Adverse Health Effects Of PM2 Research Articles

Developmental Toxicity of Fine Particulate Matter: Multifaceted Exploration from Epidemiological and Laboratory Perspectives.

Particulate matter of size ≤ 2.5 μm (PM2.5) is a critical environmental threat that considerably contributes to the global disease burden. However, accompanied by the rapid research progress in this field, the existing research on developmental toxicity is still constrained by limited data sources, varying quality, and insufficient in-depth mechanistic analysis. This review includes the currently available epidemiological and laboratory evidence and comprehensively characterizes the adverse effects of PM2.5 on developing individuals in different regions and various pollution sources. In addition, this review explores the effect of PM2.5 exposure to individuals of different ethnicities, genders, and socioeconomic levels on adverse birth outcomes and cardiopulmonary and neurological development. Furthermore, the molecular mechanisms involved in the adverse health effects of PM2.5 primarily encompass transcriptional and translational regulation, oxidative stress, inflammatory response, and epigenetic modulation. The primary findings and novel perspectives regarding the association between public health and PM2.5 were examined, highlighting the need for future studies to explore its sources, composition, and sex-specific effects. Additionally, further research is required to delve deeper into the more intricate underlying mechanisms to effectively prevent or mitigate the harmful effects of air pollution on human health.

Mixed Metal Components in PM2.5 Contribute to Chemokine Receptor CCR5-Mediated Neuroinflammation and Neuropathological Changes in the Mouse Olfactory Bulb.

Particulate matter, especially PM2.5, can invade the central nervous system (CNS) via the olfactory pathway to induce neurotoxicity. The olfactory bulb (OB) is the key component integrating immunoprotection and olfaction processing and is necessarily involved in the relevant CNS health outcomes. Here we show that a microglial chemokine receptor, CCR5, is the target of environmentally relevant PM2.5 in the OB to trigger neuroinflammation and then neuropathological injuries. Mechanistically, PM2.5-induced CCR5 upregulation results in the pro-inflammatory paradigm of microglial activation, which subsequently activates TLR4-NF-κB neuroinflammation signaling and induces neuropathological changes that are closely related to neurodegenerative disorders (e.g., Aβ deposition and disruption of the blood-brain barrier). We specifically highlight that manganese and lead in PM2.5 are the main contributors to CCR5-mediated microglial activation and neuroinflammation in synergy with aluminum. Our results uncover a possible pathway of PM2.5-induced neuroinflammation and identify the principal neurotoxic components, which can provide new insight into efficiently diminishing the adverse health effects of PM2.5.

PM2.5-induced DNA oxidative stress in A549 cells and regulating mechanisms by GST DNA methylation and Keap1/Nrf2 pathway

Fine particulate matter (PM2.5) increases the risks of lung cancer. Epigenetics provides a new toxicology mechanism for the adverse health effects of PM2.5. However, the regulating mechanisms of PM2.5 exposure on candidate gene DNA methylation changes in the development of lung cancer remain unclear. Abnormal expression of the glutathione S transferase (GST) gene is associated with cancer. However, the relationship between PM2.5 and DNA methylation-mediated GST gene expression is not well understood. In this study, we performed GST DNA methylation analysis and GST-related gene expression in human A549 cells exposed to PM2.5 (0, 50, 100 µg/mL, from Taiyuan, China) for 24 h (n = 4). We found that PM2.5 may cause DNA oxidative damage to cells and the elevation of GSTP1 promotes cell resistance to reactive oxygen species (ROS). The Kelch-1ike ECH-associated protein l (Keap1)/nuclear factor NF-E2-related factor 2 (Nrf2) pathway activates the GSTP1. The decrease in the DNA methylation level of the GSTP1 gene enhances GSTP1 expression. GST DNA methylation is associated with reduced levels of 5-methylcytosine (5mC), DNA methyltransferase 1 (DNMT1), and histone deacetylases 3 (HDAC3). The GSTM1 was not sensitive to PM2.5 stimulation. Our findings suggest that PM2.5 activates GSTP1 to defend PM2.5-induced ROS and 8-hydroxy-deoxyguanosine (8-OHdG) formation through the Keap1/Nrf2 signaling pathway and GSTP1 DNA methylation.

Systematic Evaluation of Four Satellite AOD Datasets for Estimating PM2.5 Using a Random Forest Approach

The latest epidemiological studies have revealed that the adverse health effects of PM2.5 have impacts beyond respiratory and cardio-vascular diseases and also affect the development of the brain and metabolic diseases. The need for accurate and spatio-temporally resolved PM2.5 data has thus been substantiated. While the selective information provided by station measurements is mostly insufficient for area-wide monitoring, satellite data have been increasingly applied to comprehensively monitor PM2.5 distributions. Although the accuracy and reliability of satellite-based PM2.5 estimations have increased, most studies still rely on a single sensor. However, several datasets have become available in the meantime, which raises the need for a systematic analysis. This study presents the first systematic evaluation of four satellite-based AOD datasets obtained from different sensors and retrieval methodologies to derive ground-level PM2.5 concentrations. We apply a random forest approach and analyze the effect of the resolution and coverage of the satellite data and the impact of proxy data on the performance. We examine AOD data from the Moderate resolution Imaging spectroradiometer (MODIS) onboard Terra and Aqua satellites, including Dark Target (DT) algorithm products and the Multi-Angle Implementation of Atmospheric Correction (MAIAC) product. Additionally, we explore more recent datasets from the Sea and Land Surface Temperature Radiometer (SLSTR) onboard Sentinel-3a and from the Tropospheric Monitoring Instrument (TROPOMI) operating on the Sentinel-5 precursor (S5p). The method is demonstrated for Germany and the year 2018, where a dense in situ measurement network and relevant proxy data are available. Overall, the model performance is satisfactory for all four datasets with cross-validated R2 values ranging from 0.68 to 0.77 and excellent for MODIS AOD reaching correlations of almost 0.9. We find a strong dependency of the model performance on the coverage and resolution of the AOD training data. Feature importance rankings show that AOD has less weight compared to proxy data for SLSTR and TROPOMI.

Independent risk evaluation associated with short-term black carbon exposure on mortality in two megacities of Yangtze River Delta, China

The adverse health effects of PM2.5 have been well demonstrated by many studies. However, as a component of PM2.5, evidence on the mortality risk of black carbon (BC) is still limited. In this study, based on the data of daily mean PM2.5 concentration, BC concentration, meteorological factors, total non-accidental (all-cause) and cardiovascular mortality in Shanghai and Nanjing during 2015–2016, a semi-parameter generalized additive model (GAM) in the time series and the constituent residual approach were employed to explore the exposure-response relationship between BC and human mortality in these two megacities of Yangtze River Delta, China. The main objective was to separate the health effects of BC from total PM2.5, and compare the difference of mortality ER related to BC original concentration and adjusted concentration after controlling PM2.5. Results showed that there were all significantly associated with daily mortality for PM2.5 and BC. The percentage excess risk (ER) increases in all-cause and cardiovascular categories were 1.68 % (95 % s 1.28, 2.08) and 2.16 % (95 % CI: 1.54, 2.79) with 1 μg/m3 increment in original BC concentration in Shanghai. And the ER in Nanjing was smaller than that in Shanghai. After eliminating PM2.5 confounding effects by a constituent residual approach, the BC residual concentration still had a strong significant ER. The ER for BC residual in Shanghai got an obvious increase, and ER of the cardiovascular mortality for all, females and males increased by 0.55 %, 1.46 % and 0.62 %, respectively, while the ER in Nanjing decreased slightly. It also revealed that females were more sensitive to the health risk associated with short-term BC exposure than males. Our findings provide additional important evidence and ER for mortality related to independent BC exposure. Therefore, BC emission reduction should be paid more attention in air pollution control strategies to reduce BC-related health burdens.

Prenatal exposure to PM2.5 and childhood cognition: Accounting for between-site heterogeneity in a pooled analysis of ECHO cohorts in the Northeastern United States

BackgroundEmerging studies have investigated the adverse health effects of PM2.5 using data from multiple cohorts, and results often are not generalizable across cohorts. We aimed to assess associations between prenatal PM2.5 and childhood cognition in two U.S. cohorts while accounting for between-site heterogeneity. MethodsAnalyses included 348 mother-child dyads enrolled in the dual site (New York City and Boston) PRogramming of Intergenerational Stress Mechanisms (PRISM) cohort and in the First Thousand Days of Life (FTDL) study (Northern Virginia) participating in the Environmental influences on Child Health Outcomes (ECHO) national consortium. Residential prenatal PM2.5 exposure was estimated using a validated satellite-based model and childhood cognition was measured using the NIH Toolbox Cognition Battery at three to eight years of age. We used a log-linear model applied to contingency tables formed by cross-classifying covariates by site to examine between-site heterogeneity using 3rd trimester PM2.5 exposure, age-corrected cognition scores, and covariates potentially causing heterogeneities. Multivariable linear regression models informed by the combinability analysis were used to estimate the coefficients and 95% confidence intervals (CIs) for the association between 3rd trimester PM2.5 exposure and age-corrected cognition scores (mean = 100, SD = 15). ResultsThe log-linear model indicated that inter-study associations were similar between PRISM-NYC and FTDL, which were different from those in PRISM-Boston. Accordingly, we combined the data of PRISM-NYC and FTDL cohorts. We observed associations between 3rd trimester PM2.5 and cognition scores, findings were varying by site, childsex, and test. For example, a 1 μg/m3 increase of 3rd trimester PM2.5 was associated with −4.35 (95% CI = −8.73, −0.25) mean early childhood cognition scores in females in PRISM-Boston. In the pooled NYC + FTDL site, the association between PM2.5 and childhood cognition may be modified by maternal education and urbanicity. ConclusionsWe found associations between prenatal PM2.5 and impaired childhood cognition. Since multi-site analyses are increasingly conducted, our findings suggest the needed awareness of between-site heterogeneity.

Chemical composition, oxidative potential and identifying the sources of outdoor PM2.5 after the improvement of air quality in Beijing.

Air pollution poses a serious threat to human health. The implementation of air pollution prevention and control policies has gradually reduced the level of atmospheric fine particles in Beijing. Exploring the latest characteristics of PM2.5 has become the key to further improving pollution reduction measures. In the current study, outdoor PM2.5 samples were collected in the spring and summer of Beijing, and the chemical species, oxidative potential (OP), and sources of PM2.5 were characterized. The mean PM2.5 concentration during the entire study period was 41.6 ± 30.9μgm-3. Although the PM2.5 level in summer was lower, its OP level was significantly higher than that in spring. SO42-, NH4+, EC, NO3-, and OC correlated well with volume-normalized OP (OPv). Strong positive correlations were found between OPv and the following elements: Cu, Pb, Zn, Ni, As, Cr, Sn, Cd, Al, and Mn. Seven sources of PM2.5 were identified, including traffic, soil dust, secondary sulfate, coal and biomass burning, oil combustion, secondary nitrate, and industry. Multiple regression analysis indicated that coal and biomass combustion, industry, and traffic were the main contributors to the OPv in spring, while secondary sulfate, oil combustion, and industry played a leading role in summer. The source region analysis revealed that different pollution sources were related to specific geographic distributions. In addition to local emission reduction policies, multi-provincial cooperation is necessary to further improve Beijing's air quality and reduce the adverse health effects of PM2.5.

Sensitive inflammatory biomarkers of acute fine particulate matter exposure among healthy young adults: Findings from a randomized, double-blind crossover trial on air filtration

The short-term alteration of peripheral cytokines may be an early adverse health effect of PM2.5 exposure and may be further associated with cardiovascular disease. We conducted a randomized, double-blind crossover trial using true or sham air filtration among 54 healthy college students in Beijing to investigate the potential benefits of short-term indoor air filtration and the adverse health effects of time-weighted personal PM2.5 exposure through inflammatory cytokines. The participants randomly received true or sham air filtration intervention for a week, and the treatment was changed after a two-week washout period. Peripheral blood samples were collected after each intervention period to measure 38 inflammatory cytokines. A linear mixed-effects model was applied to estimate the impacts of air purification or a 10 μg/m3 PM2.5 exposure increase on cytokines. Lag effects of PM2.5 exposure were analyzed using single-day and moving average lag models. Air filtration reduced indoor and time-weighted average personal PM2.5 concentrations by 69.0% (from 33.6 to 10.4 μg/m3) and 40.3% (from 40.6 to 24.3 μg/m3), respectively. We observed a significant association of PM2.5 exposure with growth-regulated alpha protein (GRO-α) of −11.3% (95%CI: 17.0%, −5.4%). In the lag models, significant associations between personal PM2.5 exposure and interleukin-1 receptor antagonist (IL-1Ra), monocyte chemotactic protein (MCP-1), and eotaxin were obtained at lag0, while associations with cytokines including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1β (MIP-1β), IL-4, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) were noted at relatively long lagged exposure windows (lag5-lag6). No significant alteration in cytokines was observed under true air filtration intervention. Our study indicates the effectiveness of air filtration on indoor PM2.5 reduction. PM2.5 exposure may decrease GRO-α levels and change different cytokine levels time-varyingly. Further study is still needed to explore the mechanisms of PM2.5 exposure on the inflammatory response.

Child Survival and Early Lifetime Exposures to Ambient Fine Particulate Matter in India: A Retrospective Cohort Study.

Background:Ambient fine particulate matter [PM in aerodynamic diameter ()] is a major health risk for children, particularly in South Asia, which currently experiences the highest levels globally. Nevertheless, there is comparatively little epidemiological evidence from this region to quantify the effects of on child survival.Objectives:We estimated the association between exposure and child survival in India.Methods:We constructed a large, retrospective, and nationally representative cohort of children , born between 2009–2016, from the publicly available, cross-sectional 2015–2016 Demographic Health Surveys in India. In utero and post-delivery lifetime average ambient exposures were estimated with data from satellite remote sensing, meteorology, and land use information (model 0.82). We used Cox proportional hazards regression to estimate the association between both average in utero and post-delivery lifetime and all-cause child mortality, controlling for individual- and household-level covariates, seasonality, location, and meteorology.Results:Over 7,447,724 child-months of follow-up, there were 11,559 deaths at reported by the children’s mothers. The mean concentrations of 9-month in utero and post-delivery lifetime average ambient exposure were (range: ) and (range: ), respectively. Estimated child mortality adjusted hazard ratios were 1.023 [95% confidence interval (CI): 1.008, 1.038] and 1.013 (95% CI: 1.001, 1.026) per increase of in utero and post-delivery lifetime , with both exposures in the model.Discussion:This study adds to the growing body of evidence about the adverse health effects of by demonstrating the association between exposure, both in utero and post-delivery, on child survival at the national level in India. Strategies to reduce ambient air pollution levels, including steps to minimize in utero and early life exposures, are urgently needed in India and other countries where exposures are above recommended guideline values. https://doi.org/10.1289/EHP8910

Effects of Interaction between PM2.5 and O 3 8-h max on Mortality of Cardiovascular Diseases in Chengdu

To explore the health risks of the interactive effects between PM2.5 and ozone on cardiovascular mortality in Chengdu. Daily data on the mortality of cardiovascular diseases, including data for both men and women, during 2014-2016 were collected. The meteorological data, the daily average of particulate matter with aerodynamic diameter less than 2.5 micrometers (PM2.5), and the daily ozone 8 h maximum concentration (O 3 8-h max) in Chengdu of the same period were also collected. Generalized Additive Models (GAMs) were adopted to explore the respective adverse health effects of PM2.5 and O 3 8-h max and the synergistic effects between PM2.5 and O 3 8-h max on the mortality of cardiovascular diseases in the city. The highest health risks of PM2.5 and O 3 8-h max for mortality of cardiovascular diseases were found to be the strongest for the cumulative effect of the lag of one day (lag01). For every 10 µg/m 3 increment in the mass concentration of PM2.5 (lag01), the associated increase in risks for total, male, and female cardiovascular mortalities was 0.35%, 0.26% and 0.38%, respectively. For every 10 µg/m 3 increment in the mass concentration of O 3 8-h max (lag01), the associated increase in risks for total, male, and female cardiovascular mortalities was 0.66%, 0.43%, and 1.05%, respectively. The total, male, and female cardiovascular mortalities all reached their maximum values when high concentration of PM2.5 coexisted with high concentrations of O 3 8-h max. There was a synergistic amplification effect between high concentrations of PM2.5 and high concentrations of O 3 8-h max on cardiovascular mortality.

Observed causative impact of fine particulate matter on acute upper respiratory disease: a comparative study in two typical cities in China.

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.

The impact of organic extracts of seasonal PM2.5 on primary human lung epithelial cells and their chemical characterization

Lung epithelial cells serve as the first line of defense against various inhaled pollutant particles. To investigate the adverse health effects of organic components of fine particulate matter (PM2.5) collected in Seoul, South Korea, we selected 12 PM2.5 samples from May 2016 to January 2017 and evaluated the effects of organic compounds of PM2.5 on inflammation, cellular aging, and macroautophagy in human lung epithelial cells isolated directly from healthy donors. Organic extracts of PM2.5 specifically induced neutrophilic chemokine and interleukin-8 expression via extracellular signal-regulated kinase activation. Moreover, PM2.5 significantly increased the expression of aging markers (p16, p21, and p27) and activated macroautophagy. Average mass concentrations of organic and elemental carbon had no significant correlations with PM2.5 effects. However, polycyclic aromatic hydrocarbons and n-alkanes were the most relevant components of PM2.5 that correlated with neutrophilic inflammation. Vegetative detritus and residential bituminous coal combustion sources strongly correlated with neutrophilic inflammation, aging, and macroautophagy activation. These data suggest that the chemical composition of PM2.5 is important for determining the adverse health effects of PM2.5. Our study provides encouraging evidence to regulate the harmful components of PM2.5 in Seoul.

Is Urbanization Good for the Health of Middle-Aged and Elderly People in China?—Based on CHARLS Data

The purpose of this paper is to test whether improved healthcare services can mitigate health hazards resulting from environmental pollution in the urbanization process. Specifically, using China Health and Retirement Longitudinal Study (CHARLS) data and official statistics, this paper constructs comprehensive urbanization indicators and healthcare service indicators by applying the fully arrayed polygonal graphical indication method. Then, we introduce healthcare service indicators, urbanization indicators, environmental pollution indicators, and the interaction term between environmental pollution and healthcare into an ordered-logistics regression model. Our results indicate that improvement in health conditions can decrease the health risks from multiplied emissions of industrial sulfur dioxide, industrial soot and dust, and industrial effluents, but it cannot counteract the adverse health effects of PM2.5. Furthermore, heterogeneity tests show that, when considering the multidimensionality of urbanization, the positive influence of healthcare is the greatest in residential surroundings urbanization and economic urbanization, which reduces the prevalence of chronic diseases by 18.4% and 14.9%, respectively. Among the diverse city types, mixed-economy cities have the most obvious positive effects, where healthcare has the greatest mitigating effect on the health damage caused by industrial sulfur dioxide and industrial soot and dust, decreasing the prevalence of chronic diseases among the middle-aged and elderly by 27.3% and 16.4%, respectively. When considering the regional impacts of urbanization, there is a large difference in the positive effects brought about by medical care, which is reflected mainly in eastern and western China. In eastern China, although healthcare does not offset the health damage of PM2.5, the increase in chronic diseases among the middle-aged and elderly is only 0.5%, while in western China, the increase rises to 22.4%.

Melatonin ameliorates PM2.5 -induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis.

Fine particulate matter (PM2.5) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM2.5 exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM2.5‐accelerated cardiac fibrosis. The echocardiography revealed that PM2.5 had impaired both systolic and diastolic cardiac function in ApoE−/− mice. Histopathological analysis demonstrated that PM2.5 induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM2.5‐induced cardiac dysfunction and fibrosis in mice. Results of electron microscopy and confocal scanning laser microscope confirmed that melatonin had restorative effects against impaired mitochondrial ultrastructure and augmented mitochondrial ROS generation in PM2.5‐treated group. Further investigation revealed melatonin administration could significantly reverse the PM2.5‐induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM2.5‐induced cardiac dysfunction and fibrosis via inhibiting mitochondrial oxidative injury and regulating SIRT3‐mediated SOD2 deacetylation. Our findings indicate that melatonin could be a therapy medicine for prevention and treatment of air pollution‐associated cardiac diseases.

Pollutants from primary sources dominate the oxidative potential of water-soluble PM2.5 in Hong Kong in terms of dithiothreitol (DTT) consumption and hydroxyl radical production

Increasing scientific findings show that the adverse health effects of PM2.5 are related not only to its mass but also PM2.5 sources and chemical compositions. Here, we conducted a comprehensive characterization and source apportionment of oxidative potential (OP) of water-soluble PM2.5 collected in Hong Kong for one year. Two OP indicators, namely dithiothreitol (DTT) consumption and ∙OH formation, were quantified. Six PM2.5 sources, i.e. secondary sulfate, biomass burning, secondary organic aerosol (SOA), vehicle emissions, marine vessels, and a metal-related factor, were apportioned and identified to be DTT active. The four primary sources accounted for 83.5% of DTT activity of water-soluble PM2.5, with the metal-related factor and marine vessels as the leading contributors. However, only three sources, i.e. metal-related factor, vehicle emissions, and SOA, showed ∙OH generation ability, with a predominant contribution of 96.2% from the two primary sources, especially the metal-related factor (84.5%). Based on the source apportionment results, we further evaluate the intrinsic OP of water-soluble PM2.5 from each source. Marine vessels exhibited the highest intrinsic DTT activity; while metal-related factor was most effective in ∙OH generation.

Identification of Toxicity Parameters Associated with Combustion Produced Soot Surface Chemistry and Particle Structure by in Vitro Assays.

Air pollution has become the world’s single biggest environmental health risk of the past decade, causing millions of yearly deaths worldwide. One of the dominant air pollutants is fine particulate matter (PM2.5), which is a product of combustion. Exposure to PM2.5 has been associated with decreased lung function, impaired immunity, and exacerbations of lung disease. Accumulating evidence suggests that many of the adverse health effects of PM2.5 exposure are associated with lung inflammation and oxidative stress. While the physical structure and surface chemistry of PM2.5 are surrogate measures of particle oxidative potential, little is known about their contributions to negative health effects. In this study, we used functionalized carbon black particles as surrogates for atmospherically aged combustion-formed soot to assess the effects of PM2.5 surface chemistry in lung cells. We exposed the BEAS-2B lung epithelial cell line to different soot at a range of concentrations and assessed cell viability, inflammation, and oxidative stress. Our results indicate that exposure to soot with varying particle surface composition results in differential cell viability rates, the expression of pro-inflammatory and oxidative stress genes, and protein carbonylation. We conclude that particle surface chemistry, specifically oxygen content, in soot modulates lung cell inflammatory and oxidative stress responses.

Biotoxic effects and gene expression regulation of urban PM2.5 in southwestern China

Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical composition, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1 (PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In particular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regulatory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu winter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5; and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contributes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.

The Effects of Air Pollution on Labor Supply in Japan: A Panel Data Analysis based on PM <sub>2.5</sub> Pollution and Labor Data

We empirically examine how fine particulate matter (PM2.5) pollution affects labor supply in Japan. The effects of PM2.5 pollution could be mixed. While adverse health effects of PM2.5 pollution can lead to reduced labor supply, workers can rather increase labor supply if their productivity decreases. Changes in labor demand, such as shortened operation, or lack thereof, can also affect an equilibrium labor supply. Our aim is to discuss whether and how these effects overall affect labor supply in a country with moderate levels of pollution. We use a monthly panel dataset covering entire Japan in 2013–2017 and comprising the labor supply and PM2.5 pollution monitoring data. We employ a fixed-effects framework and use precipitation as an instrument to identify the effect of PM2.5 pollution. The results show that a μg/m3-increase in the PM2.5 pollution level reduces monthly labor hours and days. However, average labor hours per labor day increases with pollution. Further, firms in certain service sectors appear to maintain labor input and this offsets the workers’ decisions to reduce labor supply. Nevertheless, these behaviors do not fully cancel out the total labor supply loss.

Acute effect of daily fine particulate matter pollution on cerebrovascular mortality in Shanghai, China: a population-based time series study

Numerous studies have investigated the impacts of ambient fine particulate matter (PM2.5) on human health. In this study, we examined the association of daily PM2.5 concentrations with the number of deaths for the cerebrovascular disease on the same day, using the generalized additive model (GAM) controlling for temporal trend and meteorological variables. We used the data between 2012 and 2014 from Shanghai, China, where the adverse health effects of PM2.5 have been of particular concern. Three different approaches (principal component analysis, shrinkage smoothers, and the least absolute shrinkage and selection operator regularization) were used in GAM to handle multicollinear meteorological variables. Our results indicate that the average daily concentration of PM2.5 in Shanghai was high, 55 μg/m3, with an average daily death for cerebrovascular disease (CVD) of 62. There was 1.7% raised cerebrovascular disease deaths per 10 μg/m3 increase in PM2.5 concentration in the unadjusted model. However, PM2.5 concentration was no longer associated with CVD deaths after controlling for meteorological variables. The results were consistent in the three modelling techniques that we used. As a large number of people are exposed to air pollution, further investigation with longer time period including individual-level information is needed to examine the association.

Pollution characteristics and risk assessment of ambient PM2.5-bound PAHs and NPAHs in typical Japanese and New Zealand cities and rural sites

Nine polycyclic aromatic hydrocarbons (PAHs) and six nitro-PAHs (NPAHs) were measured in PM2.5 samples collected over one year (2016–2017) in two cities: Kanazawa (Japan) and Auckland (New Zealand) and their respective rural background sites: Wajima in Noto Peninsula (Japan) and Tapora in Okahukura Peninsula (New Zealand). The mean concentrations of ΣPAHs and ΣNPAHs followed similar distribution profiles in both countries, with higher concentrations in the urban than rural sites. The mean of ΣPAHs in Kanazawa City was 0.53 ng/m3 and represented the highest total concentration compared to the other three sites. Conversely, the highest ΣNPAHs concentrations were measured in Auckland City (48.2 pg/m3). Diagnostic ratios and principal component analysis revealed that automobiles were the main sources of PAHs and NPAHs in both cities, whereas coal combustion and domestic wood burning were the dominant sources of PAHs and NPAHs in rural sites in Japan and New Zealand. Back trajectory analyses showed that high levels of PAHs detected at Wajima were the result of long-range transport from China and Mongolia in winter, which was not observed at the other sites. Considering the adverse health effects of PM2.5, further studies and continuous monitoring of atmospheric PAHs and NPAHs are necessary to evaluate mitigation strategies in both hemispheres.