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Brief introduction of investigation into PM 2.5. 20120701. Introduction into PM 2.5 (particulate matter). PM divided and nominated by diameter: TSP total suspended particle
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Introduction into PM2.5 (particulate matter) PM divided and nominated by diameter: TSP total suspended particle coarse particle PM10 fine particle PM2.5 ultrafine particle PM with diameter <100nm nanoparticle <10nm • 1.
Mass distributions showing multi-sources of PM <100nm 微珠 Combustion Aerosols: Factors Governing Their Size and Copmposition and Implications to Human Health, Journal of the Air&Waste Management Associat ion, 50: 9, 1565-1618
Sources of American nationwide PM2.5 扬尘 Combustion Aerosols: Factors Governing Their Size and Copmposition and Implications to Human Health, Journal of the Air&Waste Management Associat ion, 50: 9, 1565-1618
PM2.5 has highly complicated contents Particle core of carbonaceous material organic carbon:PAHs(多环芳烃), nitro-PAHs, quinones(类醌) translational metals: Fe Ni Cu V(钒) Co Cr biologic origin materials: virus, bacteria, endotoxins soluble aerosol components: nitrates(NO3-), sulfates(SO42-), ammonium(NH4+) other inorganic components
Chemical analysis of exhaust emissions showed complicated chemical components in PM2.5 多环芳烃 二烷酸 Combustion Aerosols: Factors Governing Their Size and Copmposition and Implications to Human Health, Journal of the Air&Waste Management Associat ion, 50: 9, 1565-1618
Some related hallmarks in air pollution research • three severe air pollution events: Meuse Valley(Belgium,1930) London fog(1952) Los Angeles photochemical smog(1940s) • by 1970s, correlation between acute increases in mortality and high concentrations of air particulate • 1989-1996 Epidemiological studies • 1997 EPA firstly imposed limits on PM2.5
(PM2.5) An association between air pollution and mortality in six U.S. cities. N Engl J Med. 1993:329:1753-1759
Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of American Medical Association 2002; 287:1132-1141. PM2.5 PM10
PM2.5 and cardiopulmonary disease • Long term exposure: cause DNA damage, increase risk of lung cancer induces respiratory diseases, arteriosclerosis influence children behavior • Short term exposure: cause worsening of asthma, bronchitis and other respiratory diseases change heart-rate variability
Mechanism of PM2.5-induced health effects:ROS theory Mutation Research 592 (2005) 119–137
PM exposure triggered inflammation in lung and systemic capillary
Hypothesized events taking place after exposure to PM Journal of Toxicology and Environmental Health, Part A: Current Issues, 65:20, 1571-1595
Other mechanism and signal pathways reported • induced hypermethylation of p16 promoter via ROS-JNK-DNMT1 pathway • in hypertensive rats, PM-induced inflammation was accompanied by significant increase in TLR4 • genome-wide DNA hypomethylation
PM2.5 effect is source-component dependent Particle and Fibre Toxicology 2011, 8:26
Future directions • Because of inconvenience in collection and lab exposure of PM2.5, fly ash used in many research, so a need for more convincible data • Lung Cancer morbidity rate data is deficient, also cancer development mechanism, the most plausible approach is animal model • Lab toxic experiments data of certain area is useful in assessing environment pollution risk • Identification of the most harmful component in PM2.5 is of prime importance in risk control and prevention • systemic effects of PM2.5
Acknowledgements • Thanks for Pro. J’ guidance • Thanks for everyone’ help in the lab • thanks