induced by the combination of a high-fat diet (HFD) and PM2.5 exposure. Female mice (B6129SF2/J) received HFD (58.3% of fat) or standard diet, intranasal instillation of 20 μg residual oil fly ash (ROFA: inorganic portion of PM2.5), or saline seven times per week for 19 weeks. In the 13th week, animals were submitted to moderate training or remained sedentary. Trained animals followed a progressive protocol for 6 weeks, ending at swimming with 5% body weight of workload for 60 min, while sedentary animals remained in shallow water. Aerobic moderate training attenuated weight gain and glucose intolerance and prevented muscle and pancreatic mass loss induced by a HFD plus ROFA exposure. Interestingly, a HFD combined with ROFA enhanced the catalase antioxidant activity, regardless of physical exercise. Therefore, our study highlights that, even in polluted conditions, moderate training is the most powerful non-pharmacological treatment for obesity and insulin resistance. [ABSTRACT FROM AUTHOR]

The weak potential of using the sole outdoor concentrations to represent personal exposure to PM2.5 is confirmed by the literature; therefore, it is important to account for a person's movements over time when estimating the short-term personal air pollution exposure within different microenvironments (MEs). This study is an example of applying an assessment method of the exposure to PM2.5 in different microenvironments at different temporal scales. A low-cost particle counter (the Dylos 1700) was used; its performance was validated in comparison with equivalent instruments such the SidePak AM520 Personal Aerosol Monitor (R2 = 0.89). This validation also provided a function to convert measured particle number concentrations (PNCs) into calculated particle mass concentrations. The 150 profiles that was collected on a minute-by-minute basis regarding PM2.5 concentration from December 2018 to May 2021 highlight the influence of individual activities and contextual factors on the air quality, so that Lebanon's annual PM2.5 mean (24.2 µg⁄m3) is 142% higher than the World Health Organization (WHO) annual mean guideline (10 µg⁄m3). Winter is the most polluted period due to the increased application of space heating devices. Additionally, the occurrence of dusty winds during the spring period leads to the elevated levels of dispersed PM2.5. Simultaneously, the rural zones are more polluted than urban ones due to the usage of more traditional heating equipment, in addition to the usage of chemical products like pesticides and fertilizers in agricultural activities in such areas. Furthermore, the (outdoor–indoor–transport) MEs indicate that the transport and indoor MEs have similar levels of suspended fine particulates, while outdoor MEs are less polluted. Studies based on the personal exposure to PM2.5 were generally applied on specific and limited places such as schools, workplaces, or residences. The study aims to shed light on the modern method in an attempt to estimate the personal exposure to PM2.5 and to inspire similar studies to achieve the maximum efficiency. [ABSTRACT FROM AUTHOR]

With climate change posing increasing threats and aging populations, understanding the complex relationship between extreme temperatures, PM2.5 pollution, and respiratory health among the elderly is crucial. While some research exists, there remains a significant gap in studying the combined effects of heat waves, cold spells, and PM2.5 on elderly respiratory health in high-altitude regions. We collected data from Xining (2016–2021), including respiratory disease outpatient visits, meteorological, and pollutant data. Employing a case-crossover design and conditional Poisson regression analysis, we investigated the individual and interactive impacts of heat wave, cold spell, and PM2.5 on outpatient visits for respiratory disease among the elderly. We used the relative excess odds due to interaction (REOI), proportion attributable to interaction (AP), and synergy index (S) as quantitative indicators of interaction. Our analysis revealed significant associations between heat wave, cold spell, PM2.5 exposure, and outpatient visits for respiratory disease among the elderly, with odds ratios of 1.10 (95%CI: 1.06, 1.15) and 1.16 (95%CI: 1.13, 1.20), respectively. Moreover, a synergistic effect between cold spell and PM2.5 was observed, particularly affecting vulnerable groups such as female and those aged ≥ 80. The combined exposure to cold spell and elevated PM2.5 levels was estimated to contribute to up to 0.18 (95%CI: 0.17, 0.27) of respiratory outpatient visits. This study underscores the need for urgent interventions, such as reducing PM2.5 exposure and enhancing extreme weather warning systems, to protect the respiratory health of the elderly, especially in high-altitude regions. [ABSTRACT FROM AUTHOR]

Summary: We hypothesized that air pollution could cause oxidative damage and inflammation in the human body, which was linked to bone loss. Our result showed that long-term exposure to air pollution might decrease bone mineral density (BMD) T-score and increase the prevalence of osteoporosis in Hubei province. Introduction: Osteoporosis is becoming an increasingly serious public health problem with the advent of global aging. Long-term exposure to air pollution has been linked to multitudinous adverse health outcomes, but evidence is still relatively limited and inconsistent for BMD T-score and osteoporosis. This study aimed at exploring the associations between long-term exposure to air pollution and BMD T-score and osteoporosis. Methods: The Hubei part of the China Osteoporosis Prevalence Study was extracted. Data on air pollutants were collected by the national air quality real-time release platform of China Environmental Monitoring Station. Linear mixed models and multilevel logistic regression analyses were performed to assess the associations between air pollution and BMD T-score and osteoporosis, respectively. Subgroup analyses were conducted to identify vulnerable populations. Results: A total of 1845 participants were included in this cross-section study. Per 10 ug/m3 increase in PM2.5 and SO2 were associated with 0.20 (95% CI: 0.04, 0.36) and 0.31 (95% CI: 0.11, 0.51) decrease in BMD T-score of the neck of femur, respectively. Per 10 ug/m3 increase in CO was linked with 0.03 (95% CI: 0.02, 0.05) decrease in BMD T-score of the total hip. Per 1 ug/m3 increase in PM2.5 was associated with 5% increase in the prevalence of osteoporosis in all participants. In general, the higher concentrations of PM2.5 with the more adverse effect on osteoporosis (P for trend = 0.01). The impact of PM2.5 on osteoporosis in males was higher than that in females [1.29, 95% CI (1.11, 1.50) vs 1.01, 95% CI (0.95, 1.07)]. Per 1 ug/m3 increase in PM10 corresponded with 4% elevation in the risks of osteoporosis in rural population. The ORs (95% CI) for the association of osteoporosis and NO2 in ever/current smoking and drinking population were 1.07 (1.01, 1.13) and 1.05 (1.00, 1.09), respectively. SO2 had a statistically significant positive effect on people with comorbidity [OR = 1.10, (95% CI: 1.00 to 1.21)], while none in people without comorbidity [OR = 0.96, (95% CI: 0.88 to 1.05)]. Conclusion: Our study provided evidence that long-term exposure to PM2.5 was linked with the decreased BMD T-score and increased risk of osteoporosis among all participants. The adverse impacts of PM2.5, PM10, and NO2 were larger in males than in females. People having comorbidity, living in rural areas, and current/ever smoking or drinking were more vulnerable to air pollution. Public health departments should consider air pollution to formulate better preventive measures for osteoporosis. [ABSTRACT FROM AUTHOR]

Airborne particles have been regarded as a great threat to residents' health, especially to those living in the urban area. As a passive method for fine particle reduction, the high capacity of vegetation has been widely explored. However, a limited number of researches have reported the capturing capacity of roadside plants for fine particles lower than 2.5 μm. In this study, ten common broad-leaved plants cultivated in central China were selected to evaluate their capturing capacity for water-insoluble particles lower than 2.5 μm and to explore the impacts of different planting patterns including height, location in the street, and the distance to the street curb on their deposition load. Besides, the impacts brought by different traffic pressures were discussed as well. Interspecies difference was found among the plants facing to the same direction. Ligustrum lucidum showed the highest capacity for particles over 0.45 μm. For particles between 0.22 and 0.45 μm, Xanthoceras sorbifolium showed the highest efficiency. The change of leaf orientation has impact on the capturing capacity of tested plants for fine particles larger than 0.45 μm, while for particles between 0.22 and 0.45 μm, each tested species showed a high capacity regardless of leaf orientation. In consideration of planting patterns, with the rise of height, and the distance to the street curb, the plants' capturing capacity for different-sized fine particles all declined. In addition, vegetation locating in the middle of the street had significantly higher capacity than those alongside the street. At last, roadside plants from urban-street showed significantly higher capacity than those from Uni-campus and City-park. Positive correlation was found between the capturing capacity and the traffic pressure regardless of taking all plant species as a whole or comparing them respectively. This study expands the cognition of roadside plants as an effective passive filter for water-insoluble fine particle smaller than 2.5 μm and provides insights for further roadside green infrastructure planning to improve urban air quality. [ABSTRACT FROM AUTHOR]

Numerous studies have evaluated the association between air pollution and gestational diabetes mellitus (GDM), but the findings were inconsistent. This meta-analysis aimed to provide higher grade evidence on the association of air pollution with GDM based on previous studies. PubMed, Web of science, China National Knowledge Infrastructure (CNKI), and Wanfang Data Knowledge Service Platform (Wanfang) were searched comprehensively up to September 2021. Totally, 20 eligible cohort studies were finally included, for which the pooled RR and 95% CIs were estimated. Stratified analyses by study regions and units of pollutant increase were conducted for further investigation. Sensitivity analyses were also performed to assess the robustness. The finding showed that PM2.5, PM10, NO2, and SO2 exposure increased the risk of GDM, while O3 exposure reduced GDM risk. Specifically, PM2.5 exposure in the first and second trimesters, NO2 and SO2 exposure in the first trimester significantly increased the risk of GDM, with the RR ranging from 1.015 to 1.032. In addition, the elevation of GDM risk induced by PM2.5, PM10, and O3 exposure was more pronounced in Asian subjects than in American subjects. The meta-analysis provides high-quality evidence on the effect of maternal air pollution exposure on GDM in each exposure period. [ABSTRACT FROM AUTHOR]

The emission sources and their health risks of fine particulate matter (PM2.5) in Siheung, Republic of Korea, were investigated as a middle-sized industrial city. To identify the PM2.5 sources with error estimation, a positive matrix factorization model was conducted using daily mean speciated data from November 16, 2019, to October 2, 2020 (95 samples, 22 chemical species). As a result, 10 sources were identified: secondary nitrate (24.3%), secondary sulfate (18.8%), traffic (18.8%), combustion for heating (12.6%), biomass burning (11.8%), coal combustion (3.6%), heavy oil industry (1.8%), smelting industry (4.0%), sea salts (2.7%), and soil (1.7%). Based on the source apportionment results, health risks by inhalation of PM2.5 were assessed for each source using the concentration of toxic elements portioned. The estimated cumulative carcinogenic health risks from the coal combustion, heavy oil industry, and traffic sources exceeded the benchmark, 1E-06. Similarly, carcinogenic health risks from exposure to As and Cr exceeded 1E-05 and 1E-06, respectively, needing a risk reduction plan. The non-carcinogenic risk was smaller than the hazard index of one, implying low potential for adverse health effects. The probable locations of sources with relatively higher carcinogenic risks were tracked. In this study, health risk assessment was performed on the elements for which mass concentration and toxicity information were available; however, future research needs to reflect the toxicity of organic compounds, elemental carbon, and PM2.5 itself. [ABSTRACT FROM AUTHOR]

Fine particulate matter organic extract (Po) was reported to promote inflammation in the lung. Sex differences were reported in many inflammatory diseases. In this study, we investigated the effects of Po exposure on pulmonary inflammatory response and evaluated the role of sex in this process. While mice were exposed to 100 µg/m3 Po for 12 weeks by an inhalation exposure system, the lung histopathological analysis shown obvious inflammation, the cell numbers in bronchoalveolar lavage fluid (BALF) were significantly increased, and most inflammatory cytokines in BALF were upregulated. The results of factorial analysis of variance shown that there was an interaction between sex and Po exposure in the inflammatory cell numbers and the levels of tumor necrosis factor-α (TNF-α), interleukin-5 (IL-5), and growth-related oncogene/keratinocyte chemoattractant (GRO/KC). Notably, these changes and interactions were diminished while Po-exposed mice were administered with the estrogen receptor β (ERβ) antagonist. We speculated that sex might affect the levels of inflammatory indicators in BALF of Po-exposed mice and female mice were more prone to inflammation while exposed to Po. Moreover, ERβ was involved in these processes. To our knowledge, this is the first investigation about the role of sex in Po-induced adverse effects. [ABSTRACT FROM AUTHOR]

Exposure to air pollution during prenatal or neonatal periods is associated with autism spectrum disorder (ASD) according to epidemiology studies. Furthermore, prenatal exposure to valproic acid (VPA) has also been found to be associated with an increased prevalence of ASD. To assess the association between simultaneous exposure to VPA and air pollutants, seven exposure groups of rats were included in current study (PM2.5 and gaseous pollutants exposed — high dose of VPA (PGE-high); PM2.5 and gaseous pollutants exposed — low dose of VPA (PGE-low); gaseous pollutants only exposed — high dose of VPA (GE-high); gaseous pollutants only exposed — low dose of VPA (GE-low); clean air exposed — high dose of VPA (CAE-high); clean air exposed — low dose of VPA (CAE-low) and clean air exposed (CAE)). The pollution-exposed rats were exposed to air pollutants from embryonic day (E0) to postnatal day 42 (PND42). In all the induced groups, decreased oxidative stress biomarkers, decreased oxytocin receptor (OXTR) levels, and increased the expression of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor alpha (TNF-α) were found. The volumes of the cerebellum, hippocampus, striatum, and prefrontal decreased in all induced groups in comparison to CAE. Additionally, increased numerical density of glial cells and decreased of numerical density of neurons were found in all induced groups. Results show that simultaneous exposure to air pollution and VPA can cause ASD-related behavioral deficits and air pollution reinforced the mechanism of inducing ASD ̉s in VPA-induced rat model of autism. [ABSTRACT FROM AUTHOR]

PM2.5 exposure can induce or exacerbate heart failure and is associated with an increased risk of heart failure hospitalization and mortality; however, the underlying mechanisms remain unclear. This study focuses on the potential mechanisms underlying PM2.5 induction of cardiomyocyte programmed necrosis as well as its promotion of cardiac function impairment in a mouse model of heart failure with preserved ejection fraction (HFpEF). HFpEF mice were exposed to concentrated ambient PM2.5 (CAP) (CAP group) or filtered air (FA) (FA group) for 6 weeks. Changes in myocardial pathology and cardiac function were documented for comparisons between the two groups. In vitro experiments were performed to measure oxidative stress and mitochondrial permeability transition pore (mPTP) dynamics in H9C2 cells following 24 h exposure to PM2.5. Additionally, co-immunoprecipitation was conducted to detect p53 and cyclophilin D (CypD) interactions. The results showed exposure to CAP promoted cardiac function impairment in HFpEF mice. Myocardial pathology analysis and in vitro experiments demonstrated that PM2.5 led to mitochondrial damage in cardiomyocytes and, eventually, their necrosis. Moreover, our experiments also suggested that PM2.5 increases mitochondrial reactive oxygen species (ROS), induces DNA oxidative damage, and decreases the inner mitochondrial membrane potential (ΔΨm). This indicates the presence of mPTP opening. Co-immunoprecipitation results showed a p53/CypD interaction in the myocardial tissue of HFpEF mice in the CAP group. Inhibition of CypD by cyclosporin A was found to reverse PM2.5-induced mPTP opening and H9C2 cell death. In conclusion, PM2.5 induces mPTP opening to stimulate mitochondria-mediated programmed necrosis of cardiomyocytes, and it might exacerbate cardiac function impairment in HFpEF mice. [ABSTRACT FROM AUTHOR]

To investigate the health effects of fine particulate matter (≤ 2.5 μm in aerodynamic diameter; PM2.5)-bound heavy metals and polycyclic aromatic hydrocarbons (PAHs) before and after the implementation of the Urban Natural Gas Heating Project (UNGHP), the lifetime cancer risks, hazard quotients (HQs) of heavy metals and PAHs were calculated. Seven kinds of heavy metals (Al, As, Cd, Cr, Mn, Ni and Se) and 12 kinds of PAHs including acenaphthylene (ANY), acenaphthene (ANA), fluoranthene (FLT), pyrene (PYR), chrysene (CHR), benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), benzo[a]pyrene (BaP), dibenz[a,h]anthracene (DBA), benzo[ghi]perylene (BPE) and indeno[1,2,3-cd]pyrene (IPY) were analyzed and used for the health risk assessments. It was found that HQ of Mn fell from 1.09 in the coal-burning period to 0.72 in the gas-burning period in the suburban area. And lifetime cancer risks of PAHs fell from 35.7 × 10–6 in the coal-burning period to 17.22 × 10–6 in the gas-burning period in the urban area. It could be concluded that, during the gas-burning period, downward trends were observed for the lifetime cancer risks and HQs of most kinds of heavy metals and PAHs in all regions of Tianjin compared to those during the coal-burning period. The UNGHP was effective, and we should also take other measures to control the pollution. [ABSTRACT FROM AUTHOR]

Studies have shown intriguing associations between gestational PM2.5 exposure and preeclampsia (PE), as well as fetal growth restriction (FGR). This study investigated the impact of PM2.5 exposure on gestational hypertension and fetal outcome in a preeclampsia-like rat model. Pregnant Sprague Dawley rats were exposed to either filtered (FA) or PM2.5-contaminated air during the whole pregnancy period. A PE-like rat model was established by intraperitoneal injection of L-NAME (300 mg/kg) from gestational day (GD) 12 to until GD20. Systolic blood pressure (SBP), weight gain, pup weight and placental weight were measured. The percentages of rat Treg/Th17 cells and Th17-related cytokines were examined by flow cytometry. Gene expression profiles were analyzed by microarray, and the expression of differentially expressed genes was validated by qRT-PCR. The results showed that maternal PM2.5 exposure had no effect on SBP but was associated with low birth weight (LBW) and a higher labyrinth/basal zone ratio. The percentages of splenic Th17 cells from the PM2.5 group of PE-like rats were higher than those from the FA or PM2.5 groups of healthy controls. A significantly decreased Treg/Th17 cell ratio was found in the PM2.5 group of PE-like rats. The mRNA expression of Foxp3 was downregulated, while the mRNA expression of RORα and RORγτ was upregulated after PM2.5 exposure. Furthermore, we observed that both the mRNA and protein levels of TNF-a, CCL2, CCL3 and CCR1 increased in the PM2.5 groups. Our study suggested that systemic inflammation may contribute to the development of FGR associated with PM2.5 exposure throughout pregnancy. [ABSTRACT FROM AUTHOR]

Background: Up until now, evidence pertaining to the short-term effects of fine particulate matter (PM2.5) in cardiovascular diseases (CVD) is scarce in China. In this study, we aim to estimate the association between short-term exposure to PM2.5 and hospitalizations for total and cause-specific CVD in Lanzhou of China. Methods: Daily counts of cardiovascular admissions were obtained from three large general hospitals in Lanzhou, China between 2014 and 2019. Air quality and meteorological data were obtained from the monitoring stations nearest to the admitting hospitals. We utilized Quasi-Poisson time-series regressions with distributed lag nonlinear models (DLNM) to assess the association between PM2.5 and CVD admitted in the three general hospitals. A stratified analysis was also conducted for age, sex, and disease subcategories. Results: PM2.5 was positively correlated with daily admissions for total or other cause-specific CVD under different lag patterns. For every 10 μg/m3 increase in the PM2.5 concentration, the relative risk of daily admissions for total CVD, ischemic heart disease (IHD), heart rhythm disturbances (HRD), heart failure (HF), and cerebrovascular disease (CD) was: 1.011 [95% confidence interval (CI), 1.001–1.020] in lag01; 1.020 (95% CI 1.004–1.036) in lag07; 1.013 (95% CI 1.001–1.026) in lag7; 1.018 (95% CI 1.005–1.038) in lag1; and 1.007 (95% CI 1.001–1.018) in lag1. Both low and high temperatures increased the risk of cardiovascular hospitalization. No differences were found after stratification by gender and age. We found an almost linear relationship between the exposure to PM2.5 and cause-specific CVD admissions with no threshold effect. Males as well as the elderly, aged ≥ 65 years, were more vulnerable to PM 2.5 exposure. Conclusions: Our results have demonstrated that PM2.5 has adverse impacts on cardiovascular hospitalizations in Lanzhou, especially on IHD. [ABSTRACT FROM AUTHOR]

High levels of ambient fine particulate matter (PM2.5) might increase the risk of death due to cardiovascular diseases (CVDs). As a critical risk factor for CVDs, dyslipidemia can cause CVDs or exacerbate pre-existing ones. This study aimed to investigate whether a short-time exposure to PM2.5 leads to dyslipidemia (HyperTC, HyperLDL-C, HyperTG and HypoHDL-C) in adults. The serum lipid data were provided by the Sichuan Provincial People's Hospital Medical Examination Center. We included 309,654 subjects aged 18–79 between May 10, 2015, and May 10, 2017. An advanced distributed lag nonlinear model (DLNM) was applied to investigate the acute and lag effects of ambient PM2.5 on the risk of dyslipidemia. This study was also stratified by sex, age, BMI and season to examine potential effect modification. We observed that the associations between an interquartile increase in PM2.5 (43 μg/m3) and dyslipidemia were [relative risk (RR); 95% confidence interval (CI)]: 1.042 (1.013, 1.071) for HyperLDL-C and 1.027 (1.006, 1.049) for HyperTC at lag0 day. The lag effects were found at lag6 day for HyperLDL-C, in lag4-6 days for HyperTC and lag4-7 days for HyperTG. Short-term exposure to ambient PM2.5 was related to dyslipidemia and the effect modification was observed in the subgroup analysis. The female and normal-weight populations were more susceptible to the risks of PM2.5 on HyperLDL-C and HyperTC. [ABSTRACT FROM AUTHOR]

Aim: This study seeks to examine changes in the mean annual exposure of PM2.5 air pollution from 1990 to 2000 and how they are associated with change in mortality due to tuberculosis, trachea/bronchus/lung cancer, respiratory diseases, and cardiovascular diseases from 2000 to 2016. A secondary goal of this study is to use spatial-temporal clustering to examine how PM2.5 trends differ across countries. Methods: The empirical work of this study is based on the World Bank Open Data and the World Health Organization's Global Health Observatory (GHO) Data Repository. Quantile regression and spatial-temporal cluster analysis are used to assess the aims of this study. Results: Findings from the quantile regression revealed that the number of deaths associated with these diseases differ according to the different levels of changes in PM2.5 concentration. Findings also reveal that countries assigned to different clusters are markedly different in terms of PM2.5 trends. Findings imply that air pollution inequality should be considered a factor in the elimination of health inequality. Conclusion: Efforts to integrate disease surveillance and control programs with those that reduce exposure to fine particulate matter, improve air quality, and increase people's awareness of the health implications of air pollution should be continued or encouraged. [ABSTRACT FROM AUTHOR]

Association between fine particulate matter (PM2.5) and respiratory health has attracted great concern in China. Substantial epidemiological evidences confirm the correlational relationship between PM2.5 and respiratory disease in many Chinese cities. However, the causative impact of PM2.5 on respiratory disease remains uncertain and comparative analysis is limited. This study aims to explore and compare the correlational relationship as well as the causal connection between PM2.5 and upper respiratory tract infection (URTI) in two typical cities (Beijing, Shenzhen) with rather different ambient air environment conditions. The distributed lag nonlinear model (DLNM) was used to detect the correlational relationship between PM2.5 and URTI by revealing the lag effect pattern of PM2.5 on URTI. The convergent cross mapping (CCM) method was applied to explore the causal connection between PM2.5 and URTI. The results from DLNM indicate that an increase of 10 μg/m3 in PM2.5 concentration is associated with an increase of 1.86% (95% confidence interval: 0.74%-2.99%) in URTI at a lag of 13 days in Beijing, compared with 2.68% (95% confidence interval: 0.99–4.39%) at a lag of 1 day in Shenzhen. The causality detection with CCM quantitatively demonstrates the significant causative influence of PM2.5 on URTI in both two cities. Findings from the two methods consistently show that people living in low-concentration areas (Shenzhen) are less tolerant to PM2.5 exposure than those in high-concentration areas (Beijing). In general, our study highlights the adverse health effects of PM2.5 pollution on the general public in cities with various PM2.5 levels and emphasizes the needs for the government to provide appropriate solutions to control PM2.5 pollution, even in cities with low PM2.5 concentration. [ABSTRACT FROM AUTHOR]

Exposure to fine particulate matter (PM2.5) is associated with asthma development as well as asthma exacerbation in children. PM2.5 can be directly emitted or can form in the atmosphere from pollutant precursors. PM2.5 emitted and formed in the atmosphere is influenced by meteorology; future changes in climate may alter the concentration and distribution of PM2.5. Our aim is to estimate the future burden of climate change and PM2.5 on new and exacerbated cases of childhood asthma. Projected concentrations of PM2.5 are based on the Geophysical Fluid Dynamics Laboratory Coupled Model version 3 climate model, the Representative Concentration Pathway 8.5 greenhouse gas scenario, and two air pollution emissions datasets: a 2011 emissions dataset and a 2040 emissions dataset that reflects substantial reductions in emissions of PM2.5 as compared to the 2011 inventory. We estimate additional PM2.5-attributable asthma as well as PM2.5-attributable albuterol inhaler use for four future years (2030, 2050, 2075, and 2095) relative to the year 2000. Exacerbations, regardless of the trigger, are counted as attributable to PM2.5 if the incident disease is attributable to PM2.5. We project 38 thousand (95% CI 36, 39 thousand) additional PM2.5-attributable incident childhood asthma cases and 29 million (95% CI 27, 31 million) additional PM2.5-attributable albuterol inhaler uses per year in 2030, increasing to 200 thousand (95% CI 190, 210 thousand) additional incident cases and 160 million (95% CI 150, 160 million) inhaler uses per year by 2095 relative to 2000 under the 2011 emissions dataset. These additional PM2.5-attributable incident asthma cases and albuterol inhaler use would cost billions of additional U.S. dollars per year by the late century. These outcomes could be mitigated by reducing air pollution emissions. [ABSTRACT FROM AUTHOR]

Air pollution is a serious threat to ancient sites and cultural relicts. In this study, we collected indoor and outdoor PM2.5 samples and individual particles at the Exhibition Hall of Jinsha Site Museum in June 2020, and then the chemical components, sources, morphology, and mixing state of the fine particulate matter were analyzed. Our results show that the indoor and outdoor PM2.5 concentrations at the Exhibition Hall were 33.3±6.6 and 39.4±11.4 μg m−3, respectively. Although the indoor and outdoor concentrations of OC and EC were close, the proportion of secondary organic carbon in OC outdoor (33%) was higher than that indoor (27%). The PM2.5 was alkaline both indoors and outdoors, and the outdoor alkalinity was stronger than the indoor alkalinity. SNA (SO42−, NO3−, and NH4+) was the dominant component in the water-soluble inorganic ions; Na+, Mg2+, and Ca2+ were well correlated (R2> 0.9), and Cl− and K+ were also highly correlated (R2> 0.8). Enrichment factor analysis showed that Cu (indoor) and Cd were the main anthropogenic elements and that Cd was heavily enriched. Principal components analysis showed that the main sources of PM2.5 at Jinsha Site Museum were motor vehicles, dust, secondary sources, and combustion sources. The individual particles were classified as organic matter, S-rich, soot, mineral, and fly ash/metal particles, and most of these particles were internally mixed with each other. At last, we proposed pollution control measures to improve the air quality of museums and the preservation of cultural relicts. [ABSTRACT FROM AUTHOR]

Since mobile sources are one of the most important sources of air pollution, this paper tries to estimate the health effects and economic burden due to fine particulate matter (PM2.5) concentrations from motor vehicles. In this regard, we calculate the economic costs of air pollution emitted by vehicles in Isfahan over the period from March 2018 to March 2020. The concentration of urban traffic pollution based on the generalized additive model (GAM) as well as spatial distribution of pollution is estimated. Health effects are evaluated using AirQ+ updated by the WHO European Centre for Environment and Health. Economic burden of mortality attributable air pollution from traffic is calculated using value of a statistical life (VOSL), and the value of life years (VOLY) approach. The results indicated that the number of deaths attributable to PM2.5 from motor vehicles in these two consecutive years was 136 (95%CI: 89–179), and 147 cases (95%CI: 96–194), respectively. The number of years of life lost due to premature death from air pollution was 2079 years annually. The economic costs imposed under VOSL approach were on average USD 51.7 (95%CI: 43–75) million per year, and according to VOLY approach USD 11.5 (95%CI: 9–13) million per year. These results help to analyze the cost-benefit and prioritize control measures to reduce air pollution. In addition, combination of these results with other externality cost of road traffic can take account for urban transportation planning. [ABSTRACT FROM AUTHOR]

The cardiovascular impact of fine particles has caused great concern worldwide. However, evidences on the impact of fine particulate matter (PM2.5) on emergency department (ED) admissions for circulatory system disease in Northeast China is limited. We assessed the acute, lag, cumulative, and harvesting effects of PM2.5 on ED admissions for circulatory system diseases and their exposure-response relationship. A total of 26,168 ED admissions, including those for hypertension, ischemic heart disease (IHD), arrhythmia, heart failure (HF), and cerebrovascular events (CVE), were collected from the Shenyang Emergency Center from 1 January 2017 to 31 December 2018. The relationship between PM2.5 and ED admissions for circulatory system disease was estimated using a distributed lag non-linear model and a generalized additive quasi-Poisson model. We stratified the analyses by temperature. Air pollution was positively correlated with daily ED admissions for circulatory system disease or other cause-specific diseases under different lag structures. For every 10-μg/m3 increase in the PM2.5 concentration, the relative risk of daily ED admissions for circulatory system disease was 1.007 [95% confidence interval (CI), 1.001–1.013] in lag0, 1.007 (95%CI, 1.000–1.013) in lag1, and 1.011 (95%CI, 1.002–1.021) in lag03. A lag effect was found in IHD, a cumulative effect was found in CVE, and both lag and cumulative effects were found in hypertension and arrhythmia. A harvesting effect was observed in daily ED admissions for circulatory system disease and HF. We found no interaction between pollutants and temperature. We observed a monotonic and almost linear exposure-response relationship between PM2.5 and circulatory system disease with no threshold effect.PM2.5 contributes to obvious acute, lag, cumulative, and harvesting effects on circulatory system disease. PM2.5 was associated with the risk of daily ED admissions for circulatory system disease, hypertension, IHD, arrhythmia, HF, and CVE. Therefore, air quality management must be strengthened. [ABSTRACT FROM AUTHOR]

Due to the rapid economic development and acceleration of industrialization, most cities in China are experiencing severe air pollution. Exposure to fine particulate matter (PM2.5) has been associated with acute lower respiratory tract infection (ALRI). To estimate associations between short-term exposure to PM2.5 and ALRI hospitalization in Yancheng City, China. This was a 6-year time-series study from 2014 to 2019. Data on hospitalization were collected from four high-ranked general hospitals, including for community-acquired pneumonia (CAP), acute exacerbation of chronic bronchitis (AECB), acute exacerbation of chronic obstructive pulmonary disease (AECOPD), and acute exacerbation of bronchiectasis (AEB), and the sum was termed total ALRIs. We obtained pollutant exposure data from five fixed monitoring stations. The association between PM2.5 and ALRI hospitalization was estimated using the generalized linear model with quasi-Poisson regression. Two-pollutant models were applied to test the robustness of the observed correlations. Subgroup analyses included sex, age, and season. During the study period, a total of 43,283 cases of total ALRIs were recorded. The average annual mean PM2.5 concentration was 45.4 ± 32.3 μg/m3. A 10-μg/m3 increase in PM2.5 concentration (lag 0) was significantly associated with increases in hospitalizations for total ALRIs (at 0.73%; 95% CI: 0.40%, 1.06%), in CAP (at 0.80%; 95% CI: 0.02%, 1.57%), in for AECOPD (1.08%; 95% CI: 0.38%, 1.78%), and AECB (0.67%; 95% CI: 0.23%, 1.11%). The estimated effects for total ALRIs and AECB were relatively robust with adjustment for other air pollutants. Associations between PM2.5 and total ALRIs were stronger in females, in the elderly, and in the cold season. PM2.5 exposure was significantly associated with ALRI morbidity, and females and older people were more susceptible to PM2.5 air pollution, especially in the cold season. [ABSTRACT FROM AUTHOR]