Measurement methods of Air Pollution Combustion Emissions with considering Causative Agents and Cardiovascular Effects

Emissions from the combustion fossil fuels result in generation of a large number of particle and gaseous products in outdoor and/or indoor air, which create health and environmental risks. Of particular importance are the very small particles that are emitted in large quantities from all the combustion sources, and that could be potentially more significant in terms of their impact on health and the environment than larger particles. It is important to quantify particle emissions from combustion sources for regulatory and control purposes in relation to air quality. Combustion emissions account for over half of the fine particle (PM2.5) air pollution and most of the primary particulate organic matter. Human exposure to combustion emissions including the associated airborne fine particles and mutagenic and carcinogenic constituents (e.g., polycyclic aromatic compounds (PAC), nitro-PAC) .A number of these components are significant sources of human exposure to mutagenic and carcinogenic chemicals that may also cause oxidative and DNA damage that can lead to reproductive and cardiovascular effects.Chemical and physical tracers have been used to apportion outdoor and indoor and personal exposures to airborne particles between various combustion emissions and other sources. there is substantial evidence that PAH or substituted PAH may be causative agents in cancer and reproductive effects, an increasing number of studies investigating cardiopulmonary and cardiovascular effects are investigating these and other potential causative agents from air pollution combustion sources .The current methods for measuring particle physical characteristics (mass and number concentrations) and principles of methodologies for measuring emission factors are discussed in the paper too

کلیدواژه ها:

air pollution ، Combustion emissions ، fine particles (PM 2.5) ، particulate matter (PM ) ، exposure ، source apportionment ، DNA damage ، carcinogenicity ، cardiovascular disease