1989-1996epidemiologicalstudies1997epafirstly-中国pm25.ppt

Brief introduction of investigation into PM2.5 1. Mass distributions showing multi-sources of PM Scale drawing comparing PM to structures in human alveoli Sources of American nationwide PM2.5 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 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 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 PM exposure triggered inflammation in lung and systemic capillary 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 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