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.

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.

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.

Impact of Lockdown on Air Quality in the Most Polluted Cities of India.

Background: COVID-19 has become a global pandemic, prompting lockdowns in practically every country. To prevent the spread of the disease, India has enforced a rigorous nationwide lockdown that commenced in March 2020. The lockdown imposed amid the pandemic ensured that most commercial activities and vehicle transportation ceased, resulting in a significant reduction in air pollution levels. Material and Methods: The value of air pollutants PM10, PM2.5, NO2, and SO2 from January to May 2020 was obtained from the Indian Central Pollution Control Board. Before lockdown and during lockdown, relative fluctuations in ambient concentrations of four air contaminants were investigated. The Box-Jenkins approach was used to estimate future air pollution data points using time series data analysis. Results: The PM10 level reduced by 61%, 30%, 68%, 37%, and 43% in the selected cities, respectively. Comparison of other pollutant concentrations before and after the lockdown also found a reduction in ambient pollutant concentrations, resulting in improved air quality. Inference of predicted model values to observed values revealed a significant increase in the concentrations of all pollutants. The percentage increases in AQImean from predicted to observed values were 206% in Ghaziabad, 148% in Delhi, 59% in Hyderabad, and 160% in Cochin. Conclusion: The strict lockdown has resulted in a significant drop in air pollutant levels. Upgrading present technologies could help keep pollution to a minimum of 37% under control. The findings would prompt the government to consider how to strictly reduce vehicle and industrial pollution to improve air quality and maintain improved public health.

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.

The joint effects of prenatal exposure to PM2.5 constituents and reduced fetal growth on children's accelerated growth in the first 3 years: a birth cohort study.

BACKGROUND: Prenatal fine particulate matter (PM2.5) constituents exposure and reduced fetal growth may be risk factors for accelerated growth in early childhood, an important indicator for lifelong health. OBJECTIVE: The study investigated whether the joint effects are present between PM2.5 constituents and reduced fetal growth. METHODS: The study was embedded in a birth cohort in China, including 5424 mother-child pairs. Prenatal PM2.5 and its constituents' [organic carbon (OC), elementary carbon (EC), ammonium (NH4+), nitrate (NO3-), and sulfate (SO42-)] concentrations were estimated based on maternal residential addresses. Fetal growth was evaluated by fetal growth trajectory in utero and preterm birth (PTB), low birth weight (LBW), and small for gestational age (SGA). Children's accelerated growth was defined as body mass index (BMI) Z-score change of >0.67 between birth and 3 years. Generalized logistic regression was used to analyze the effects of prenatal PM2.5 constituents exposure and fetal growth on children's accelerated growth. Joint effect was tested on multiplicative scale and additive scale with the relative excess risk due to interaction (RERI). RESULTS: Children with lower fetal growth trajectory, PTB, LBW, and SGA had increased odds of children's accelerated growth, with odds ratios (ORs) ranging from 1.704 to 11.605. Compared with lower exposure (≤median), higher exposure (>median) of PM2.5, OC, and SO42- were significantly associated with increased odds of children's accelerated growth, varying in ORs from 1.163 to 1.478. Prenatal exposure to OC had joint effects with lower fetal growth on children's accelerated growth. We observed that the interaction was statistically significant on an additive scale in OC and lower fetal growth trajectory (RERI: 0.497, 95% CI: 0.033,0.962). IMPACT: Fine particulate matter (PM2.5) is a huge threat to human health worldwide, causing 6.7 million death globally in 2019. According to the theory of DOHaD, prenatal PM2.5 exposure could influence early childhood growth, which is important for lifelong health. We found that prenatal exposure to PM2.5, OC, and SO42- was associated with higher risk of accelerated childhood growth in the first 3 years. More importantly, reduced fetal growth moderated these associations. Our findings highlight the need for policies and interventions on PM2.5 constituents to improve lifelong health, especially for those vulnerable populations with reduced fetal growth.

Triple dip La-Nina, unorthodox circulation and unusual spin in air quality of India.

The recent La-Nina phase of the El Nino Southern Oscillation (ENSO) phenomenon unusually lasted for third consecutive year, has disturbed global weather and linked to Indian monsoon. However, our understanding on the linkages of such changes to regional air quality is poor. We hereby provide a mechanism that beyond just influencing the meteorology, the interactions between the ocean and the atmosphere during the retreating phase of the La-Niña produced secondary results that significantly influenced the normal distribution of air quality over India through disturbed large-scale wind patterns. The winter of 2022-23 that coincided with retreating phase of the unprecedented triple dip La-Niña, was marred by a mysterious trend in air quality in different climatological regions of India, not observed in recent decades. The unusually worst air quality over South-Western India, whereas relatively cleaner air over the highly polluted North India, where levels of most toxic pollutant (PM2.5) deviating up to about ±30 % from earlier years. The dominance of higher northerly wind in the transport level forces influx and relatively slower winds near the surface, trapping pollutants in peninsular India, thereby notably increasing PM2.5 concentration. In contrast, too feeble western disturbances, and unique wind patterns with the absence of rain and clouds and faster ventilation led to a significant improvement in air quality in the North. The observed findings are validated by the chemical-transport model when forced with the climatology of the previous year. The novelty of present research is that it provides an association of air quality with climate change. We demonstrate that the modulated large-scale wind patterns linked to climatic changes may have far-reaching consequences even at a local scale leading to unusual changes in the distribution of air pollutants, suggesting ever-stringent emission control actions.

The role of lysosomes in airborne particulate matter-induced pulmonary toxicity.

An investigation of the potential role of lysosomes in airborne particulate matter (APM) induced health risks is essential to fully comprehend the pathogenic mechanisms of respiratory diseases. It is commonly accepted that APM-induced lung injury is caused by oxidative stress, inflammatory responses, and DNA damage. In addition, there exists abundant evidence that changes in lysosomal function are essential for cellular adaptation to a variety of particulate stimuli. This review emphasizes that disruption of the lysosomal structure/function is a key step in the cellular metabolic imbalance induced by APMs. After being ingested by cells, most particles are localized within lysosomes. Thus, lysosomes become the primary locus where APMs accumulate, and here they undergo degradation and release toxic components. Recent studies have provided incontrovertible evidence that a wide variety of APMs interfere with the normal function of lysosomes. After being stimulated by APMs, lysosome rupture leads to a loss of lysosomal acidic conditions and the inactivation of proteolytic enzymes, promoting an inflammatory response by activating the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Moreover, APMs interfere with autophagosome production or block autophagic flux, resulting in autophagy dysfunction. Additionally, APMs disrupt the normal function of lysosomes in iron metabolism, leading to disruption on iron homeostasis. Therefore, understanding the impacts of APM exposure from the perspective of lysosomes will provide new insights into the detrimental consequences of air pollution.

Oil mistparticulate matter exposure induces hyperlipidemia-related inflammation via microbiota/ SCFAs/GPR43 axis inhibition and TLR4/NF-κB activation.

Metabolites produced by the human gut microbiota play an important role in fighting and intervening in inflammatory diseases. It remains unknown whether immune homeostasis is influenced by increasing concentrations of air pollutants such as oil mist particulate matters (OMPM). Herein, we report that OMPM exposure induces a hyperlipidemia-related phenotype through microbiota dysregulation-mediated downregulation of the anti-inflammatory short-chain fatty acid (SCFA)-GPR43 axis and activation of the inflammatory pathway. A rat model showed that exposure to OMPM promoted visceral and serum lipid accumulation and inflammatory cytokine upregulation. Furthermore, our research indicated a reduction in both the "healthy" microbiome and the production of SCFAs in the intestinal contents following exposure to OMPM. The SCFA receptor GPR43 was downregulated in both the ileum and white adipose tissues (WATs). The OMPM treatment mechanism was as follows: the gut barrier was compromised, leading to increased levels of lipopolysaccharide (LPS). This increase activated the Toll-like receptor 4 Nuclear Factor-κB (TLR4-NF-κB) signaling pathway in WATs, consequently fueling hyperlipidemia-related inflammation through a positive-feedback circuit. Our findings thus imply that OMPM pollution leads to hyperlipemia-related inflammation through impairing the microbiota-SCFAs-GPR43 pathway and activating the LSP-induced TLR4-NF-κB cascade; our findings also suggest that OMPM pollution is a potential threat to humanmicrobiota dysregulation and the occurrence of inflammatory diseases.

Influence of atmospheric oxidation capacity on atmospheric particulate matters concentration in Lanzhou.

The atmospheric oxidation capacity (AOC) reflects the removal rate of atmospheric pollutants, and this index is typically characterized by the oxidant concentration or total reaction rate. The AOC plays a crucial role in the formation of atmospheric particulate matters and serves as an important indicator for studying changes in the concentration. In this study, we analyse the characteristics of atmospheric oxidants in Lanzhou based on data in the year of 2020 and 2021 retrieved from the Atmospheric Comprehensive Observation Station in Lanzhou. Empirical equations are applied to estimate the impact of atmospheric oxidative properties secondary generation concentrations of atmospheric particulate matters with different particle sizes. The results indicate that the annual average values of Ox were 146 µg/m3 in 2020 and 139 µg/m3 in 2021. The AOC was the highest in summer and lowest in winter. The correlation coefficient between O3 and Ox was significantly higher than that between NO2 and Ox, suggesting that O3 exerted a greater impact on the AOC in Lanzhou. A low AOC (MDA8 O3 ≤ 100 µg/m3) promoted the oxidation process of VOCs and other precursors, leading to the generation of secondary aerosols and subsequent formation of secondary particles. There were negative correlations between Ox and atmospheric particulate matters, secondary inorganic components, sulfur oxidation ratio (SOR) and nitrogen oxidation ratio (NOR), indicating that excessively high levels of Ox could inhibit the conversion rate of SO2 and NO2 into their respective forms to a certain extent.

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.

Assessing occupational exposure of airborne PMs and TVOCs in the nail salons in Tehran city, Iran.

There are concerns about the health of nail salon technicians due to the inherently harmful agents such as volatile organic compounds (VOCs) and released particles in the salons. For this reason, this study was conducted to investigate the occupational exposure of nail salon technicians to VOCs and particulate matters (PMs) in the nail salons in Tehran, Iran. In this cross-sectional study, indoor air quality and measurement continually Total VOCs and PMs in the various size of PM1-PM10 using PhoCheck Tiger and particle counter device investigated, respectively. site observation, and an interview with the manager in 49 salons in Tehran. Data was analyzed using SPSS software (version 22). Mean concentrations of PM1 with 2.56 µÉ¡/m3 was the lowest amount and PM10 with 346.86µÉ¡/m3 had the highest concentration. Also, the mean concentration of TVOCs was equal 2.61 ppm. The results of the regression model showed that there is a statistically significant between the number of services with airborne PMs (PM2.5), (p-Value≤0.050). In salons only with nail activities, the concentration of PM4 was less than the others, although this correlation was statistically significant just for PM1 (p-Value = 0.010). By implementing effective local exhaust ventilation systems equipped with dust collectors and utilizing safe products, the emission of particles and chemical compounds within salons can be significantly reduced.

Targeting Mitochondrial Dysfunction With LncRNAs in a Wistar Rat Model of Chronic Obstructive Pulmonary Disease.

BACKGROUND/AIM: Chronic obstructive pulmonary disease (COPD) has become a prominent healthcare issue in recent years. Cigarette smoking (CS) and fine particulate matter (PM2.5) are important causative factors for COPD. This study assessed the aberrant lncRNA profiles in the tissue of rats with COPD caused by CS or PM2.5 Materials and Methods: A COPD rat model was developed using CS (CSM) or PM2.5 (PMM), and lung tissue RNA was extracted. The Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) were used to investigate the correlations between the distinct lncRNAs and mRNA pathways. A coding-non-coding gene co-expression network (CNC) was constructed by establishing connections between differentially expressed long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) associated with mitochondrial dysfunction and the inflammatory response. RESULTS: A quantitative real-time reverse transcription PCR (qRT-PCR) experiment was performed to verify the expression of the particular lncRNAs. Microarray analysis of lung tissue from the COPD model revealed that 123 and 444 lncRNAs were substantially raised and reduced in PMM vs. the control group (Ctrl), respectively, as were 621 and 1,178 mRNAs. Meanwhile, 81 and 340 lncRNAs were consistently raised and lowered in CSM vs. Ctrl, respectively, as were 408 and 931 mRNAs. GO enrichment and KEGG pathway analysis indicated that the COPD model was connected to inflammatory responses, mitochondrial dysfunction, and others. CONCLUSION: XR_340674, ENSRNOT00000089642, XR_597045, and XR_340651 were decreased, and XR_592469 was elevated. These lncRNAs were shown to be related to mitochondrial dysfunction in the lung tissue of animals exposed to CS or PM2.5.

Effects of pre-natal and post-natal exposures to air pollution on onset and recurrence of childhood otitis media.

BACKGROUND: Despite mounting evidence linking outdoor air pollution with otitis media (OM), the role of air pollutant(s) exposure during which critical window(s) on childhood OM remains unknown. OBJECTIVES: We sought to identify the key air pollutant(s) and critical window(s) associated with the onset and recurrent attacks of OM in kindergarten children. METHODS: A combined cross-sectional and retrospective cohort study involving 8689 preschoolers aged 3-6 years was performed in Changsha, China. From 2013-2020, data on air pollutants were collected from ambient air quality monitoring stations in Changsha, and the exposure concentration to each child at their home address was calculated using the inverse distance weighted (IDW) method. The relationship between air pollution and OM in kindergarten children was studied using multiple logistic regression models. RESULTS: Childhood lifetime OM was associated with PM2.5, SO2 and NO2, with ORs (95% CI) of 1.43 (1.19-1.71), 1.18 (1.01-1.37) and 1.18 (1.00-1.39) by per IQR increase in utero exposure and with PM2.5, PM2.5-10 and PM10, with ORs = 1.15 (1.00-1.32), 1.25 (1.13-1.40) and 1.49 (1.28-1.74) for entire post-natal exposure, respectively. The 2nd trimester in utero and the post-natal period, especially the 1st year, were key exposure time windows to PM2.5 and PM10 associated with lifetime OM and the onset of OM. Similarly, the 4th gestational month was a critical window for all pollutants except CO exposure in relation to lifetime OM and OM onset, but not recurrent OM attacks. PM2.5 exposure during the nine gestational months and PM10 exposure during the first three years had cumulative effects on OM development. Our subgroup analysis revealed that certain children were more susceptible to the OM risk posed by air pollution. CONCLUSIONS: Early-life exposure to air pollution, particularly PM2.5 during the middle of gestation and PM10 during the early post-natal period, was associated with childhood OM.

A novel approach for the prediction and analysis of daily concentrations of particulate matter using machine learning.

Traditional air quality analysis and prediction methods depend on the statistical and numerical analyses of historical air quality data with more information related to a specific region; therefore, the results are unsatisfactory. In particular, fine particulate matter (PM2.5, PM10) in the atmosphere is a major concern for human health. The modelling (analysis and prediction) of particulate matter concentrations remains unsatisfactory owing to the rapid increase in urbanization and industrialization. In the present study, we reconstructed a prediction model for both PM2.5 and PM10 with varying meteorological conditions (windspeed, temperature, precipitation, specific humidity, and air pressure) in a specific region. In this study, a prediction model was developed for the two observation stations in the study region. The analysis of particulate matter shows that seasonal variation is a primary factor that highly influences air pollutant concentrations in urban regions. Based on historical data, the maximum number of days (92 days in 2019) during the winter season exceeded the maximum permissible level of particulate matter (PM2.5 = 15 µg/m3) concentration in air. The prediction results showed better performance of the Gaussian process regression model, with comparatively larger R2 values and smaller errors than the other models. Based on the analysis and prediction, these novel methods may enhance the accuracy of particulate matter prediction and influence policy- and decision-makers among pollution control authorities to protect air quality.

[Chemical Characteristics and Source Apportionment of Organic Aerosols in Urban Shanghai During Cold Season Based on High Time-resolution Measurements of Organic Molecular Markers].

Organic aerosols (OA) are closely related to the formation of both PM2.5 and O3 in the atmosphere. In this study, a thermal desorption aerosol GC/MS (TAG) online system was adopted to measure hourly concentrations of 94 total organic molecular markers in PM2.5 at an urban site in Shanghai from November 6th to December 31st, 2021. Combined with air mass cluster analysis and other online measurement data, the chemical characteristics of OA under the influence of different air masses, oxidant levels, and relative humidity (RH) levels were investigated. The results showed that OA was characterized by higher mass percentages of primary organic molecular markers (e.g., saturated fatty acids, unsaturated fatty acids, and alkanes) under the influence of local air masses. Further, high loadings of biomass burning tracers were observed in OA under the influence of long-range transported air masses. In contrast, OA impacted by marine air masses was laden with significantly higher fractions of secondary organic molecular markers, such as dicarboxylic acids and hydroxyl dicarboxylic acids, which were formed from a wide range of volatile organic precursors through photochemical and aqueous-phase processing. With the application of the positive matrix factorization (PMF) model, seven total primary source factors and five secondary source factors were resolved for PM2.5 and OA during the observation. Among them, secondary nitrate was the highest contributor to PM2.5 mass with a mass percentage of 25.2%, whereas vehicle emissions were the top contributor (24.0%) to OA mass. Primary source factors, including coal combustion, vehicle emission, and cooking emission as well as their corresponding secondary source factors (e.g., secondary nitrate, secondary organic aerosols 2, etc.) showed elevated contributions in PM2.5 and OA with the increase in PM2.5 masses, indicating that more stringent controls of local emission sources (e.g., coal combustion, vehicle emission, and cooking emission) are needed to further lower PM2.5 pollution and improve air quality in Shanghai.

Active living wall for particulate matter and VOC remediation: potential and application.

Particulate matters (PM) and volatile organic compounds (VOCs) are the sources of toxic substances that hurt human health and can cause human carcinogens. An active living wall was applied to reduce PM and VOC contamination, while Sansevieria trifasciata cv. Hahnii, a high-performance plant for VOC removal, was selected to grow on the developing wall and used to treat PM and VOCs. The active living wall operating in a 24 m3 testing chamber showed the ability to remediate more than 90% PM within 12 h. The VOC removal can be approximately 25-80% depending on each compound. In addition, the suitable flow velocity of the living wall was also investigated. The flow rate of 1.7 m3 h-1 in front of the living wall was found as the best inlet flow velocity for the developed active living wall. The suitable condition for PM and VOC removal in the active living wall application on the real side was presented in this study. The result confirmed that the application of an active living wall for PM phytoremediation can be an alternative effective technology.

Effects of intrauterine and post-natal exposure to air pollution on children's pneumonia: Key roles in different particulate matters exposure during critical time windows.

BACKGROUND: Despite mounting evidence linked pneumonia with air pollution, it is unclear what main pollutant(s) exposure in which critical window(s) play a key role in pneumonia. OBJECTIVE: To examine effects of intrauterine and post-natal exposure to air pollution on children's doctor-diagnosed pneumonia (DDP). METHODS: A combination of cross-sectional and retrospective cohort study was conducted at Changsha, China during 2019-2020. Personal exposure to outdoor air pollutants at each child's home address was estimated using inverse distance weighted (IDW) method based on data from 10 air quality monitoring stations. Associations between personal air pollution exposure and DDP were evaluated. RESULTS: Children's DDP was associated with intrauterine and post-natal exposure to PM2.5, PM2.5-10, and PM10, adjusted ORs (95% CI) of 1.17 (1.04-1.30), 1.09 (1.01-1.17), and 1.07 (1.00-1.14) for IQR increase in intrauterine exposure and 1.12 (1.02-1.22), 1.13 (1.06-1.21), and 1.28 (1.16-1.41) for post-natal exposure. Intrauterine PM2.5 exposure and post-natal PM10 exposure were associated with a higher risk of pneumonia. We identified the 2nd trimester, 3rd trimester, and first year as critical windows respectively for PM2.5, PM2.5-10, and PM10 exposure. Daytime exposure to traffic-related air pollution especially during early life increased DDP. CONCLUSION: Intrauterine and post-natal exposure to particulate matters played a dominant role in children's DDP.

Individual exposure of ambient particulate matters and eosinophilic chronic rhinosinusitis with nasal Polyps: Dose-Response, mediation effects and recurrence prediction.

PURPOSE: We evaluated the association between ambient particulate matter (PM) exposure and eosinophilic chronic rhinosinusitis with nasal polyps (CRSwNP), and predicted the CRSwNP recurrence risk using machine learning algorithms. METHODS: In total, 1,086 patients with CRSwNP were recruited from nine hospitals in China during 2014-2019. The average annual concentrations of ambient PMs before surgery were assessed using satellite-based daily concentrations of PM2.5 and PM10 for a 1 × 1-km2 area. Linear regression and logistic regression models were used to evaluate the associations of PM exposure with eosinophilia and risks of eosinophilic CRSwNPs. In addition, mediation effect analysis was used to validate the interrelationships of the aforementioned factors. Finally, machine learning algorithms were used to predict the recurrence risks of CRSwNPs. RESULTS: There was a significantly increased risk of eosinophilic CRSwNPs with each 10 µg/m3 increase in PMs, with odds ratios (ORs) of 1.039 (95% confidence interval [CI] = 1.007-1.073) for PM10 and 1.058 (95% CI = 1.007- 1.112) for PM2.5. Eosinophils had a significant mediation effect, which accounted for 52% and 35% of the relationships of CRSwNP recurrence with PM10 and PM2.5, respectively. Finally, we developed a naïve Bayesian model to predict the risk of CRSwNP recurrence based on PM exposure, inflammatory data, and patients' demographic factors. CONCLUSIONS: Increased PM exposure is associated with an increased risk of eosinophilic CRSwNP in China. Therefore, patients with eosinophilic CRSwNP should reduce PM exposure to mitigate its harmful impacts.

Intrauterine and early postnatal exposure to air pollution associated with childhood allergic rhinitis.

BACKGROUND: Despite mounting evidence linking allergic rhinitis (AR) to air pollution, it remains unclear which major air pollutant(s) and critical window(s) of exposure play important roles in children's AR. OBJECTIVE: To examine the effects of intrauterine and early postnatal exposure to outdoor air pollution on children with doctor-diagnosed allergic rhinitis (DDAR). METHODS: A retrospective cohort study involving 8689 kindergarten children was conducted in Changsha, China, from 2019 to 2020. A questionnaire survey was conducted to collect information on the health status of children and their family members, as well as their living habits and home environment. Personal exposure to daily outdoor air pollutants (PM2.5, PM2.5-10, PM10, SO2, NO2, and CO) was estimated during 40 gestational weeks, three trimesters, the entire pregnancy, and the first year after birth. Multiple logistic regression models were used to assess the associations between air pollution and children's DDAR. RESULTS: Children's DDAR was associated with intrauterine CO exposure, with adjusted ORs (95% CI) of 1.18 (1.03-1.34) for each IQR increase in CO exposure. The second and third trimesters were critical windows for PM2.5 and CO exposure in relation to DDAR. Furthermore, early postnatal exposure to PM2.5-10 and PM10 in first year of life was associated with DDAR development, with adjusted ORs (95% CI) of 1.11 (1.01-1.22) and 1.27 (1.09, 1.47). The entire pregnancy and the first year of life were critical windows for CO and PM10 exposure. Some children were predisposed to DDAR risk due to exposure to traffic-related air pollution (TRAP). CONCLUSION: Our findings support the hypothesis of "fetal origin of allergic rhinitis" by demonstrating that intrauterine and early postnatal exposure to air pollution plays an important role in children's DDAR.