Passage of exogeneous fine particles from the lung into the brain in humans and animals.

There are still significant knowledge gaps in understanding the intrusion and retention of exogeneous particles into the central nervous system (CNS). Here, we uncovered various exogeneous fine particles in human cerebrospinal fluids (CSFs) and identified the ambient environmental or occupational exposure sources of these particles, including commonly found particles (e.g., Fe- and Ca-containing ones) and other compositions that have not been reported previously (such as malayaite and anatase TiO2), by mapping their chemical and structural fingerprints. Furthermore, using mouse and in vitro models, we unveiled a possible translocation pathway of various inhaled fine particles from the lung to the brain through blood circulation (via dedicated biodistribution and mechanistic studies). Importantly, with the aid of isotope labeling, we obtained the retention kinetics of inhaled fine particles in mice, indicating a much slower clearance rate of localized exogenous particles from the brain than from other main metabolic organs. Collectively, our results provide a piece of evidence on the intrusion of exogeneous particles into the CNS and support the association between the inhalation of exogenous particles and their transport into the brain tissues. This work thus provides additional insights for the continued investigation of the adverse effects of air pollution on the brain.

The cross-linking between DNA damage, oxidative stress and epidermal barrier in keratinocytes after exposure to particulate matters and carbon black.

As the largest organ, the skin provides the first line of defence against environmental pollutants. Different pollutants have varied damage to the skin due to their own physical-chemical properties. A previous epidemiological study by our team revealed that eczema was positively correlated with different air pollutants. However, the mechanism of action from different pollutants on the skin is less known. In this work, the differences among the genotoxicity, intracellular reactive oxygen species, and barrier-related parameters caused by two kinds of air pollutants, that is, S1650b and carbon black (CB) were investigated by Western blot, TUNEL, comet assay and RNA-sequences. The results indicated that both S1650b and CB caused DNA damage of keratinocytes. With the content of lipophilic polycyclic aromatic hydrocarbons (PAH), S1650b leaked into the keratinocytes easily, which activated the aromatic hydrocarbon receptor (AhR) in keratinocytes, leading to worse damage to barrier-related proteins than CB. And CB-induced higher intracellular ROS than S1650b due to the smaller size which make it enter the keratinocytes easier. RNA-sequencing results revealed that S1650b and CB both caused DNA damage of keratinocytes, and the intervention of S1650b significantly upregulated AhR, cytochrome oxidase A1 and B1 (CYP1A1 and CYP1B1) genes, while the results showed oppositely after CB intervention. The mechanism of keratinocyte damage caused by different air particle pollutants in this study will help to expand our understanding on the air pollutant-associated skin disease at cell levels.

Contribution of Particulates to Airborne Disease Transmission and Severity: A Review.

The emergence of coronavirus disease 2019 (COVID-19) has catalyzed great interest in the spread of airborne pathogens. Airborne infectious diseases are classified into viral, bacterial, and fungal infections. Environmental factors can elevate their transmission and lethality. Air pollution has been reported as the leading environmental cause of disease and premature death worldwide. Notably, ambient particulates of various components and sizes are harmful pollutants. There are two prominent health effects of particles in the atmosphere: (1) particulate matter (PM) penetrates the respiratory tract and adversely affects health, such as heart and respiratory diseases; and (2) bioaerosols of particles act as a medium for the spread of pathogens in the air. Particulates contribute to the occurrence of infectious diseases by increasing vulnerability to infection through inhalation and spreading disease through interactions with airborne pathogens. Here, we focus on the synergistic effects of airborne particulates on infectious disease. We outline the concepts and characteristics of bioaerosols, from their generation to transformation and circulation on Earth. Considering that microorganisms coexist with other particulates as bioaerosols, we investigate studies examining respiratory infections associated with airborne PM. Furthermore, we discuss four factors (meteorological, biological, physical, and chemical) that may impact the influence of PM on the survival of contagious pathogens in the atmosphere. Our review highlights the significant role of particulates in supporting the transmission of infectious aerosols and emphasizes the need for further research in this area.

Screening Organic Components and Toxicogenic Structures from Regional Fine Particulate Matters Responsible for Myocardial Fibrosis in Male Mice.

Numerous studies indicate that fine particulate matters (PM2.5) and its organic components are urgent risk factors for cardiovascular diseases (CVDs). Combining toxicological experiments, effect-directed analyses, and nontarget identification, this study aims to explore whether PM2.5 exposure in coal-combustion areas induces myocardial fibrosis and how to identify the effective organic components and their toxic structures to support regional risk control. First, we constructed an animal model of real-world PM2.5 exposure during the heating season and found that the exposure impaired cardiac systolic function and caused myocardial fibrosis, with chemokine Ccl2-mediated inflammatory response being the key cause of collagen deposition. Then, using the molecular event as target coupled with two-stage chromatographic isolation and mass spectrometry analyses, we identified a total of 171 suspect organic compounds in the PM2.5 samples. Finally, using hierarchical characteristic fragment analysis, we predicted that 40 of them belonged to active compounds with 6 alert structures, including neopentane, butyldimethylamine, 4-ethylphenol, hexanal, decane, and dimethylaniline. These findings provide evidence for risk management and prevention of CVDs in polluted areas.

Enhanced Intrusion of Exogenous Airborne Fine Particles toward Eyes in Humans and Animals: Where Damaged Blood-Ocular Barrier Plays a Crucial Role.

Emerging data suggest a close correlation between ambient fine particle (AFP) exposure and eye disorders and pinpoint potential threats of AFPs to eye health in humans. However, the possible passage (including direct intrusion) and the interactions of AFPs with the eye microenvironment in addition to morphological and physiological injuries remain elusive. To this end, the likely transport of AFPs into the eyes via blood-ocular barrier (BOB) in humans and animals was investigated herein. Exogenous particles were recognized inside human eyes with detailed structural and chemical fingerprints. Importantly, comparable AFPs were found in sera with constant structural and chemical fingerprints, hinting at the translocation pathway from blood circulation into the eye. Furthermore, we found that the particle concentrations in human eyes from patients with diabetic retinopathy were much higher than those from patients with no fundus pathological changes (i.e., myopia), indicating that the damaged BOB increased the possibility of particle entrance. Our diseased animal model further corroborated these findings. Collectively, our results offer a new piece of evidence on the intrusion of exogenous particles into human eyes and provide an explanation for AFP-induced eye disorders, with substantially increased risk in susceptible individuals with BOB injuries.

Unveiling the potent effect of vitamin D: harnessing Nrf2/HO-1 signaling pathways as molecular targets to alleviate urban particulate matter-induced asthma inflammation.

BACKGROUND: Asthma is the most common allergic disease characterized by an inflammatory response in the airways. Mechanismly, urban particulate matter (PM) is the most widely air pollutant associated with increased asthma morbidity and airway inflammation. Current research found that vitamin D is an essential vitamin with anti-inflammatory, antioxidant and other medical efficacy. Inadequate or deficient vitamin D often leads to the pathogenesis and stability of asthma. NGF exacerbates airway inflammation in asthma by promoting smooth muscle cell proliferation and inducing the Th2 immune response. Activation of the Nrf2/HO-1 signaling pathway can exert a protective effect on the inflammatory response in bronchial asthma. However, the specific mechanism of this pathway in PM-involved asthmatic airway smooth muscle cells remains unclear. METHODS: Mice were sensitized and challenged with Ovalbumin (OVA) to establish an asthma model. They were then exposed to either PM, vitamin D or a combination of both, and inflammatory responses were observed. Including, acetylcholine stimulation at different concentrations measured airway hyperresponsiveness in mice. Bronchoalveolar lavage fluid (BALF) and serum were collected for TNF-α, IL-1ß, IL-6, and Nerve growth factor (NGF) analysis. Additionally, lung tissues underwent histopathological examination to observe alveolar structure and inflammatory cell infiltration. Specific ELISA kits were utilized to determine the levels of the inflammatory factors TNF-α, IL-1ß, IL-6, and Nerve growth factor (NGF). Nrf2/HO-1 signaling pathways were examined by western blot analysis. Meanwhile, we constructed a cell system with low HO-1 expression by lentiviral transfection of airway smooth muscle cells. The changes of Nrf2, HO-1, and NGF were observed after the treatment of OVA, PM, and Vit D were given. RESULTS: The in vivo results showed that vitamin D significantly alleviated pathological changes in lung tissue of PM-exposed mice models. Mechanismly, vitamin D decreased substantial inflammatory cell infiltration in lung tissue, as well as the number of inflammatory cells in BALF. Furthermore, vitamin D reduced the heightened inflammatory factors including of TNF-α, IL-1ß, IL-6, and NGF caused by PM exposure, and triggered the activity of nucleus Nrf2 and HO-1 in PM-exposed asthmatic mice. Notably, knockdown HO-1 weakens the Vitamin D- mediated inhibition to pollution toxicity in asthma. Importantly, in vitro experiments on OVA-stimulated mice airway smooth muscle cells, the results showed that OVA and PM, respectively, reduced Nrf2/HO-1 and increased NGF's expression, while vitamin D reversed the process. And in the HO-1 knockdown cell line of Lenti-si-HO-1 ASMCs, OVA and PM reduced Nrf2's expression, while HO-1 and NGF's expression were unchanged. CONCLUSIONS: The above results demastrate that vitamin D downregulated the inflammatory response and the expression of NGF by regulating the Nrf2/HO-1 signaling pathways in airway smooth muscle cells, thereby showing potent anti-inflammatory activity in asthma.

Airway bacterial microbiome signatures correlate with occupational pneumoconiosis progression.

Recent evidence has pinpointed a key role of the microbiome in human respiratory health and disease. However, significant knowledge gaps still exist regarding the connection between bacterial communities and adverse effects caused by particulate matters (PMs). Here, we characterized the bacterial microbiome along different airway sites in occupational pneumoconiosis (OP) patients. The sequencing data revealed that OP patients exhibited distinct dysbiosis in the composition and function of the respiratory microbiota. To different extents, there was an overall increase in the colonization of microbiota, such as Streptococcus, implying a possible intrusion pathway provided by exogenous PMs. Compared to those of healthy subjects, unhealthy living habits (i.e., smoking) had a greater impact on microbiome changes in OP patients. Importantly, the associations between the bacterial community and disease indicators indicated that specific bacterial species, including Prevotella, Actinobacillus, and Leptotrichia, might be surrogate markers of OP disease progression. Collectively, our results highlighted the potential participation of the bacterial microbiota in the pathogenesis of respiratory diseases and helped in the discovery of microbiome-based diagnostics for PM-induced disorders.

Lung Cancer and Risk Factors in Lebanon: Epidemiology, Temporal Trends, and Comparison to Countries From Different Regions in the World.

BACKGROUND: Lung cancer (Lca) is the leading cause of cancer morbidity and mortality worldwide. This study examines the Lca incidence and trends in Lebanon and compares them to regional and global ones. It also discusses Lca risk factors in Lebanon. METHODS: Lung cancer data from the Lebanese National Cancer Registry for 2005 to 2016 was obtained. The age-standardized incidence rates (ASRw) and age-specific rates per 100 000 population were calculated. RESULTS: Lung cancer ranked second for cancer incidence in Lebanon from 2005-2016. Lung cancer ASRw ranged from 25.3 to 37.1 per 100 000 males and 9.8 to 16.7 per 100 000 females. Males 70-74 and females 75+ had the highest incidence. Lung cancer ASRw in males increased significantly at 3.94% per year from 2005 to 2014 (P > .05), then decreased non-significantly from 2014 to 2016 (P < .05). Lung cancer ASRw in females increased significantly at 11.98% per year from 2005 to 2009 (P > .05), then increased non-significantly from 2009 to 2016 (P < .05). Males' Lca ASRw in Lebanon was lower than the global average in 2008 and became similar in 2012 (34.1 vs 34.2 per 100 000); However, females' Lca ASRw was almost comparable to the global average in 2008 and exceeded it in 2012 (16.5 vs 13.6, respectively, per 100 000). Males' and Females' Lca ASRw in Lebanon were among the highest in the Middle East and North Africa (MENA) region but lower than those estimated for North America, China and Japan, and several European countries. The proportion of Lca cases attributed to smoking among Lebanese males and females was estimated at 75.7% and 66.3% for all age groups, respectively. The proportion of Lca cases attributed to air pollution with PM10 and PM2.5 in Lebanon was estimated at 13.5% for all age groups. CONCLUSION: Lung cancer incidence in Lebanon is among the highest in the MENA region. The leading known modifiable risk factors are tobacco smoking and air pollution.

PM2.5 exposure increases dry eye disease risks through corneal epithelial inflammation and mitochondrial dysfunctions.

Dry eye disease (DED) is the most common disease affecting vision and quality of life. PM2.5 was a potential risk of DED. Herein, we conducted animal exposure and cell-based studies to evaluate the pathogenic effect of PM2.5 exposure on the ocular surface and DED etiological mechanisms. C57 mice were exposed to filtered air and PM2.5 aerosol. We assessed health conditions and inflammation of the ocular surface by corneal fluorescein staining and immunohistochemistry. In parallel, cultured human corneal epithelial cells (HCETs) were treated with PM2.5, followed by characterization of cell viability, intracellular ATP level, mitochondrial activities, and expression level of DED relevant mRNA and proteins. In mice, PM2.5 exposure induced severe superficial punctate keratopathy and inflammation in their cornea. In HCETs, cell proliferation and ROS generation followed dose-response and time-dependent manner; meanwhile, mitochondrial ROS (mtROS) level increased and mitochondrial membrane potential (MMP) level decreased. Inflammation cascade was triggered even after short-term exposure. The reduction of ATP production was alleviated with Nrf2 overexpression, NF-κB P65 knockdown, or ROS clearance. Nrf2 overexpression and P65 knockdown reduced inflammatory reaction through decreasing expression of P65 and increasing of Nrf2, respectively. They partly alleviated changes of ROS/mtROS/MMP. This research proved that PM2.5 would cause DED-related inflammation reaction on corneal epithelial cells and further explored its mechanism: ROS from mitochondrial dysfunctions of corneal epithelial cells after PM2.5 exposure partly inhibited the expression of anti-inflammatory protein Nrf2 led the activation of inflammatory protein P65 and its downstream molecules, which finally caused inflammation reaction.

Association of air pollution with dementia: a systematic review with meta-analysis including new cohort data from China.

It remains unclear whether a total exposure to air pollution (AP) is associated with an increased risk of dementia. Little is known on the association in low- and middle-income countries. Two cohort studies in China (in Anhui cohort 1402 older adults aged ≥ 60 followed up for 10 years; in Zhejiang cohort 6115 older adults followed up for 5 years) were conducted to examine particulate matter - PM2.5 associated with all dementia and air quality index (AQI) with Alzheimer's disease, respectively. A systematic literature review and meta-analysis was performed following worldwide literature searched until May 20, 2020 to identify 15 population-based cohort studies examining the association of AP with dementia (or any specific type of dementia) through PubMed, MEDLINE, PsycINFO, SocINDEX, CINHAL, and CNKI. The cohort studies in China showed a significantly increased relative risk (RR) of dementia in relation to AP exposure; in Anhui cohort the adjusted RR was 2.14 (95% CI 1.00-4.56) in people with PM2.5 exposure at ≥ 64.5 µg/m3 versus <63.5 µg/m3 and in Zhejiang cohort the adjusted RR was 2.28 (1.07-4.87) in AQI>90 versus ≤ 80. The systematic review revealed that all 15 studies were undertaken in high income countries/regions, with inconsistent findings. While they had reasonably good overall quality of studies, seven studies did not adjust smoking in analysis and 13 did not account for depression. Pooling all eligible data demonstrated that dementia risk increased with the total AP exposure (1.13, 1.08-1.19). Data analysis of air pollutants showed that the RR significantly increased with PM2.5 (1.06, 1.03-1.10 in 2nd tertile exposure; 1.13, 1.07-1.19 in 3rd tertile versus 1st tertile), PM10 (1.05, 0.86-1.29; 1.62, 0.60-4.36), carbon monoxide (1.69, 0.72-3.93; 1.52, 1.35-1.71), nitrogen dioxide (1.06, 1.03-1.09; 1.18, 1.10-1.28) and nitrogen oxides (1.09, 1.04-1.15; 1.26, 1.13-1.41), but not ozone. Controlling air pollution and targeting on specific pollutants would reduce dementia globally.

Effects of fine ambient particulate matters on de novo hypertensive disorders of pregnancy and blood pressure before 20 weeks.

The effects of fine particulate matter (PM) on de novo hypertensive disorders of pregnancy (HDP) were inconsistent during the first and second trimesters. This study aimed to assess the trimester-specific effects of PM2.5 and PM1 prior to diagnosis of de novo HDP. The exposure of fine PM was predicted by satellite remote sensing data according to maternal residential addresses. De novo HDP was defined as gestational hypertension and preeclampsia during the current pregnancy. A logistic regression model was performed to assess the association of PM2.5 and PM1 with HDP during the first and early second trimesters (0-13 weeks and 14-20 weeks). The generalized estimating equation model was conducted to assess the effect of PM2.5 and PM1 on blood pressure. The present study included 22,821 pregnant women (mean age, 29.1 years) from 2013 to 2017. PM2.5 and PM1 were significantly associated with an increased risk of de novo HDP during the first trimester (OR = 1.070, 95% CI: 1.013-1.130; OR = 1.264, 95% CI: 1.058-1.511 for per 10 µg/m3) and early second trimester (OR = 1.045, 95% CI: 1.003-1.088; OR = 1.170, 95% CI: 1.002-1.366 for per 10 µg/m3). Significant trends of increased de novo HDP risk was also observed with the increment of PM (all P for trend <0.05). The stratified analyses demonstrated that the associations between exposure to fine PM and the risk of HDP were more pronounced among the pregnant women with maternal age above 35 and low maternal education level (all OR >1.047). Each 10 µg/m3 increase of PM1 and PM2.5 before diagnosis of de novo HDP elevated 0.204 (95% CI: 0.098-0.310) and 0.058 (95%CI: 0.033-0.083) mmHg of systolic blood pressure. Exposure to PM2.5 and PM1 during the first and early second trimester were positively associated with the risk of de novo HDP. The fine PM before diagnosis of de novo HDP elevated the systolic blood pressure.

Loliolide in Sargassum horneri Alleviates Ultrafine Urban Particulate Matter (PM 0.1)-Induced Inflammation in Human RPE Cells.

Owing to increasing air pollution due to industrial development, fine dust has been associated with threatening public health. In particular, ultrafine urban particulate matter (uf-UP, PM 0.1) can easily enter our bodies, causing inflammation-related diseases. Therefore, in the present study, we evaluated the effects of hydrothermal extracts of Sargassum horneri and its bioactive compound, loliolide, on uf-UP-induced inflammation as a potential treatment strategy for retinal disorders. Human retinal pigment epithelial cells (ARPE-19) stimulated with TNF-α or uf-UPs were treated with S. horneri extract and loliolide. S. horneri extracts exhibited anti-inflammatory effects on uf-UP-induced inflammation without cell toxicity through downregulating the mRNA expression of MCP-1, IL-8, IL-6, and TNF-α. UPLC-QTOF/MS analysis confirmed that the hydrothermal extract of S. horneri contained loliolide, which has anti-inflammatory effects. Loliolide effectively reduced the mRNA expression and production of proinflammatory chemokines (IL-8) and cytokines (IL-1ß and IL-6) by downregulating the MAPK/NF-ĸB signaling pathway on TNF-α-stimulated inflammatory ARPE-19 cells. These effects were further confirmed in inflammatory ARPE-19 cells after stimulation with uf-UPs. Collectively, these results suggested the application of S. horneri as a functional ingredient for treating ocular disorders caused by particular matters.

Spatiotemporal analysis and forecasting of air quality in the greater Dhaka region and assessment of a novel particulate matter filtration unit.

Bangladesh is one of the most polluted nations in the world, with an average Air Quality Index (AQI) of 161 in 2021; its capital, Dhaka, has the worst air quality of any major city in the world. The present study aims to analyze the spatiotemporal distribution of air quality indicators in the greater Dhaka region, forecast weekly AQI, and assess the performance of a novel particulate matter filtration unit in removing particulate matter. Air quality indicators remained highest during the dry season with an average of 128.5 µm/m3, while the lowest concentration was found in the monsoon season with an average of 19.096 µm/m3. Analysis revealed a statistically significant annual increasing trend of CO, which was associated with the growing number of brick kilns and usage of high-sulfur diesel. Except for the pre-monsoon AQI, concentrations of both seasonal and yearly AQI and PM2.5 showed decreasing trend, though predominantly insignificant, demonstrating the improvement in air quality. Prevailing winds influenced the seasonal distribution of tropospheric CO & NO2. The study also employed a seasonal autoregressive integrated moving average (ARIMA) model to forecast weekly AQI values. ARIMA (3,0,4) (3,1,3) at the 7-periodicity level performed best forecasting the AQI values among all developed models with low root mean square error (RMSE)-29.42 and mean absolute percentage error (MAPE)-13.11 values. The predicted AQI values suggested that the air quality would remain unhealthy for most weeks. The experimental simulation of the particulate matter filtration unit, designed in the shape of a road divider, generated substantial cyclonic motion while maintaining a very minimal pressure drop. In the real-world scenario, using only cyclonic separation and dry deposition, the suggested air filtration system removed 40%, 44%, and 42% of PM2.5, PM10, and TSP, respectively. Without employing filters, the device removed significant amounts of particulate matter, implying enormous potential to be used in the study area. The study could be useful for policy makers to improve urban air quality and public health in Bangladesh and in other developing countries.

Gastrointestinal tissue as a "new" target of pollution exposure.

Airborne pollution has become a leading cause of global death in industrialized cities and the exposure to environmental pollutants has been demonstrated to have adverse effects on human health. Among the pollutants, particulate matter (PM) is one of the most toxic and although its exposure has been more commonly correlated with respiratory diseases, gastrointestinal (GI) complications have also been reported as a consequence to PM exposure. Due to its composition, PM is able to exert on intestinal mucosa both direct damaging effects, (by reaching it either via direct ingestion of contaminated food and water or indirect inhalation and consequent macrophagic mucociliary clearance) and indirect ones via generation of systemic inflammation. The relationship between respiratory and GI conditions is well described by the lung-gut axis and more recently, has become even clearer during coronavirus disease 2019 (COVID-19) pandemic, when respiratory symptoms were associated with gastrointestinal conditions. This review aims at pointing out the mechanisms and the models used to evaluate PM induced GI tract damage.

Long-term exposure to ambient air pollution is associated with an increased incidence and mortality of acute respiratory distress syndrome in a large French region.

INTRODUCTION: Air pollution exposure is suspected to alter both the incidence and mortality in acute respiratory distress syndrome (ARDS). The impact of chronic air pollutant exposure on the incidence and mortality of ARDS from various aetiologies in Europe remains unknown. The main objective of this study was to evaluate the incidence of ARDS in a large European region, 90-day mortality being the main secondary outcome. METHODS: The study was performed in the Provence-Alpes-Cote-d'Azur (PACA) region. Nitrogen dioxide (NO2), particulate matter (PM2.5 and PM10) and ozone (O3) were measured. The Programme de Médicalisation des Systèmes d'Information (PMSI), which captures all patient hospital stays in France, was used to identify adults coded as ARDS in an intensive care unit. RESULTS: From 2016 to 2018, 4733 adults with ARDS treated in intensive care units were analysed. The incidence rate ratios for 1-year average exposure to PM2.5 and PM10 were 1.207 ([95% confidence interval (95% CI), 1.145-1.390]; P < 0.01) and 1.168 (95% CI, 1.083-1.259; P < 0.001), respectively. The same trend was observed for both 2- and 3-year exposures, while only chronic 1- and 2-year exposure NO2 exposures were related to a higher incidence of ARDS. Increased PM2.5 exposure was associated with a higher 90-day mortality for both 1- and 3-year exposures (OR 1.096 (95% CI, 1.001-1.201) and 1.078 (95% CI, 1.009-1.152), respectively). O3 was not associated with either of incidence nor mortality. CONCLUSIONS: While chronic exposure to NO2, PM2.5, and PM10 was associated with an increased ARDS incidence and a higher mortality rate (for PM2.5) in those patients presenting with ARDS, further research on this topic is required.

Real-time detection of vehicle-originated condensable particulate matter through thermodenuder integrated aerosol measurement method at tailpipes.

Condensable particulate matter (CPM) corresponds to primary particulate matter ≤2.5 µm (PM2.5) obtained through the condensation of gaseous air pollutants caused by temperature drops in the atmosphere. The internal combustion of vehicle engines can produce CPM because of the condensable compounds in the exhaust gas. Conventional CPM measurement methods have been developed for coal-fired power plants with stable emissions through sampling and off-site analyses. They are therefore unsuitable for detecting the rapidly changing vehicle-originated CPM. In addition, the current system for evaluating PM2.5 from vehicles, based on the particle measurement program (PMP) protocol, provides only the emission factors of total PM2.5 (and not CPM separately) at a fixed temperature (∼25 °C) and dilution ratio (∼ × 35). This study reports, for the first time, the development of a real-time detection method for vehicle-originated CPM through a thermodenuder (TD) integrated with real-time aerosol instruments. This method was designed to reduce the loss of CPM due to condensation and diffusion while sampling the exhaust gas. It permits the investigation of the effects of dilution gas temperature (5-45 °C) and dilution ratio (up to × 30) on the formation of CPM. During the feasibility test of this method using a diesel vehicle (Euro-4), the real-time total particle number concentrations (PNs) matched well with those obtained by a PMP protocol-based evaluation system. Moreover, this method detected PNs concentrations ten times higher than the detection limit (4 × 106 particles/cm3) of the PMP-based system. The emission factors of the total PM2.5 with a bulk density (1 g/cm3) measured by this method also showed consistency with the results of the PMP protocol. The mass emission factor of CPM determined by deploying the TD was ∼14.57 mg/km (∼63% contribution to the total PM2.5).

Emission characteristics, sources, and airborne fate of speciated organics in particulate matters in a Hong Kong residence.

A growing number of studies warn of the adverse health effects of indoor particulate matters (PM). However, little is known about the molecular compositions and emission characteristics of PM-bound organics (OM) indoors, a critical group of species with highest concentration and complexity in indoor PM. In a Hong Kong residence where prescribed activities were performed with normal frequency and intensity, we found that the activities significantly elevated not only the total concentration but also the fraction of OM in indoor PM. However, the concentration of the total PM-bound OM outdoors (10.3 ± 0.7 µg/m3 ) surpassed that for the indoor counterpart during the undisturbed period (8.2 ± 0.1 µg/m3 ), that is, period when there was no activity with high emission of PM but the residual effects of previous activities might remain. Emissions of indoor activities involving combustion or high-temperature processes significantly elevated the indoor-to-outdoor (I/O) ratios for a majority of organic species. In addition, gas-to-particle partitioning, secondary formation, carrying-over (residues of pollutants in the air), and re-emission also modulated the I/O ratios of some compounds. Chemically comprehensive emission profiles of speciated organics were obtained for 5 indoor activities in the residence. While the indoor contribution to PM-bound OM was estimated to be not higher than 13.1% during the undisturbed period, carrying-over and/or re-emission seemed to exist for certain compounds emitted from cigarette smoking and incense burning. This study enhances knowledge on emissions and airborne fate of speciated organics in indoor PM.

Insight into urban PM2.5 chemical composition and environmentally persistent free radicals attributed human lung epithelial cytotoxicity.

Fine particulate matter (PM2.5) is detrimental to the human respiratory system. However, the toxicity of PM2.5 and its associated potentially harmful species, notably novel pollutants like environmentally persistent free radicals (EPFRs), remains unclear. Therefore, one-year site monitoring and ambient air PM2.5 sampling in the Nanjing urban area was designed to investigate the relationships between chemical compositions (carbon fractions, metallic elements, and water-soluble ions) and EPFRs, and change in cytotoxicity with varying PM2.5 components. Oxidative stress (reactive oxygen species, ROS), inflammatory injury (IL-6 and TNF-α), and membrane injury (LDH) of human lung epithelial cells (A549) induced by PM2.5 were analyzed using in vitro cytotoxicity test. Both the composition and toxicity of PM2.5 from different seasons were compared. The average daily exposure of urban PM2.5 associated EPFRs load in Nanjing were 2.29 × 1011 spin m-3. Their exposure concentration and cytotoxic damage ability were stronger in the cold season than warm. The particle compositions of metals and carbon fractions were significantly positively correlated with EPFRs. The airborne EPFRs, organic carbon (OC), and heavy metal Cu, As, and Pb may pose principal cell damage ability, which is worthy of further study interlinking aerosol pollution and health risks.

The impact of air pollution on skin and related disorders: A comprehensive review.

As the largest organ in the body, human skin is constantly exposed to harmful compounds existing in the surrounding environment as the first-line barrier. Studies have indicated that exposure to high concentrations of many environmental factors, such as ultraviolet (UV) radiation, outdoor air pollutants, including polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), particulate matter (PM), heavy metals, gaseous pollutants, such as carbon monoxide (CO), nitric oxides (NOx ), sulfur oxide (SO2 ), ozone (O3 ), and indoor air pollutants (solid fuels consumption), might interrupt the skin's normal barrier function. Besides, the intensity of the pollutants and the length of exposure might be a contributing factor. Air pollutants are believed to induce or exacerbate a range of skin conditions, such as aging, inflammatory diseases (atopic dermatitis, cellulitis, and psoriasis), acne, hair loss, and even skin cancers (mainly melanoma and Squamous Cell Carcinoma) through various mechanisms. The interaction between pollutants and the skin might differ based on each agent's particular characteristics. Also, damaging the skin barrier seems to be closely related to the increased production of reactive oxygen species (ROS), induction of oxidative stress, activation of aryl hydrocarbon receptor (AhR), and inflammatory cytokines. This article reviews recent studies on the correlation between air pollutants and skin diseases, along with related mechanisms.

Spatiotemporal variation in residential PM2.5 and PM10 concentrations in China: National on-site survey.

BACKGROUND: Significant efforts have been directed toward addressing the adverse health effects of particulate matter, while few data exist to evaluate indoor exposure nationwide in China. OBJECTIVES: This study aimed to investigate dwellings particulate matter levels in the twelve cities in China and provide large data support for policymakers to accelerate the legislative process. METHODS: The current study was based on the CIEHS 2018 study and conducted in 12 cities of China. A total of 2128 air samples were collected from 610 residential households during the summer and winter. Both PM10 and PM2.5 were detected with a light-scattering dust meter in both the living room and bedroom. The Wilcoxon rank-sum test was performed to evaluate the correlations between PM2.5 and PM10 concentrations and both sampling season and site. Ratios of the living room to bedroom were calculated to evaluate the particulate matter variation between rooms. Hierarchical clustering was used to probe the question of whether the concentration varies between cities throughout China. RESULTS: The geometric means of the PM2.5 in living rooms and bedrooms were 39.80 and 36.55 µg/m3 in the summer, and 70.97 and 67.99 µg/m3 in the winter, respectively. In the summer, approximately 70 % of indoor dwelling PM2.5 exceeded the limit of 25 µg/m3, and for PM10 approximately 60 % of dwellings demonstrated levels higher than 50 µg/m3; the corresponding values were over 90 % and 80 % in winter, respectively. In Shijiazhuang, Lanzhou, Luoyang and Qingdao, the geometric means of the PM2.5 concentrations were observed to be 1.5 to 4.3 times higher during winter than during summer; similar concentrations in summer and winter were observed in Harbin, Wuxi, and Shenzhen, while the PM2.5 concentrations in Panjin were approximately 1.5 times higher in summer than in winter. There was no significant difference in particulate matter concentrations between the living rooms and bedrooms. Scatter plots showed that cities with low GDP and a small population had higher concentrations, while Shenzhen, which has a higher GDP and a large permanent population, had a relatively low concentration of particulate matter. CONCLUSIONS: Our results suggest that indoor air pollution is a severe problem in China. It is necessary to continue monitoring indoor air quality to observe the changing trend under the tremendous effort of the Chinese government.