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Ambient fine particulate matter (PM2.5) is a mixture consisting of a wide range of chemical constituents including carbonaceous aerosols, water soluble ions and inorganic elements, and has become the major air pollutant in most cities in China. Evidence suggests that exposure to ambient PM2.5 induces damage on the cardiovascular system and can increase risk of the development and mortality of ischemic heart diseases (IHD). However, the effects of exposure to specific PM2.5 constituents on IHD remain unclear, and its underlying mechanisms are yet to be investigated. Here we reviewed studies investigating the association of short- and long-term exposure to specific PM2.5 constituents with IHD, which may provide useful clues for future relevant studies.
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Objective To evaluate the antagonistic effects of N-acetylcysteine (NAC) on mitogen-activated protein kinases (MAPK) pathway activation, oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter (PM2.5). Methods Forty eight male Wistar rats were randomly divided into six groups: blank control group (C1), water drip control group (C2), PM2.5 exposed group (P), low-dose NAC treated and PM2.5 exposed group (L), middle-dose NAC treated and PM2.5 exposed group (M), and high-dose NAC treated and PM2.5 exposed group (H). PM2.5 suspension (7.5 mg/kg) was administered tracheally once a week for four times. NAC of 125 mg/kg, 250 mg/kg and 500 mg/kg was delivered intragastrically to L, M and H group respectively by gavage (10 ml/kg) for six days before PM2.5 exposure. The histopathological changes and human mucin 5 subtype AC (MUC5AC) content in lung tissue of rats were evaluated. We investigated IL-6 in serum and bronchoalveolar lavage fluid (BALF) by Enzyme-linked immunosorbent assay (ELISA), MUC5AC in lung tissue homogenate by ELISA, glutathione peroxidase (GSH-PX) in serum and BALF by spectrophotometry, and the expression of p-ERK1/2, p-JNK1/2 and p-p38 proteins by Western blot. All the measurements were analyzed and compared statistically. Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells. Rats receiving NAC treatment showed less histological destruction and mucus secretion. Of P, L, M and H group, MUC5AC in lung tissue, IL-6 in serum and BALF were higher than controls (C1 and C2) (all P<0.05), with the highest levels found in the P group and a decreasing trend with increase of NAC dose. The activity of GSH-PX in serum and BALF of PM2.5 exposed rats (P, L, M and H) was lower than that of controls (all P<0.05), with higher activities found in NAC treated rats (L, M, and H), and an increasing trend with increase of NAC dose. The expressions of p-ERK1/2, p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue (P, L, M and H) was higher than controls (all P<0.05), with decreased levels and dose dependent downregulation found in NAC treated rats. Conclusion NAC can antagonize major MAPK pathway activation, lung oxidative stress and inflammatory injury induced by PM2.5 in rats.
Subject(s)
Animals , Male , Acetylcysteine/pharmacology , Bronchoalveolar Lavage Fluid , Enzyme Activation/drug effects , Glutathione Peroxidase/metabolism , Inflammation/pathology , Interleukin-6/metabolism , Lung/pathology , Lung Injury/pathology , Mitogen-Activated Protein Kinases/metabolism , Mucin 5AC/metabolism , Mucus/metabolism , Oxidative Stress/drug effects , Particle Size , Particulate Matter/toxicity , Phosphorylation/drug effects , Rats, WistarABSTRACT
Objective@#To study the effect of particulate matter 2.5 (PM2.5) on oncogene expression in human bronchial epithelial (HBE) cells.@*Methods@#HBE cells were selected as the study subjects, and PM2.5 treatment group (10 μg/ml and 50 μg/ml) , negative control group and positive control group (10 μmol/L Cr6+) were set. CCK8 assay was used to test the IC50 value of PM2.5. HBE cells were treated with PM2.5 for 24 h at 10 μg/ml and 50 μg/ml, additionally, cells were treated with blank as negative control, 10 μmol/L Cr6+ as a positive control for 24 h. After the treatment, mRNA expression of oncogenes including c-myc, c-fos, k-ras and p53 were detected by fluorescent quantitative RT-PCR, the protein expression of oncogenes were detected with western blot.@*Results@#The IC50 value of PM2.5 in HBE cells is 70.12 μg/ml. The qRT-PCR data showed that compared with the control group, the expression level of c-myc gene increased by respectively 500.1%、780.7%、305.3% after exposure to 10、50 μg/ml PM2.5 and positive control group; c-fos gene increased respectively 34.0%、76.7%、131.3% after exposure to 10、50 μg/ml PM2.5 and positive control group; k-ras gene increased respectively 50.3%、107.0%、49.7% after exposure to 10、50 μg/ml PM2.5 and positive control group; p53 gene decreased by 28.3%、28.7%、59.7% after exposure to 10、50 μg/ml PM2.5 and positive control group. The western blot results showed that compared with the control group, c-myc protein increased respectively 29.7%、77.3% after exposure to 50 μg/ml PM2.5 and positive control group; c-fos protein increased respectively 200.3%、137.0% after exposure to 50 μg/ml PM2.5 and positive control group; k-ras protein increased respectively 106.3%、130.3%、116.7% after exposure to 10、50 μg/ml PM2.5 and positive control group; p53 protein decreased by 43.7%、53.3%、52.1% after exposure to 10、50 μg/ml PM2.5 and positive control group.@*Conclusion@#PM2.5 could promote the expression of oncogenes in HBE cells, the carcinogenicity of haze might be related to promotion of oncogenes expression induced by PM2.5.
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With the improvement of quality of life, the life expectancy of residents is generally prolonged, and people suffering from Alzheimer’s disease (AD) is increasing. Epidemiological and animal experiments have found that atmospheric particulate matter is associated with AD. This article briefly reviews the mechanisms of AD-related oxidative stress damage and neuroinflammation caused by atmospheric fine particulate matter entering the brain via olfactory bulb pathway.
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Aims: To determine the lung function of cleaners exposed to particulate matter of aerodynamic diameter less than 2.5 micrometer (PM2.5) in the streets and offices in Lusaka, Zambia. Study Design: This was a cross sectional study between two groups. Place and Duration of Study: Lusaka city, central business area, between June and August 2014. Methodology: The study included women between 18-50 years of age who had been working as street or office cleaners for 6 months or more. Males and individuals in both groups who used to smoke or were currently smokers, as well as those with a history of respiratory related illnesses or had cardiopulmonary conditions were excluded from the study. The cleaners were interviewed to get information on socio-demographic characteristics and other information using a structured interview schedule. The participants’ lung volumes, forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and their ratio (FEV1/FVC) were measured using a MRI spirobank G spirometer. On the day of the interview, PM2.5 in their work environment was sampled using a personal aerosol monitor (SIDEPAK AM510). Results: Out of the 90 participants, 45 were street sweepers and 45 were office cleaners. More street sweepers had impaired lung function (FEV1/FVC) 15(75%) than office cleaners 5(25%) p=0.01. FEV1 was also significantly different among street sweepers 12(70.6%) and office cleaners 5(29.4%) p=0.05. PM2.5 measurements revealed significantly high levels of exposure among street sweepers (p=0.001). Participants with impaired lung function (p=.005) and those with reduced FEV1percent predicted were exposed to significantly high concentrations of PM2.5 (p=0.012). Conclusion: Exposure to high PM2.5 concentration is associated with pulmonary function impairment and reduced FEV1 % predicted among cleaners.
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Objective To explore the association between atmospheric particulate matter (PM10/PM2.5) levels and hospital admissions due to lower respiratory tract infection in Shijiazhuang. Methods Data of air pollution, meteorologic data, and the data of patients admitted to hospital due to lower respiratory tract infection were retrospectively analyzed. Pearson's correlation coefficients were calculated to analyze correlations between atmospheric particulate matter and meteorologic factors. Data of hospital admission due to lower respiratory tract infection and of atmospheric air pollution levels in Shijiazhuang were obtained, a bidirectional case-crossover design was used to investigate the association between hospital admissions due to lower respiratory tract infection and levels of atmospheric particles. Stratified analyses of exposure based on age, gender, complications and season were performed to evaluate the effect. Results Pearson's correlation analysis showed positive correlations among PM2.5, PM10, SO2, NO2 and CO. The concentration of all these five pollutants were negatively correlated with O3 and daily mean temperature, while a positive correlation was found between concentrations of the 5 pollutants and daily average temperature and O3. In single-pollutant model, every 10μg/m3 increase in PM2.5 and PM10 at lag5 brought the corresponding OR values (95%CI) up to 1.010(1.005-1.015) and 1.006(1.003-1.009) respectively. In the multi-pollutant models, the observed effects of PM2.5 remained significant. Stratified analysis based on gender, age, season and comorbidities showed that the effect of PM2.5 exposure on lower respiratory tract infection admissions was stronger in males, persons younger than 60 years of age and persons without comorbidities, and even more stronger in cold season. The effect of PM10 exposure on lower respiratory tract infection admissions was stronger in females, persons older than 60 years of age and persons with comorbidities, and even more stronger in cold season. Conclusion Our study demonstrates that higher levels of atmospheric particulate matter (PM10/PM2.5) may increase the risk of hospital admissions due to lower respiratory tract infection.