Brief introduction of investigation into PM2.5

20120701

• 1.

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

＜ 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, 1565-1618

微珠

Scale drawing comparing PM to structures in human alveoli

Sources of American nationwide PM2.5

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

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(NO3-), sulfates(SO4

2-), ammonium(NH4

+)

other inorganic components

PM2.5 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, 1565-1618

多环芳烃

二烷酸

Chemical analysis of exhaust emissions showed complicated chemical components in PM2.5

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

• 1989-1996 Epidemiological studies

• 1997 EPA firstly imposed limits on PM2.5

An association between air pollution and mortality in six U.S. cities. N Engl J Med. 1993:329:1753-1759

(PM2.5）

PM2.5 PM10

Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of American Medical Association 2002; 287:1132-1141.

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 PM2.5-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, 1571-1595

Hypothesized events taking place after exposure to PM

Environmental Health Perspectives. 2001,109(4):523-527

• 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 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

Future directions

Acknowledgements

• Thanks for Pro. J’ guidance

• Thanks for everyone’ help in the lab

• thanks