Brief introduction of investigation into PM

1. Introduction into PM 2.5 (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

＜ 100nm Mass distributions showing multi-sources of PM Combustion Aerosols: Factors Governing Their Size and Copmposition and Implications to Human Health, Journal of the Air&Waste Management Associat ion, 50: 9, 微珠

Scale drawing comparing PM to structures in human alveoli

Sources of American nationwide PM 2.5 Combustion Aerosols: Factors Governing Their Size and Copmposition and Implications to Human Health, Journal of the Air&Waste Management Associat ion, 50: 9, 扬尘

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(NO 3 - ), sulfates(SO 4 2- ), ammonium(NH 4 + ) other inorganic components PM 2.5 has highly complicated contents

Combustion Aerosols: Factors Governing Their Size and Copmposition and Implications to Human Health, Journal of the Air&Waste Management Associat ion, 50: 9, 多环芳烃 二烷酸 Chemical analysis of exhaust emissions showed complicated chemical components in PM 2.5

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 Epidemiological studies 1997 EPA firstly imposed limits on PM 2.5

An association between air pollution and mortality in six U.S. cities. N Engl J Med. 1993:329: (PM 2.5 ）

PM 2.5 PM 10 Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of American Medical Association 2002; 287:

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

JOURNAL OF AEROSOL MEDICINE,2005,18:1-22

Mechanism of PM 2.5 -induced health effects ： ROS theory Mutation Research 592 (2005) 119–137

PM exposure triggered inflammation in lung and systemic capillary

Journal of Toxicology and Environmental Health, Part A: Current Issues, 65:20, Hypothesized events taking place after exposure to PM

Environmental Health Perspectives. 2001,109(4):

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 Other mechanism and signal pathways reported

PM2.5 effect is source-component dependent Particle and Fibre Toxicology 2011, 8:26

Because of inconvenience in collection and lab exposure of PM 2.5, 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 PM 2.5 is of prime importance in risk control and prevention systemic effects of PM2.5 Future directions

Acknowledgements Thanks for Pro. J’ guidance Thanks for everyone’ help in the lab thanks