Background Particulate Matter Research Articles

PM2.5-induced oxidative stress upregulates PLA2R expression in the lung and is involved in the pathogenesis of membranous nephropathy through extracellular vesicles

BackgroundParticulate matter (PM2.5) has been implicated in the development of membranous nephropathy (MN), but the underlying mechanism has yet to be fully understood. Oxidative stress is an essential factor of PM2.5-related toxicity and plays a significant role in the exposure of target antigenic epitopes in MN. This study aims to explore the pathogenic effects of PM2.5 in facilitating the crosstalk between the lung and kidney in MN.MethodWe examined oxidative stress indicators and the circulating levels of extracellular vesicles (EVs) in patients diagnosed with MN. Additionally, we assessed the expression of M-type phospholipase A2 receptor (PLA2R) in human lung tissue ex vivo. To verify the impact of PM2.5 on PLA2R expression in the lung and the kidney, we stimulated human bronchial epithelial cells (Beas-2B) with lipopolysaccharide (LPS) or PM2.5. We then treated podocytes in vitro with the supernatants from PM2.5-exposed Beas-2B cells, intervening with GW4869, an inhibitor of EV release, to explore the role of EV-mediated cell-cell interactions.ResultsWe found that elevated serum markers of oxidative stress and increased levels of PLA2R + EVs correlated positively with anti-PLA2R antibody levels in the serum of patients with idiopathic MN (IMN). Notably, PLA2R expression was significantly higher in the lung tissue of smokers, suggesting a possible link between PLA2R and oxidative stress. In vitro experiments demonstrated that PLA2R expression in Beas-2B cells was upregulated upon stimulation with LPS and PM2.5, an effect that could be reversed by the antioxidant glutathione (GSH). Furthermore, the supernatants from PM2.5-exposed Beas-2B cells were found to induce PLA2R overexpression and injury in podocytes, with this effect being mitigated by GW4869, an inhibitor of EVs release.ConclusionOur study contributes new knowledge to the understanding of how environmental pollutants, such as PM2.5, cause kidney damage through oxidative stress and EV-mediated signaling. The findings pave the way for further research into therapeutic strategies targeting oxidative stress and EVs, which could potentially improve patient outcomes of MN, particularly in high-risk populations like smokers and those exposed to air pollution.

Dynamics of the airway microbiome in response to exposure to particulate matter 2.5 in patients with chronic obstructive pulmonary disease

BackgroundParticulate matter (PM) and air pollution have been suggested to be associated with chronic obstructive pulmonary disease (COPD), contributing significantly to global respiratory disease-related mortality. This study aimed to investigate whether seasonal exposure to PM influences dysbiosis in the respiratory microbiota of patients with COPD. MethodsSputum samples were collected four times over 1 year from 102 patients with COPD, and 16S rRNA sequencing was performed. The dynamics of the airway microbiota were analyzed depending on PM exposure levels and season. ResultsThe PM-low exposure group had higher α-diversity compared to the PM-high exposure group, particularly noted in spring. Some bacterial groups, including seven species such as Treponema socranskii, were more abundant in the low exposure group. Additionally, the bacterial community structure in summer significantly differed from that in other seasons, with significantly increased α-diversity in this season. The difference in the airway microbiome due to PM exposure was prominent in patients with moderate COPD. ConclusionsPM exposure may influence changes in the sputum microbiome depending on exposure levels and seasonal variations. Our results suggest that airway microbiomes could vary with PM exposure according to seasonal trends.

Anti-inflammatory diet mitigate cardiovascular risks due to particulate matter exposure in women during pregnancy: A perspective cohort study from China

BackgroundParticulate matter (PM) exposure during pregnancy may increase cardiovascular risk (CVR). However, the specific time windows of exposure contributing to this association and the potential biological mechanisms underlying it remain unclear. ObjectiveTo determine the sensitive time window for CVR related to PM exposure. We investigated whether levels of inflammatory biomarkers mediate the relationship between PM exposure and CVR, and examined the potential impact of an anti-inflammatory diet on this association. MethodsFrom 2015 to 2021, 9294 pregnant women from three Hefei hospitals were included. We used a 1 × 1 km satellite dataset to assess PM1, PM2.5, and PM10 exposure. High-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured as inflammatory biomarkers. The empirical dietary inflammatory pattern (EDIP) score, based on a validated food frequency questionnaire. The CVR score was calculated using five clinical metrics based on American Heart Association criteria. ResultsWe found a significant association between PM exposure and increased CVR score, especially during the 2nd to 8th weeks of the first trimester. For every increase of 10-μg/m3 of PM1, PM2.5, and PM10, there was an associated increase in CVR of 0.51 (95%CI: 0.21, 082), 0.25 (95% CI: 0.11 to 0.39), and 0.29 (95% CI: 0.09 to 0.37), respectively. Mediation analysis revealed that the proportion of the association between PM1, PM2.5, and PM10 exposure and CVR mediated by inflammatory biomarkers was 24.3%, 22.4%, and 20.1%, respectively. Stratified analyses showed no positive correlation between PM exposure and CVR in the anti-inflammatory diet (low EDIP) group. The β coefficients were 0.52 for PM1 (95% CI: -0.06 to 1.11), 0.31 for PM2.5 (95% CI: -0.04 to 0.79), and 0.25 for PM10 (95% CI: -0.03 to 0.54). ConclusionsPM exposure, particularly during weeks 2–8 of pregnancy, correlates with CVR, partly mediated by levels of inflammatory biomarkers. An anti-inflammatory diet mitigates CVR associated with PM exposure.

The association between cumulative exposure to PM2.5 and DNA methylation measured using methyl-capture sequencing among COPD patients

BackgroundParticulate matter with a diameter of < 2.5 μm (PM2.5) influences gene regulation via DNA methylation; however, its precise mechanism of action remains unclear. Thus, this study aimed to examine the connection between personal PM2.5 exposure and DNA methylation in CpG islands as well as explore the associated gene pathways.MethodsA total of 95 male patients with chronic obstructive pulmonary disease (COPD) were enrolled in this study. PM2.5 concentrations were measured for 12 months, with individual exposure recorded for 24 h every 3 months. Mean indoor and estimated individual PM2.5 exposure levels were calculated for short-term (7 days), mid-term (35 days), and long-term (90 days). DNA methylation analysis was performed on the blood samples, which, after PCR amplification and hybridization, were finally sequenced using an Illumina NovaSeq 6000 system. Correlation between PM2.5 exposure and CpG methylation sites was confirmed via a mixed-effects model. Functional enrichment analysis was performed on unique CpG methylation sites associated with PM2.5 exposure to identify the relevant biological functions or pathways.ResultsThe number of CpG sites showing differential methylation was 36, 381, and 182 for the short-, mid-, and long-term indoor models, respectively, and 3, 98, and 28 for the short-, mid-, and long-term estimated exposure models, respectively. The representative genes were TMTC2 (p = 1.63 × 10-3, R2 = 0.656), GLRX3 (p = 1.46 × 10-3, R2 = 0.623), DCAF15 (p = 2.43 × 10-4, R2 = 0.623), CNOT6L (p = 1.46 × 10-4, R2 = 0.609), BSN (p = 2.21 × 10-5, R2 = 0.606), and SENP6 (p = 1.59 × 10-4, R2 = 0.604). Functional enrichment analysis demonstrated that the related genes were mostly associated with pathways related to synaptic transmission in neurodegenerative diseases and cancer.ConclusionA significant association was observed between PM2.5 exposure and DNA methylation upon short-term exposure, and the extent of DNA methylation was the highest upon mid-term exposure. Additionally, various pathways related to neurodegenerative diseases and cancer were associated with patients with COPD.ClinicalTrials.gov identifierNCT04878367.

Biomarkers of Airway Disease, Barrett’s and Underdiagnosed Reflux Noninvasively (BAD-BURN) in World Trade Center exposed firefighters: a case–control observational study protocol

BackgroundParticulate matter exposure (PM) is a cause of aerodigestive disease globally. The destruction of the World Trade Center (WTC) exposed first responders and inhabitants of New York City to WTC-PM and caused obstructive airways disease (OAD), gastroesophageal reflux disease (GERD) and Barrett’s Esophagus (BE). GERD not only diminishes health-related quality of life but also gives rise to complications that extend beyond the scope of BE. GERD can incite or exacerbate allergies, sinusitis, bronchitis, and asthma. Disease features of the aerodigestive axis can overlap, often necessitating more invasive diagnostic testing and treatment modalities. This presents a need to develop novel non-invasive biomarkers of GERD, BE, airway hyperreactivity (AHR), treatment efficacy, and severity of symptoms.MethodsOur observational case-cohort study will leverage the longitudinally phenotyped Fire Department of New York (FDNY)-WTC exposed cohort to identify Biomarkers of Airway Disease, Barrett’s and Underdiagnosed Reflux Noninvasively (BAD-BURN). Our study population consists of n = 4,192 individuals from which we have randomly selected a sub-cohort control group (n = 837). We will then recruit subgroups of i. AHR only ii. GERD only iii. BE iv. GERD/BE and AHR overlap or v. No GERD or AHR, from the sub-cohort control group. We will then phenotype and examine non-invasive biomarkers of these subgroups to identify under-diagnosis and/or treatment efficacy. The findings may further contribute to the development of future biologically plausible therapies, ultimately enhance patient care and quality of life.DiscussionAlthough many studies have suggested interdependence between airway and digestive diseases, the causative factors and specific mechanisms remain unclear. The detection of the disease is further complicated by the invasiveness of conventional GERD diagnosis procedures and the limited availability of disease-specific biomarkers. The management of reflux is important, as it directly increases risk of cancer and negatively impacts quality of life. Therefore, it is vital to develop novel noninvasive disease markers that can effectively phenotype, facilitate early diagnosis of premalignant disease and identify potential therapeutic targets to improve patient care.Trial registrationName of Primary Registry: “Biomarkers of Airway Disease, Barrett's and Underdiagnosed Reflux Noninvasively (BADBURN)”. Trial Identifying Number: NCT05216133. Date of Registration: January 31, 2022.

Dust particulate matter increases pulmonary embolism onset: A nationwide time-stratified case-crossover study in China

BackgroundParticulate matter (PM) has been found to elevate the risk of pulmonary embolism (PE) onset. Among the contributors to PM, dust PM stands as the second natural source, and its emissions are escalating due to climate change. Despite this, information on the effect of dust PM on PE onset is scarce. Hence, this study aims to investigate the impacts of dust PM10, dust PM2.5–10, and dust PM2.5 on PE onset. MethodsA nationwide time-stratified case-crossover study was conducted between 2015 and 2020, using data from 18,616 PE onset cases across 1,921 hospitals in China. The analysis employed a conditional logistic regression model to quantify the associations between dust PM10, dust PM2.5–10, and dust PM2.5 and PE onset. Furthermore, the study explored the time-distributed lag pattern of the effect of dust PM on PE development. Stratified analyses were performed based on sex, age, region, and season. ResultsDust PM10, dust PM2.5–10, and dust PM2.5 exhibited significant health effects on PE onset, particularly concerning exposure on the same day. The peak estimates were observed at lag 01 day, with the odds ratio being 1.011 [95 % confidence interval (CI): 1.003, 1.019], 1.014 (95 % CI: 1.003, 1.026), and 1.039 (95 % CI: 1.011, 1.068), for a 10 μg/m3 increase in the concentration of dust PM10, dust PM2.5–10, and dust PM2.5, respectively. In addition, the study identified a higher risk of PE onset associated with dust PM exposure during the warm season than that in cool season, particularly for dust PM2.5. ConclusionsThe findings from this study suggest that short-term exposure to dust PM, particularly dust PM2.5, may trigger PE onset, posing a significant health threat. Implementing measures to mitigate dust PM emissions and protect patients with PE from dust PM exposure is imperative.

Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure

BackgroundParticulate matter 2.5 (PM2.5) deposition in the lung’s alveolar capillary region (ACR) is significantly associated with respiratory disease development, yet the molecular mechanisms are not completely understood. Adverse responses that promote respiratory disease development involve orchestrated, intercellular signaling between multiple cell types within the ACR. We investigated the molecular mechanisms elicited in response to PM2.5 deposition in the ACR, in an in vitro model that enables intercellular communication between multiple resident cell types of the ACR.MethodsAn in vitro, tri-culture model of the ACR, incorporating alveolar-like epithelial cells (NCI-H441), pulmonary fibroblasts (IMR90), and pulmonary microvascular endothelial cells (HULEC) was developed to investigate cell type-specific molecular responses to a PM2.5 exposure in an in-vivo-like model. This tri-culture in vitro model was termed the alveolar capillary region exposure (ACRE) model. Alveolar epithelial cells in the ACRE model were exposed to a suspension of diesel exhaust particulates (DEP) (20 µg/cm2) with an average diameter of 2.5 µm. Alveolar epithelial barrier formation, and transcriptional and protein expression alterations in the directly exposed alveolar epithelial and the underlying endothelial cells were investigated over a 24 h DEP exposure.ResultsAlveolar epithelial barrier formation was not perturbed by the 24 h DEP exposure. Despite no alteration in barrier formation, we demonstrate that alveolar epithelial DEP exposure induces transcriptional and protein changes in both the alveolar epithelial cells and the underlying microvascular endothelial cells. Specifically, we show that the underlying microvascular endothelial cells develop redox dysfunction and increase proinflammatory cytokine secretion. Furthermore, we demonstrate that alveolar epithelial MAPK signaling modulates the activation of NRF2 and IL-8 secretion in the underlying microvascular endothelial cells.ConclusionsEndothelial redox dysfunction and increased proinflammatory cytokine secretion are two common events in respiratory disease development. These findings highlight new, cell-type specific roles of the alveolar epithelium and microvascular endothelium in the ACR in respiratory disease development following PM2.5 exposure. Ultimately, these data expand our current understanding of respiratory disease development following particle exposures and illustrate the utility of multicellular in vitro systems for investigating respiratory tract health.

Mediation of metabolic syndrome in the association between long-term exposure to particulate matter and incident cardiovascular disease: Evidence from a population-based cohort in Chengdu

BackgroundParticulate matter (PM) exposure has been linked with cardiovascular disease (CVD) and metabolic syndrome (MetS), the latter characterized by concurrent multiple metabolic disorders. As a result, the mechanisms assumption from PM to CVD through MetS have emerged, thus requiring further epidemiological evidence. This cohort study aimed to assess whether MetS mediates the associations of PM with CVD risk. MethodsThis study included 14,195 participants from the Chengdu cohort of the China Multi-Ethnic Cohort (CMEC) study in 2018. The primary outcome of incident CVD diagnoses was identified using matched hospital records from the Health Information Center of Sichuan Province. Residence-specific levels of PM with aerodynamic diameters of ≤ 1 µm (PM1), ≤ 2.5 µm (PM2.5), and ≤ 10 µm (PM10) were estimated by spatiotemporal models. Causal mediation analyses were applied to evaluate the indirect effect of MetS. ResultsIncreased exposure levels to PM were significantly associated with MetS and CVD. Mediation analyses indicated that the associations between PM exposure and CVD were mediated by MetS, with the proportion of multiple mediations being 19.3%, 12.1%, and 13.5% for PM1, PM2.5, and PM10, respectively. Further moderated mediation analyses suggested that male, overweight individuals, alcohol drinkers, and those suffering from indoor air pollution may experience more significant adverse effects from PM exposure on CVD via MetS than others. ConclusionsOur findings suggest that MetS partially mediates the association between long-term exposure to PM and CVD. These mediation effects appear to be amplified by demographic characteristics and unhealthy lifestyles.

Ambient atmospheric PM worsens mouse lung injury induced by influenza A virus through lysosomal dysfunction

BackgroundParticulate matter (PM) air pollution poses a significant risk to respiratory health and is especially linked with various infectious respiratory diseases such as influenza. Our previous studies have shown that H5N1 virus infection could induce alveolar epithelial A549 cell death by enhancing lysosomal dysfunction. This study aims to investigate the mechanisms underlying the effects of PM on influenza virus infections, with a particular focus on lysosomal dysfunction.ResultsHere, we showed that PM nanoparticles such as silica and alumina could induce A549 cell death and lysosomal dysfunction, and degradation of lysosomal-associated membrane proteins (LAMPs), which are the most abundant lysosomal membrane proteins. The knockdown of LAMPs with siRNA facilitated cellular entry of both H1N1 and H5N1 influenza viruses. Furthermore, we demonstrated that silica and alumina synergistically increased alveolar epithelial cell death induced by H1N1 and H5N1 influenza viruses by enhancing lysosomal dysfunction via LAMP degradation and promoting viral entry. In vivo, lung injury in the H5N1 virus infection-induced model was exacerbated by pre-exposure to silica, resulting in an increase in the wet/dry ratio and histopathological score.ConclusionsOur findings reveal the mechanism underlying the synergistic effect of nanoparticles in the early stage of the influenza virus life cycle and may explain the increased number of respiratory patients during periods of air pollution.

Heavy metal deposition and parameter change of soft contact lenses by exposure to particulate matter

BackgroundParticulate matter (PM) is known to contain heavy metals and be harmful to the tissues and organs of the human body including the eyes. As such, in this study, the deposition of heavy metals from PM on soft contact lenses was examined, and changes in the lens parameters were further investigated.MethodsSix types of soft contact lenses were exposed to captured PM10 for eight hours. The central thickness, water content, refractive power, and oxygen transmissibility of each contact lens were measured after analyzing the amounts of six heavy metals adsorbed on the contact lenses.ResultsLead, manganese, barium, arsenic, vanadium, and cadmium were detected in the captured PM, and only lead was adsorbed on all soft contact lenses except senofilcon C. The largest deposition was 23.21 ± 0.70 (10− 3)µg/lens of the lead on lotrafilcon B. The oxygen transmissibility of nelfilcon A exhibited statistically significant changes, however, it was within the ISO standard tolerance. Nevertheless, changes in the central thickness, water content, and refractive power of each soft contact lens were not statistically significant.ConclusionsThis study revealed that a considerable amount of lead in PM10 was adsorbed on soft contact lenses. Amongst lens parameters, only oxygen transmissibility changed significantly. Thus, wearing soft contact lenses under high PM10 concentration might affect the physiology of the eyes.

Particulate Matter Pollution Remains a Threat for Cardiovascular Health: Findings From the Global Burden of Disease 2019.

Background Particulate matter (PM) pollution is a significant risk factor for cardiovascular diseases, causing substantial disease burden and deaths worldwide. This study aimed to investigate the global burden of cardiovascular diseases attributed to PM from 1990 to 2019. Methods and Results We used the GBD (Global Burden of Disease) study 2019 to investigate disability-adjusted life-years (DALYs), years of life lost (YLLs), years lived with disability (YLDs), and deaths attributed to PM as well as its subgroups. It was shown that all burden measures' age-standardized rates for PM were in the same decreasing trend, with the highest decline recorded for deaths (-36.7%). However, the all-age DALYs increased by 31%, reaching 8.9 million in 2019, to which YLLs contributed the most (8.2 million [95% uncertainty interval, 7.3 million-9.2 million]). Men had higher deaths, DALYs, and YLLs despite lower years lived with disability in 2019 compared with women. There was an 8.1% increase in the age-standardized rate of DALYs for ambient PM; however, household air pollution from solid fuels decreased by 65.4% in the assessed period. Although higher in men, the low and high sociodemographic index regions had the highest and lowest attributed YLLs/YLDsratio for PM pollution in 2019, respectively. Conclusions Although the total age-standardized rate of DALYs for PM-attributed cardiovascular diseases diminished from 1990 to 2019, the global burden of PM on cardiovascular diseases has increased. The differences between men and women and between regions have clinical and policy implications in global health planning toward more exact funding and resource allocation, in addition to addressing inequity in health care access.

Risk of De Novo Hypertensive Disorders of Pregnancy After Exposure to PM1 and PM2.5 During the Period From Preconception to Delivery: Birth Cohort Study.

Particulate matter (PM) is detrimental to the respiratory and circulatory systems. However, no study has evaluated the lag effects of weekly exposure to fine PM during the period from preconception to delivery on the risk of hypertensive disorders of pregnancy (HDPs). We set out to investigate the lag effect windows of PM on the risk of HDPs on a weekly scale. Data from women with de novo HDPs and normotensive pregnant women who were part of the Peking University Retrospective Birth Cohort, based on the hospital information system of Tongzhou district, were obtained for this study. Meteorological data and data on exposure to fine PM were predicted by satellite remote sensing data based on maternal residential address. The de novo HDP group consisted of pregnant women who were diagnosed with gestational hypertension or preeclampsia. Fine PM was defined as PM2.5 and PM1. The gestational stage of participants was from preconception (starting 12 weeks before gestation) to delivery (before the 42nd gestational week). A distributed-lag nonlinear model (DLNM) was nested in a Cox regression model to evaluate the lag effects of weekly PM exposure on de novo HDP hazard by controlling the nonlinear relationship of exposure-reaction. Stratified analyses by employment status (employed or unemployed), education level (higher or lower), and parity (primiparity or multiparity) were performed. A total of 22,570 pregnant women (mean age 29.1 years) for whom data were available between 2013 and 2017 were included in this study. The prevalence of de novo HDPs was 6.7% (1520/22,570). Our findings showed that PM1 and PM2.5 were significantly associated with an elevated hazard of HDPs. Exposure to PM1 during the 5th week before gestation to the 6th gestational week increased the hazard of HDPs. A significant lag effect of PM2.5 was observed from the 1st week before gestation to the 6th gestational week. The strongest lag effects of PM1 and PM2.5 on de novo HDPs were observed at week 2 and week 6 (hazard ratio [HR] 1.024, 95% CI 1.007-1.042; HR 1.007, 95% CI 1.000-1.015, respectively, per 10 μg/m3 increase). The stratified analyses indicated that pregnant women who were employed, had low education, and were primiparous were more vulnerable to PM exposure for de novo HDPs. Exposure to PM1 and PM2.5 was associated with the risk of de novo HDPs. There were significant lag windows between the preconception period and the first trimester. Women who were employed, had low education, and were primiparous were more vulnerable to the effects of PM exposure; more attention should be paid to these groups for early prevention of de novo HDPs.

The association between ambient particulate matter exposure and the telomere–mitochondrial axis of aging in newborns

BackgroundParticulate matter (PM) is associated with aging markers at birth, including telomeres and mitochondria. It is unclear whether markers of the core-axis of aging, i.e. tumor suppressor p53 (p53) and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), are associated with prenatal air pollution and whether there are underlying mechanisms. Methods556 mother-newborn pairs from the ENVIRONAGE birth cohort were recruited at the East Limburg Hospital in Genk (Belgium). In placenta and cord blood, telomere length (TL) and mitochondrial DNA content (mtDNAc) were measured using quantitative real-time polymerase chain reaction (qPCR). In cord plasma, p53 and PGC-1α protein levels were measured using ELISA. Daily ambient PM2.5 concentrations during gestation were calculated using a spatial temporal interpolation model. Distributed lag models (DLMs) were applied to assess the association between prenatal PM2.5 exposure and each molecular marker. Mediation analysis was performed to test for underlying mechanisms. ResultsA 5 µg/m3 increment in PM2.5 exposure was associated with −11.23 % (95 % CI: −17.36 % to −4.65 %, p = 0.0012) and −7.34 % (95 % CI: −11.56 % to −2.92 %, p = 0.0014) lower placental TL during the entire pregnancy and second trimester respectively, and with −12.96 % (95 % CI: −18.84 % to −6.64 %, p < 0.001) lower placental mtDNAc during the third trimester. Furthermore, PM2.5 exposure was associated with a 12.42 % (95 % CI: −1.07 % to 27.74 %, p = 0.059) higher cord plasma p53 protein level and a −3.69 % (95 % CI: −6.97 % to −0.31 %, p = 0.033) lower cord plasma PGC-1α protein level during the third trimester. Placental TL mediated 65 % of the negative and 17 % of the positive association between PM2.5 and placental mtDNAc and cord plasma p53 protein levels, respectively. ConclusionAmbient PM2.5 exposure during pregnancy is associated with markers of the core-axis of aging, with TL as a mediating factor. This study strengthens the hypothesis of the air pollution induced core-axis of aging, and may unravel a possible underlying mediating mechanism in an early-life epidemiological context.

TAPaC—tobacco-associated particulate matter emissions inside a car cabin: establishment of a new measuring platform

BackgroundParticulate matter (PM) emission caused by tobacco combustion leads to severe health burdens worldwide. Second-hand smoke exposure is extraordinarily high in enclosed spaces (e.g., indoor rooms, car cabins) and poses a particular threat to the health of vulnerable individuals (e.g., children, elderly, etc.). This study aimed to establish a new measuring platform and investigate PM emissions under four different ventilation conditions inside a car cabin without exposing any person to harmful tobacco smoke.MethodsPM concentrations were measured during the smoking of 3R4F reference cigarettes in a Mitsubishi Space Runner (interior volume 3.709 m3). The cigarettes were smoked with a machine, eliminating exposure of the researchers. Cigarettes were extinguished 4.5 min after ignition, and PM measurements continued until 10 min after ignition.ResultsHigh mean PM concentrations were measured for cigarettes without ventilation after 4.5 min (PM10: 1150 µg/m3, PM2.5: 1132 µg/m3, PM1: 861.6 µg/m3) and after 10 min (PM10: 1608 µg/m3, PM2.5: 1583 µg/m3, PM1: 1133 µg/m3). 3R4F smoked under conditions with turned on ventilation resulted in reduction of PM compared to those smoked without ventilation after 4.5 min (PM10:-47.5 to -58.4%, PM2.5:-47.2 to -58%, PM1:-39.6 to -50.2%) and after 10 min (PM10:-70.8 to -74.4%, PM2.5:-70.6 to -74.3%, PM1:-64.0 to -68.0%). Cigarettes smoked without ventilation generated high PM peaks at 4.5 min (PM10: 2207 µg/m3, PM2.5: 2166 µg/m3, PM1: 1421 µg/m3) and at 10 min (PM10: 1989 µg/m3, PM2.5: 1959 µg/m3, PM1: 1375 µg/m3). PM peaks of cigarettes smoked under different ventilation modes varied at 4.5 min (PM10: 630-845 µg/m3, PM2.5: 625-836 µg/m3, PM1: 543 - 693 µg/m3) and 10 min (PM10: 124 - 130 µg/m3, PM2.5: 124 - 129 µg/m3, PM1: 118 - 124 µg/m3).ConclusionThe new measuring platform provides a safer way for researchers to investigate PM emissions of cigarettes. These data are comparable to published research and show that smoking in a parked vehicle with the windows closed generates harmful PM emissions even when the vehicle ventilation is in operation. Future studies should be carried out using the new measuring platform investigating PM exposure and PM distribution of in-vehicle smoking under a wide range of conditions.

New insights into the treatment mechanisms of Vitamin D on PM2.5-induced toxicity and inflammation in mouse renal tubular epithelial cells

BackgroundParticulate matter (PM2.5) could induce renal injury other than lung and heart damage. The renal injury always displays in the way of renal inflammation. Vitamin D (VitD) has been identified as renal-protective factor with its anti-inflammatory effect. Aim of the studyThis study explored the therapeutic effect of VitD receptor (VDR) agonist (paricalcitol) on PM2.5-induced toxicity and inflammation in mouse renal tubular epithelial cells (mRTECs) and its molecular mechanisms. MethodsThe variation between PM2.5 and paricalcitol solution was investigated in different concentration solutions with transmission electron microscopy (TEM), laser-induced fluorescence (LIF) and liquid chromatography-mass spectrometry (LC-MS). The detoxication and anti-inflammation effects of paricalcitol on PM2.5 in vitro were analyzed by LIF, MTT, western blot (WB), ELISA and flow cytometry (FCM). Results and ConclusionPM2.5 became more compact after paricalcitol treatment on account of stripped polycyclic aromatic hydrocarbons (PAHs). In the cellular experiments, PM2.5 (160 μg/ml) evoked mRTECs inflammation and apoptosis through the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) /IL-1β axis, while paricalcitol (120 μg/ml) reversed these processes. The fluorescence intensity of cell supernatant detected by PAH-LIF was weakened after adding paricalcitol, compared with.PM2.5 treatment alone. Interestingly, paricalcitol can significantly reduce the concentration of highly toxic PAHs and increase the proportion of nontoxic small PAHs. Furthermore, VDR expression was negatively correlated with the inflammation and cell apoptosis. In summary, VitD and VDR promote biological detoxication on PM2.5 though PAH degradation from a molecular effect, and exert anti-inflammatory effects against NLRP3/IL-1β axis caused by PM2.5.

Current status of herbal medicine research for respiratory diseases induced by particulate matter: a protocol for a scoping review

BackgroundParticulate matter (PM) is an important environmental risk factor for the initiation and exacerbation of respiratory disease. Various herbal medicines have exhibited a reduction in symptoms of respiratory diseases induced by PM in animal models. However, the types and characteristics of studies on herbal medicine for respiratory diseases by PM have not been reviewed. This scoping review will focus on the currents status and research gap of herbal medicines for respiratory diseases caused by PM.MethodsWe will follow the scoping review framework developed by Arksey and O’Malley. MEDLINE (via PubMed), EMBASE, and the Cochrane Central Register of Controlled Trials will be searched for relevant English-language publications, and only peer-reviewed, controlled comparative in vivo/in-vitro/human studies examining the effects of herbs on respiratory disease induced by PM will be included. The basic characteristics, research methods, detailed regimens, possible mechanisms, outcomes, and results will be extracted using a predefined standardized data extraction form. Outcomes will be presented in the following categories: pulmonary function, inflammatory markers, reactive oxygen species, histology and mechanisms, and adverse events. Two researchers will independently perform the study selection, data extraction, and quality assessment. We will also present the research map and implications for further study.Ethics and disseminationEthical approval is not required because individual patient data will not be included. The findings will be disseminated through peer-reviewed publications or conference presentations.Systematic review registrationThis review protocol has been registered with the Open Science Framework on February 12, 2021 (https://osf.io/s7uvk/)

Association of ambient PM1 with hospital admission and recurrence of stroke in China

BackgroundParticulate matter (PM) pollution is a well-known risk factor of stroke. However, little is known about the association between PM1 (aerodynamic diameter ≤ 1.0 μm) and stroke. We estimated the associations of short-term exposure to PM1 with hospital admission and recurrence of stoke in China. MethodsStroke data were derived from the Chinese Stroke Center Alliance (CASA) program conducted in 1458 hospitals in 292 Chinese cities from 2015 to 2019. Daily air pollution and meteorological data were collected in the cities where studied hospitals were located. Daily PM1 concentration was estimated by a generalized additive model (GAM) using PM2.5 and meteorological variables. A time-stratified case-crossover design was applied to estimate the associations of short-term exposure to PM1 with hospital admission of stroke. A GAM model was used to estimate the association between average PM1 exposure during hospitalization and the recurrence of stroke. ResultsA total of 989,591 stroke cases were included in the study. Each 10 μg/m3 increase in PM1 (lag06-day) was associated with a 0.53% (95%CI, 0.39%, 0.67%) increment in hospital admission for stroke. The adverse effects of PM1 on ischemic stroke was stronger than on intracerebral hemorrhage. We found the associations were significant in Northeast (0.94%, 95%CI, 0.51%, 1.38%), North (0.47%, 95%CI, 0.20%, 0.75%), Central (0.57%, 95%CI, 0.30%, 0.85%), and East China (0.63%, 95%CI, 0.27%, 0.99%). Of all stroke cases, 62,988 (6.4%) had recurrent stoke attack during their hospitalization. Each 10 μg/m3 increase in PM1 was associated with a 1.64% (95%CI, 1.28%, 2.01%) increment in recurrence of stroke during hospitalization. ConclusionsShort-term exposure to PM1 may increase the risk of incidence and recurrence of stroke in China, and the effects varied across different types of stroke and regions. Geographically targeted strategies and measures are needed to control air pollution for reducing the burden of stroke from PM1.

Effects of

BackgroundParticulate matter (PM) is one of the air pollutants that can damage human skin; the recent increase in the amount of PM may be detrimental to skin health.ObjectiveWe aimed to investigate the effects of PM on cultured human sebocytes and outer root sheath (ORS) cells and the effects of Siegesbeckia Herba extract (SHE) on PM-treated cultured cells.MethodsSebocytes and ORS cells were cultured. The cultured cells were treated with various concentrations of PM of <10 µm in size (PM10) (10 µg/ml, 25 µg/ml, 50 µg/ml, and 100 µg/ml) for 24 h. Real-time polymerase chain reaction, measurement of reactive oxygen species (ROS), small interfering (si) RNA transfection, Oil Red O and Nile red staining, and immunofluorescence staining were performed to analyze the presence of inflammatory cytokines, matrix metalloproteinases (MMPs), aryl hydrocarbon receptor (AhR), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ROS, and lipid production. In addition, PM10 (100 µg/ml)-treated cultured cells were treated with 10 mg/ml of SHE.ResultsPM10 upregulates the expression of inflammatory cytokines, MMPs, AhR, NF-κB, and ROS in cultured human sebocytes and ORS cells. The production of ROS was dramatically reduced in AhR siRNA-transfected cells. In addition, PM10 upregulates sebum production in cultured sebocytes. SHE inhibited the upregulation of inflammatory cytokines, MMPs, AhR, NF-κB, ROS, and sebum production in cultured human sebocytes and/or ORS cells by PM10.ConclusionEffects of PM10 on cultured human sebocytes and ORS cells can be regulated by SH.

Exposure to combustion derived particulate matter exacerbates influenza infection in neonatal mice by inhibiting IL22 production

BackgroundParticulate matter (PM) containing environmentally persistent free radicals (EPFRs) are formed during various combustion processes, including the thermal remediation of hazardous wastes. Exposure to PM adversely affects respiratory health in infants and is associated with increased morbidity and mortality due to acute lower respiratory tract infections. We previously reported that early-life exposure to PM damages the lung epithelium and suppresses immune responses to influenza virus (Flu) infection, thereby enhancing Flu severity. Interleukin 22 (IL22) is important in resolving lung injury following Flu infection. In the current study, we determined the effects of PM exposure on pulmonary IL22 responses using our neonatal mouse model of Flu infection.ResultsExposure to PM resulted in an immediate (0.5–1-day post-exposure; dpe) increase in IL22 expression in the lungs of C57BL/6 neonatal mice; however, this IL22 expression was not maintained and failed to increase with either continued exposure to PM or subsequent Flu infection of PM-exposed mice. This contrasts with increased IL22 expression in age-matched mice exposed to vehicle and Flu infected. Activation of the aryl hydrocarbon receptor (AhR), which mediates the induction and release of IL22 from immune cells, was also transiently increased with PM exposure. The microbiome plays a major role in maintaining epithelial integrity and immune responses by producing various metabolites that act as ligands for AhR. Exposure to PM induced lung microbiota dysbiosis and altered the levels of indole, a microbial metabolite. Treatment with recombinant IL22 or indole-3-carboxaldehyde (I3A) prevented PM associated lung injury. In addition, I3A treatment also protected against increased mortality in Flu-infected mice exposed to PMs.ConclusionsTogether, these data suggest that exposure to PMs results in failure to sustain IL22 levels and an inability to induce IL22 upon Flu infection. Insufficient levels of IL22 may be responsible for aberrant epithelial repair and immune responses, leading to increased Flu severity in areas of high PM.

Evaluation of anti-inflammatory and immunomodulatory activity of Chyawanprash on particulate matter-induced pulmonary disease in mice

BackgroundParticulate matter (PM) is the major component of air pollution, which includes emissions from both anthropogenic and natural sources. PM, with aerodynamic diameter of 2.5 ± 10 μm can remain in the air for a long time and be deposited in the lungs through inhalation and hence, is a major threat to human health. ObjectiveThe objective of the present study was to examine the protective effect of Chyawanprash (CP) on PM-induced pulmonary disease through estimation of cytokines and immunoglobulins. Materials and methodsCP, standard drug, and vehicle (Group G1 to Group G7) were administered orally at the dose volume of 10 ml/kg, for 28 consecutive days (Prophylactic treatment; i.e., Day 1 to Day 28) and next 10 days (i.e., Day 29 to Day 38) of co-treatment with inducing agent PM2.5 intratracheally. Animals of group G6 (Inhalation + control) and G7 (Inhalation + CP) were exposed group-wise to PM2.5 aerosol (2 mg/5 ml, 15 min) via inhalation in histamine chamber on Days 29, 31, 33, 35, and 37. On Day 38, animals were anesthetised and blood and broncho alveolar lavage fluid (BALF) were collected. Animals were sacrificed and lungs were collected for histology. ResultsProphylactic benefit of CP against pulmonary pathology was evidenced by the inhibition of inflammatory cytokines (BALF: TNF a, IFN-g, IL-7, IL-6 and lung: TNFa, Histamine and IL-6), chemokines (Lung: MMP-9), inflammatory cell infiltration (cell counts in BALF), and histopatholoy in experimental mice model. ConclusionThese findings suggest that CP has potential benefit in protecting from harmful effects caused by air pollutants such as PM2.5.