Brief introduction of investigation into PM 2.5
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Transcript of Brief introduction of investigation into PM 2.5
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