Humans ; Diabetes Mellitus, Type 2/epidemiology* ; Air Pollution/adverse effects* ; Air Pollutants/toxicity* ; Risk Assessment ; Particulate Matter ; Environmental Exposure

Ozone/toxicity* ; Air Pollution/analysis* ; Air Pollutants/analysis* ; China/epidemiology* ; Environmental Exposure/analysis* ; Mortality ; Particulate Matter/analysis*

Ambient fine particulate matters (PM_2.5) refer to particulate matters with an aerodynamic diameter less than or equal to 2.5 μm. PM_2.5 enter the body through the target organ-lung, and can induce a variety of adverse health effects (such as cardiovascular diseases, diabetes, respiratory diseases, neurodegenerative diseases and adverse birth outcomes). PM_2.5 are known to have complex compositions (including water-soluble/-insoluble components and biological components), diverse sources and capacity of secondary transformation. Numerous epidemiological and toxicological studies indicated that different components of PM_2.5 may induce adverse health effects through different biological mechanisms. In adddition, co-exposure of different components and their interaction should also be considered. Thus here we have systematically reviewed studies in recent years about the toxicological effects and underlying mechanisms of different components of ambient fine particulate matters, including inflammatory response, oxidative stress, endoplasmic reticulum stress, activation of the NF-κB signaling pathway and so on. The information may give some insights into the prevention and treatment of adverse health effects caused by exposure to different components of PM_2.5.
Air Pollutants/toxicity* ; Cardiovascular Diseases/chemically induced* ; Humans ; Lung ; Oxidative Stress ; Particulate Matter/toxicity*

Objective: To screen the differential methylation sites, genes and pathways of air pollution fine particles (PM(2.5)) on human bronchial epithelial (HBE) cells by methylation chip and bioinformation technology, so as to provide scientific basis for further study of the toxicological mechanism of PM(2.5) on HBE cells. Methods: In August 2020, HBE cells were infected with 10 μg/ml and 50 μg/ml PM(2.5) aqueous solution for 24 h, namely PM(2.5) 10 μg/ml exposure group (low dose group) and PM(2.5) 50 μg/ml exposure group (high dose group) ; uninfected HBE cells were used as control group. The DNA fragments were hybridized with the chip, the chip scanned and read the data, analyzed the data, screened the differential methylation sites, carried out GO analysis and KEGG analysis of the differential methylation sites, and analyzed the interaction relationship of the overall differential methylation sites by functional epigenetic modules (FEMs). Results: Compared with the control group, 127 differential methylation sites were screened in the low-dose group, including 89 genes, including 55 sites with increased methylation level and 72 sites with decreased methylation level. The differential methylation sites were mainly concentrated in the Body region and UTR region. Compared with the control group, 238 differential methylation sites were screened in the high-dose group, including 168 genes, of which 127 sites had increased methylation level and 111 sites had decreased methylation level. The differential heterotopic sites were mainly concentrated in the Body region and UTR region. Through FEMs analysis, 8 genes with the most interaction were screened, of which 6 genes had significant changes in methylation level. MALT1 gene related to apoptosis was found in the heterotopic site of methylation difference in low-dose group; PIK3CA and ARID1A genes related to carcinogenesis were found in the heterotopic sites of methylation difference in high-dose group; TNF genes related to tumor inhibition were found in the results of FEMs analysis. Conclusion: After PM(2.5) exposure to HBE cells, the DNA methylation level is significantly changed, and genes related to apoptosis and carcinogenesis are screened out, suggesting that the carcinogenic mutagenic effect of PM(2.5) may be related to DNA methylation.
Air Pollutants/toxicity* ; Basic Helix-Loop-Helix Transcription Factors/analysis* ; Carcinogenesis ; DNA Methylation ; Humans ; Particulate Matter/toxicity* ; Technology

Objective To quantitatively evaluate the associations of PM
Air Pollutants/toxicity* ; Air Pollution/adverse effects* ; Child, Preschool ; China ; Dermatitis, Atopic/epidemiology* ; Female ; Humans ; Male ; Outpatients ; Particulate Matter/analysis*

Objective: Epidemiological studies reveal that exposure to fine particulate matter (aerodynamic diameter ≤ 2.5 μm, PM Methods: EVs were isolated from the serum of healthy subjects, quantified Results: PM Conclusions EVs treatment promotes cell survival and attenuates PM
A549 Cells ; Air Pollutants/toxicity* ; Apoptosis/drug effects* ; Cell Survival/drug effects* ; Extracellular Vesicles ; Humans ; Male ; Middle Aged ; Particulate Matter/toxicity* ; Protective Agents/pharmacology* ; Proto-Oncogene Proteins c-akt/metabolism* ; Serum

OBJECTIVES: The association between concentrations of sulfur dioxide (SO), nitrogen dioxide (NO), carbon monoxide (CO), ozone (O), and emergency ambulance dispatches (EADs) for asthma was explored in the central Sichuan Basin of southwestern China for the first time. METHODS: EADs for asthma were collected from the Chengdu First-Aid Command Center. Pollutant concentrations were collected from 24 municipal environmental monitoring centers and including SO, NO, CO, daily 8-h mean concentrations of O (O-8 h), and particulate matter less than 2.5 μm in aerodynamic diameter (PM). The climatic data were collected from the Chengdu Municipal Meteorological Bureau. All data were collected from years spanning 2013-2017. A time-stratified case-crossover design was used to analyze the data. RESULTS: After controlling for temperature, relative humidity, and atmospheric pressure, IQR increases in SO (13 μg/m), NO (17 μg/m), and CO (498 μg/m) were associated with 18.8%, 11.5%, and 3.1% increases in EADs for asthma, respectively. The associations were strongest for EADs and SO, NO, and CO levels with 3-, 5-, and 1-day lags, respectively. CONCLUSIONS This study provides additional data to the limited body of literature for potential health risks arising from ambient gaseous pollutants. The results of the study suggest that increased concentrations of SO, NO, and CO were positively associated with emergency ambulance dispatches for asthma in Chengdu, China. Further studies are needed to investigate the effects of individual air pollutants on asthma.
Air Pollutants ; analysis ; toxicity ; Asthma ; chemically induced ; epidemiology ; Carbon Monoxide ; analysis ; toxicity ; China ; epidemiology ; Cities ; Cross-Over Studies ; Emergency Medical Dispatch ; statistics & numerical data ; Environmental Monitoring ; statistics & numerical data ; Humans ; Nitrogen Dioxide ; analysis ; toxicity ; Ozone ; analysis ; toxicity ; Particle Size ; Particulate Matter ; analysis ; toxicity ; Risk ; Sulfur Dioxide ; analysis ; toxicity

Exposure to traffic-related air pollutants(TRAP)has been implicated in airway allergic diseases.Recent findings include epidemiologic and mechanistic studies that shed new light on the impact of TRAP on allergic rhinitis(AR)and the biology underlying this impact.These studies have found that oxidative stress induced by TRAP could affect the axis of epithelial cell-dendritic cell-T cell towards a T-helper 2 immune response,which is the major mechanism between TRAP and AR.Further,epigenetics and microRNA might be involved in this process.Our review will summarize the most recent findings in each of these areas.
Air Pollutants ; toxicity ; Air Pollution ; Humans ; Oxidative Stress ; Rhinitis, Allergic ; etiology ; Vehicle Emissions ; toxicity

BACKGROUND: Plastic resins are complex chemicals that contain toluene diisocyanate (TDI) and/or trimellitic anhydride (TMA), which cause occupational allergies (OA), including respiratory allergies. Serum IgGs against TDI and TMA have been suggested as potential markers of the exposure status and as exploring cause of OA. Although TDI-specific IgG has been examined for suspected OA, TMA-specific IgG is not commonly evaluated in a urethane foam factory. This study therefore investigated both TDI- and TMA-specific IgGs in suspected OA patients and to evaluate the usefulness of the measurement of multiple chemical-specific IgG measurement for practical monitoring. METHODS: Blood samples were collected from two male workers who developed respiratory allergies supposedly caused by occupational exposure to TDI and/or TMA for the presence of TDI- and TMA-specific IgGs. In addition, blood samples from 75 male workers from a urethane foam factory, along with 87 male control subjects, were collected in 2014 and tested for the same IgGs in 2014. The presence and levels of TDI- and TMA-specific serum IgGs were measured using dot blot assays. RESULTS: We found that controls had mean concentrations of TDI- and TMA-specific IgGs of 0.98 and 2.10 μg/mL, respectively. In the two workers with respiratory allergies, the TDI-specific IgG concentrations were 15.6 and 9.51 μg/mL, and TMA-specific IgG concentrations were 4.56 and 14.4 μg/mL, which are clearly higher than those in controls. Mean concentrations of TDI- and TMA-specific IgGs in the factory workers were 1.89 and 2.41 μg/mL, respectively, and are significantly higher than those of the controls (P < 0.001 and P < 0.026 for TDI- and TMA-specific IgGs, respectively). CONCLUSION The workers suspected of OA showed an evidently high level of TDI- and TMA-specific IgG, and these levels in workers at the urethane foam factory were also significantly higher than those in controls. In conclusion, the measurement of TDI- and TMA-specific IgG among workers using plastic resins is helpful to monitor their exposure status.
Adult ; Air Pollutants, Occupational ; adverse effects ; immunology ; Environmental Monitoring ; Humans ; Immunoglobulin G ; blood ; immunology ; Japan ; Male ; Manufacturing and Industrial Facilities ; statistics & numerical data ; Middle Aged ; Occupational Diseases ; blood ; chemically induced ; Occupational Exposure ; adverse effects ; statistics & numerical data ; Phthalic Anhydrides ; immunology ; toxicity ; Respiratory Hypersensitivity ; blood ; chemically induced ; Toluene 2,4-Diisocyanate ; immunology ; toxicity ; Workforce

BackgroundAsthma is a common chronic respiratory disease and is related to air pollution exposure. However, only a few studies have concentrated on the association between air pollution and adult asthma. Moreover, the results of these studies are controversial. Therefore, the present study aimed to analyze the influence of various pollutants on hospitalization due to asthma in adults.

MethodsA total of 1019 unrelated hospitalized adult asthma patients from Northeast China were recruited from 2014 to 2016. Daily average concentrations of air pollutants (particulate matter <2.5 μm [PM], particulate matter <10 μm [PM], sulfur dioxide [SO], nitrogen dioxide [NO], and carbon monoxide [CO]) were obtained from the China National Environmental Monitoring Centre website from 2014 to 2016. Cox logistic regression analysis was used to analyze the relationship between air pollutants and hospital admissions in adult asthma.

ResultsThe maximum odds ratio (OR) value for most air pollutants occurred on lag day 1. Lag day 1 was chosen as the exposure period, and 8 days before onset was chosen as the control period. Three pollutants (PM, CO, and SO) were entered into the regression equation, and the corresponding OR (95% confidence interval) was 0.995 (0.991-0.999), 3.107 (1.607-6.010), and 0.979 (0.968-0.990), respectively.

ConclusionsA positive association between hospital admissions and the daily average concentration of CO was observed. CO is likely to be a risk factor for hospital admissions in adults with asthma.

Air Pollutants ; toxicity ; Air Pollution ; adverse effects ; Asthma ; epidemiology ; Carbon Monoxide ; toxicity ; China ; Environmental Monitoring ; statistics & numerical data ; Female ; Hospitalization ; statistics & numerical data ; Humans ; Male ; Odds Ratio ; Particulate Matter ; toxicity ; Risk Factors ; Sulfur Dioxide ; toxicity