1.Potential Toxicological and Cardiopulmonary Effects of PM2.5 Exposure and Related Mortality: Findings of Recent Studies Published during 2003-2013.
Mohammed O A MOHAMMED ; Wei Wei SONG ; Wan Li MA ; Wen Long LI ; Yi Fan LI ; Afed Ullah KHAN ; Mohammed A E M IBRAHIM ; Osman Adam MAAROUF ; Alshebli A AHMED ; John J AMBUCHI
Biomedical and Environmental Sciences 2016;29(1):66-79
2.Physical and chemical characteristics of PM2.5 and its toxicity to human bronchial cells BEAS-2B in the winter and summer.
Hui-Hui ZHANG ; Zheng LI ; Yu LIU ; Ping XINAG ; Xin-Yi CUI ; Hui YE ; Bao-Lan HU ; Li-Ping LOU
Journal of Zhejiang University. Science. B 2018;19(4):317-326
With the increasing occurrence of haze during the summer, the physicochemical characteristics and toxicity differences in PM2.5 in different seasons are of great concern. Hangzhou is located in an area that has a subtropical monsoon climate where the humidity is very high during both the summer and winter. However, there are limited studies on the seasonal differences in PM2.5 in these weather conditions. In this test, PM2.5 samples were collected in the winter and summer, the morphology and chemical composition of PM2.5 were analyzed, the toxicity of PM2.5 to human bronchial cells BEAS-2B was compared, and the correlation between PM2.5 toxicity and the chemical composition was discussed. The results showed that during both the winter and summer, the main compounds in the PM2.5 samples were water-soluble ions, particularly SO42-, NO3-, and NH4+, followed by organic components, while heavy metals were present at lower levels. The higher the mass concentration of PM2.5, the greater its impact on cell viability and ROS levels. However, when the mass concentration of PM2.5 was similar, the water extraction from the summer samples showed a greater impact on BEAS-2B than that from the winter samples. The cytotoxicity of PM2.5 was closely associated with heavy metals and organic pollutants but less related to water-soluble ions.
Air Pollutants/toxicity*
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Bronchi/metabolism*
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Carbon/chemistry*
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Environmental Monitoring
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Humans
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Ions
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Metals, Heavy
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Organic Chemicals
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Particle Size
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Particulate Matter/toxicity*
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Seasons
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Temperature
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Water
3.Impact of traffic emissions on local air quality and the potential toxicity of traffic-related particulates in Beijing, China.
Lei TIAN ; Wei ZHANG ; Zhi Qing LIN ; Hua Shan ZHANG ; Zhu Ge XI ; Jian Hua CHEN ; Wei WANG
Biomedical and Environmental Sciences 2012;25(6):663-671
OBJECTIVEAir-borne particulates from different sources could have different physicochemical properties and inflammatory potentials. This study aims to characterize the chemical compositions and the toxicity of ambient particulate matter (PM) associated with traffic emissions.
METHODSThe concentrations of trace elements, organic carbon (OC), elemental carbon (EC) and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 and PM10 were measured in samples collected at sites in Beijing, China. Their toxic effects on the pulmonary system of rats were investigated. Biochemical parameters (LDH, T-AOC, TP) and inflammatory cytokine(IL-6, IL-1, TNF-a) levels were measured in the lungs of rats exposed to traffic-related PM. Oxidative damage was observed. PM samples were taken from a near road site and an off road site in summer time in 2006.
RESULTSThe concentrations of the USEPA priority pollutant PAHs in both PM10 and PM2.5 were higher (299.658 and 348.412) at the near road site than those (237.728 and 268.472) at the off road site. The similar trend was observed for the concentrations of trace elements in PM. Compared to coarse particles (PM10), fine particles (PM2.5) have a greater adsorption capacity to enrich toxic elements than inhalable particles. Decrease in antioxidant capacity and an increase in the amount of lipid peroxidation products in rat lung tissues was observed.
CONCLUSIONThe findings of the present study suggest that the differing inflammatory responses of PM collected from the two road sites might have been mediated by the differing physicochemical characteristics.
Air Pollutants ; chemistry ; toxicity ; Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; China ; Cities ; Cytokines ; genetics ; metabolism ; Gene Expression Regulation ; physiology ; Lung ; drug effects ; metabolism ; Male ; Particle Size ; Particulate Matter ; toxicity ; Rats ; Rats, Wistar ; Vehicle Emissions ; toxicity
4.Physical Activity- and Alcohol-dependent Association Between Air Pollution Exposure and Elevated Liver Enzyme Levels: An Elderly Panel Study.
Kyoung Nam KIM ; Hyemi LEE ; Jin Hee KIM ; Kweon JUNG ; Youn Hee LIM ; Yun Chul HONG
Journal of Preventive Medicine and Public Health 2015;48(3):151-169
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
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Aged, 80 and over
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Air Pollutants/analysis/*toxicity
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Alanine Transaminase/blood
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*Alcohol Drinking
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Aspartate Aminotransferases/blood
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Environmental Exposure
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*Exercise
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Female
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Humans
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Linear Models
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Liver/*drug effects/enzymology
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Male
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Nitrogen Dioxide/chemistry/toxicity
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Ozone/chemistry/toxicity
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Particulate Matter/analysis/toxicity
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Sulfur Dioxide/chemistry/toxicity
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gamma-Glutamyltransferase/blood
5.Pulmonary Toxicity in Rats Caused by Exposure to Intratracheal Instillation of SiO2 Nanoparticles.
Hong YANG ; Qiu Yun WU ; ; Ming Yue LI ; Can Shan LAO ; Ying Jian ZHANG ;
Biomedical and Environmental Sciences 2017;30(4):264-279
OBJECTIVEThe effect of the silica nanoparticles (SNs) on lungs injury in rats was investigated to evaluate the toxicity and possible mechanisms for SNs.
METHODSMale Wistar rats were instilled intratracheally with 1 mL of saline containing 6.25, 12.5, and 25.0 mg of SNs or 25.0 mg of microscale SiO2 particles suspensions for 30 d, were then sacrificed. Histopathological and ultrastructural change in lungs, and chemical components in the urine excretions were investigated by light microscope, TEM and EDS. MDA, NO and hydroxyproline (Hyp) in lung homogenates were quantified by spectrophotometry. Contents of TNF-α, TGF-β1, IL-1β, and MMP-2 in lung tissue were determined by immunohistochemistry staining.
RESULTSThere is massive excretion of Si substance in urine. The SNs lead pulmonary lesions of rise in lung/body coefficients, lung inflammation, damaged alveoli, granuloma nodules formation, and collagen metabolized perturbation, and lung tissue damage is milder than those of microscale SiO2 particles. The SNs also cause increase lipid peroxidation and high expression of cytokines.
CONCLUSIONThe SNs result into pulmonary fibrosis by means of increase lipid peroxidation and high expression of cytokines. Milder effect of the SNs on pulmonary fibrosis comparing to microscale SiO2 particles is contributed to its elimination from urine due to their ultrafine particle size.
Air Pollutants ; toxicity ; Animals ; Dose-Response Relationship, Drug ; Lung ; drug effects ; pathology ; ultrastructure ; Male ; Microscopy, Electron, Transmission ; Nanoparticles ; toxicity ; Pulmonary Fibrosis ; chemically induced ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Wistar ; Silicon Dioxide ; toxicity ; Specific Pathogen-Free Organisms ; Spectrometry, X-Ray Emission ; Urine ; chemistry
6.Comparative study of PM2.5 - and PM10 - induced oxidative stress in rat lung epithelial cells.
Jin Hyuk CHOI ; Jun Sung KIM ; Young Chul KIM ; Yoon Shin KIM ; Nam Hyun CHUNG ; Myung Haing CHO
Journal of Veterinary Science 2004;5(1):11-18
Accurate estimation of the exposure-response relationship between ambient urban particulate matters (PM) and public health is important for regulatory perspective of ambient urban particulate matters (PM). Ambient PM contains various transition metals and organic compounds. PM10 (aerodynamic diameter less than 10 microgram) is known to induce diverse diseases such as chronic cough, bronchitis, chest illness, etc. However, recent evaluation of PM2.5 (aerodynamic diameter less than 2.5 microgram) against health outcomes has suggested that the fine particles may be more closely associated with adverse respiratory health effects than particles of larger size. This study was performed to evaluate PM2.5-induced oxidative stress in rat lung epithelial cell in order to provide basic data for the risk assessment of PM2.5. PM2.5 showed higher cytotoxicity than PM10. Also, PM 2.5 induced more malondialdehyde (MDA) formation than PM10. In Hoechst 33258 dye staining and DNA fragmentation assay, apopotic changes were clearly detected in PM2.5 treated cells in compared to PM10. Expression of catalase mRNA was increased by PM2.5 rather than PM10. PM2.5 induced higher Mth1 mRNA than PM10. In pBR322 DNA treated with PM2.5, production of single strand breakage of DNA was higher than that of PM10. In Western blot analysis, PM2.5 induced more Nrf-2 protein, associated with diverse transcriptional and anti-oxidative stress enzymes, compared to PM10. Our data suggest that PM2.5 rather than PM10 may be responsible for PM-induced toxicity. Additional efforts are needed to establish the environmental standard of PM2.5.
Air Pollutants/chemistry/*toxicity
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Animals
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Apoptosis/physiology
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Benzimidazoles/metabolism
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Blotting, Western
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Cell Line
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Cell Survival/physiology
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DNA Fragmentation/physiology
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DNA Repair Enzymes/genetics/metabolism
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DNA-Binding Proteins/metabolism
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Epithelial Cells/drug effects/enzymology/pathology
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Formazans/metabolism
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GA-Binding Protein Transcription Factor
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Lipid Peroxides/metabolism
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Lung Diseases/*chemically induced/enzymology/pathology
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Oxidative Stress/*physiology
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RNA, Messenger/chemistry/genetics
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Rats
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Reverse Transcriptase Polymerase Chain Reaction
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Tetrazolium Salts/metabolism
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Transcription Factors/metabolism