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

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*

BACKGROUNDAirborne fine particulate matter (PM) can induce pulmonary inflammation which may adversely affect human health, but very few reports about its effect on the neonate rats are available. This study aimed to observe the potential impact and toxicity of fine PMs on the airway in neonate rats.

METHODSPulmonary inflammation, cytotoxicity, histopathology, and antioxidants as well as oxidant products were assessed 24 hours after intratracheal instillation of fine PM consecutively for 3 days. Cytotoxicity of fine PM was measured in HEp-2 cells.

RESULTSRats treated with high dose fine PM developed significant pulmonary inflammation characterized by neutrophil and macrophage infiltration. The inflammatory process was related to elevated level of TNF-α and prooxidant/antioxidant imbalance in the lung. Cytotoxicity studies performed in human epithelial cells indicated that high dose fine PM significantly reduced cell viability.

CONCLUSIONThe study demonstrated acute exposure to fine PM induced airway inflammation as well as increased oxidative stress in addition to its direct toxic effect on airway epithelium cells.

Animals ; Animals, Newborn ; Bronchoalveolar Lavage Fluid ; chemistry ; Glutathione ; metabolism ; Male ; Oxidative Stress ; Particulate Matter ; toxicity ; Pneumonia ; etiology ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; analysis

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

OBJECTIVETo investigate the short-term association between outdoor air pollution and outpatient visits for acute bronchitis, which is a rare subject of research in the mainland of China.

METHODSA time-series analysis was conducted to examine the association of outdoor air pollutants with hospital outpatient visits in Shanghai by using two-year daily data (2010-2011).

RESULTSOutdoor air pollution was found to be associated with an increased risk of outpatient visits for acute bronchitis in Shanghai. The effect estimates of air pollutants varied with the lag structures of the concentrations of the pollutants. For lag06, a 10 μg/m(3) increase in the concentrations of PM10, SO(2), and NO(2) corresponded to 0.94% (95% CI: 0.83%, 1.05%), 11.12% (95% CI: 10.76%, 11.48%), and 4.84% (95% CI: 4.49%, 5.18%) increases in hospital visits for acute bronchitis, respectively. These associations appeared to be stronger in females (P<0.05). Between-age differences were significant for SO(2) (P<0.05), and between-season differences were also significant for SO(2) (P<0.05).

CONCLUSIONOur analyses have provided the first evidence that the current air pollution level in China has an effect on acute bronchitis and that the rationale for further limiting air pollution levels in Shanghai should be strengthened.

Acute Disease ; Adolescent ; Adult ; Age Factors ; Aged ; Air Pollutants ; analysis ; toxicity ; Ambulatory Care ; statistics & numerical data ; Bronchitis ; epidemiology ; Child ; Child, Preschool ; China ; epidemiology ; Cities ; Data Interpretation, Statistical ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Middle Aged ; Nitrogen Dioxide ; analysis ; toxicity ; Particulate Matter ; analysis ; toxicity ; Seasons ; Sex Factors ; Sulfur Dioxide ; analysis ; toxicity ; Young Adult

OBJECTIVETo investigate the association between ambient fine particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) and the risk on preterm birth.

METHODSA total of 1 882 pregnant women with local residency of Taiyuan city and underwent delivery at the First Hospital of Shanxi Medical University with the dates of conception between January 1 and December 31, 2013, were enrolled in the study. Information on general demographics, home address and history on pregnancy, lifestyle and related environmental factors were collected through in-person interview. Birth outcomes and maternal complications were abstracted from medical records. Data on the amount of daily average PM2.5 from 8 monitor points in Taiyuan city, between March 1, 2012 and December 31, 2013 were also collected. Individual exposure during pregnancy were calculated using the inverse-distance weighting method, based on home address. Multivariate unconditional logistic regression model was used to examine the associations among PM2.5 exposure, risk of preterm birth and related clinical subtypes.

RESULTSThe overall incidence of preterm birth was 8.21% (151/1 839)in 1 839 pregnant women. Exposure to ambient PM2.5 during the second week prior to delivery was associated with an increased risk of preterm birth (OR=1.087, 95% CI: 1.001-1.182 per 10 μg/m(3) increase) and mild preterm birth (OR=1.099, 95% CI: 1.007-1.200 per 10 μg/m(3)). Compared to data from the China Environmental Air Quality Standard, higher level of exposure (≥75 μg/m(3)) of PM2.5 during the second week before delivery was associated with an increased risk of preterm birth (OR=1.008, 95%CI: 1.000-1.017) but the association was mainly seen for mild preterm birth (OR=1.010, 95%CI: 1.001-1.018).

CONCLUSIONSRESULTS from our study showed that exposure to high level of PM2.5 during late pregnancy would increase the risk of preterm birth. Future large studies are needed to examine the association by preterm clinical subtypes and to elucidate potential underlying mechanisms.

China ; epidemiology ; Environmental Exposure ; adverse effects ; analysis ; Female ; Humans ; Incidence ; Infant, Newborn ; Logistic Models ; Maternal Exposure ; Particle Size ; Particulate Matter ; analysis ; toxicity ; Pregnancy ; Pregnancy Complications ; Premature Birth ; chemically induced ; epidemiology ; Public Health ; statistics & numerical data

OBJECTIVES: The deleterious effects of air pollution on various health outcomes have been demonstrated. However, few studies have examined the effects of air pollution on liver enzyme levels. METHODS: Blood samples were drawn up to three times between 2008 and 2010 from 545 elderly individuals who regularly visited a community welfare center in Seoul, Korea. Data regarding ambient air pollutants (particulate matter < or =2.5 mum [PM2.5], nitrogen dioxide [NO2], ozone [O3], carbon monoxide, and sulfur dioxide) from monitoring stations were used to estimate air pollution exposure. The effects of the air pollutants on the concentrations of three liver enzymes (aspartate aminotransferase [AST], alanine aminotransferase [ALT], and gamma-glutamyltranspeptidase [gamma-GTP)]) were evaluated using generalized additive and linear mixed models. RESULTS: Interquartile range increases in the concentrations of the pollutants showed significant associations of PM2.5 with AST (3.0% increase, p=0.0052), ALT (3.2% increase, p=0.0313), and gamma-GTP (5.0% increase, p=0.0051) levels; NO2 with AST (3.5% increase, p=0.0060) and ALT (3.8% increase, p=0.0179) levels; and O3 with gamma-GTP (5.3% increase, p=0.0324) levels. Significant modification of these effects by exercise and alcohol consumption was found (p for interaction <0.05). The effects of air pollutants were greater in non-exercisers and heavy drinkers. CONCLUSIONS: Short-term exposure to air pollutants such as PM2.5, NO2, and O3 is associated with increased liver enzyme levels in the elderly. These adverse effects can be reduced by exercising regularly and abstinence from alcohol.
Aged ; Aged, 80 and over ; Air Pollutants/analysis/*toxicity ; Alanine Transaminase/blood ; *Alcohol Drinking ; Aspartate Aminotransferases/blood ; Environmental Exposure ; *Exercise ; Female ; Humans ; Linear Models ; Liver/*drug effects/enzymology ; Male ; Nitrogen Dioxide/chemistry/toxicity ; Ozone/chemistry/toxicity ; Particulate Matter/analysis/toxicity ; Sulfur Dioxide/chemistry/toxicity ; gamma-Glutamyltransferase/blood

To explore the therapeutic effect of honokiol on particulate matter 2.5 (PM2.5)-induced lung injury in asthmatic mice and the possible mechanisms.
 Methods: A total of 32 BALB/C mice were randomly divided into four groups: a normal saline group, a model group, a PM2.5 group and a honokiol group (n=8 in each group). The asthma mouse model was established by ovalbumin treatment. The mice were treated with physiological saline, ovalbumin, PM2.5 and honokiol, respectively. Lung tissues and serum were collected. The pathological changes of lung tissues were evaluated. The levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were measured and the expressions of Toll like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), retinoid-related orphan receptor gamma-t (RORγt) and forkhead box protein 3 (Foxp3) in lung tissues were detected.
 Results: 1) The lung tissues of mice in the asthma group showed obvious pathological changes and inflammatory state, suggesting that the asthma model was established successfully. PM2.5 could aggravate the pathological condition of inflammatory injury in lung tissues in asthmatic mice. 2) Compared to the PM2.5 group, the pathological symptoms in the lung tissues were alleviated in the honokiol group and the percentage of inflammatory cells in BALF and the levels of inflammatory cytokines in BALF and serum were significantly reduced (all P<0.05). 3) Compared to the PM2.5 group, the expressions of TLR4, NF-κB (p-p65) and RORγt in lung tissues were significantly decreased, while the expression of Foxp3 was increased; the ratio of RORγt/Foxp3 was also decreased in the honokiol group (all P<0.05).
 Conclusion: Honokiol can resist lung injury induced by PM2.5 in asthmatic mice. These effects are through inhibiting TLR4-NF-κB pathway-mediated inflammatory response or regulating the balance of Th17/Treg cells.
Animals ; Asthma ; chemically induced ; complications ; Biphenyl Compounds ; pharmacology ; Bronchoalveolar Lavage Fluid ; chemistry ; Cytokines ; analysis ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Inflammation Mediators ; analysis ; Lignans ; pharmacology ; Lung ; metabolism ; pathology ; Lung Injury ; drug therapy ; etiology ; metabolism ; pathology ; Mice ; Mice, Inbred BALB C ; NF-kappa B ; metabolism ; Ovalbumin ; Particulate Matter ; toxicity ; Random Allocation ; Toll-Like Receptor 4 ; metabolism