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HOW PARTICLES MAY CAUSE HARM?

by Meena Pandey | 08-10-2019 01:58





Kathmandu is enlisted as the 7th most polluted city in the world. Dust is formed from the finest, smallest particles of dirt and sand that become airborne due to the forces of erosion present on the Earth. The figure mentioned is of Shesmati, Kathmandu valley. The place is nearby my residence. When I was waiting for the vehicle to move to my nearer and dearer ones, I could hardly seat there, due to dust and its irritation on me. Majority of the people were wearing the masks passing by. Tarakeshwor municipality however is acting against on it.The act is not enough until the effective plans and policies along with its effective implementation is put into an effect. Here I have presented the effects of air particulates in human health.
About 50% of nanometer particles are deposited by Brownian movement. Soluble particles will increase in diameter by absorption of water as they pass down the airway, but on reaching the alveoli they make contact with a water-repellant surface and will be handled by the lung¡¯s defenses like other particles of similar size. Insoluble particles are predominantly carbon, of complex shape and high surface-to-volume ratio, and will be handled similarly. There is evidence that particles below about 100 nm in diameter behave differently from larger respirable ones and a particle which is non-toxic in the micrometer size range may be toxic in the nanometer range. Thus, rats exposed to equal weights of titanium dioxide in two aerosol size ranges, fine and ultra-fine (around 0-25 and 0-02 pm, respectively), retain more ultra-fine particles in the interstitial tissue of the lung, developing a marked airspace inflammatory response.20,21 This interstitial retention probably arises from the failure of alveolar macrophages to phagocytose the large numbers of small particles, together with the action of surfactant in impelling them into the alveolar space.22 These studies were carried out at a high airborne-mass concentration, but Teflon fume particles, 30 nm in diameter at only 200 !-lg/m3, have also been shown to cause acute pulmonary toxicity in rats.23 The Teflon-generating system produces more ultra-fine particles than does the titanium dioxide system. It is part of our hypothesis that very small but chemically reactive particles in urban air pollution produce such a reaction in human beings. That transport of chemicals on the surface of particles may be important in the cause of lung ¡®inflammation has been shown in recent studies in which iron complexed on the surface of fly-ash particles promoted oxidative lung injury, and this effect was reduced after removal of surface iron by washing. 24 Whatever the precise mechanism of induction, we propose that alveolar inflammation provoked by ultra-fine particles, in addition to promoting exacerbations of lung disease, has an additional effect on the coagulability of blood, increasing the susceptibility of individuals to acute episodes of cardiovascular disease. Several hematological factors, including plasma viscosity, fibrinogen, factor VII, and plasminogen activator inhibitor, are not only known to be predictive of cardiovascular disease¡¯-5 but also rise as a consequence of inflammatory reactions. Such low-grade inflammation may in part be responsible for the otherwise unexplained variations in fibrinogen and white-cell counts seen in the general population.26 Low-grade inflammation may be particularly important in altering the coagulability of blood as a result of activation of mononuclear cells in the lung.27 Activated white cells have been shown to initiate and promote coagulation28 by releasing tissue factor, which initiates the conversion of factor X to factor Ax, the first reaction of the final common clotting pathway. 29 Alveolar inflammations may also cause the release of interleukin-6 from macrophages and thus stimulate hepatocytes to secrete fibrinogen. 

Source: Seaton, A., Godden, D., MacNee, W., & Donaldson, K. (1995). Particulate air pollution and acute health effects. The Lancet, 345(8943), 176–178. doi:10.1016/s0140-6736(95)90173-6