Finally, there are the air fine particles often monitored in many countries as PM10 (less than 10 m in aerodynamic diameter). These consist of a mixture of particle components, including traffic- and combustion-derived carbon-centered ultrafine particles (less than 100 nm in diameter), secondary particles (nitrates and sulfates, wind-blown dust of geological origin, potentially containing endotoxin), and biological particles (e.g., spores, pollens) with their associated allergens.
Because of the complex nature of PM10, many studies have used model components or surrogates such as ultrafine carbon black, solutions of metals, or direct treatment with endotoxins.
There is epidemiological evidence of an association of PM10 levels with cardiovascular and respiratory mortality and morbidity. The precise mechanisms underlying the cardiovascular effects of PM10 remain uncertain. Current attention is particularly focused on ultrafine particles (diameter larger than 0.05 to 0.10 mm), which are highly reactive and are present in large numbers in the urban environment. Ultrafine particles can penetrate the epithelium and vascular walls and enter the bloodstream and, in animal models, have been reported to produce alterations in blood coagulability and increased rates of cardiovascular disorders, as well as increased carcinogenicity and potentiation of autoimmune disorders.
Some other epidemiological studies have reported that patients with asthma are adversely affected by PM pollution. As with the cardiovascular effects, there seems to be no threshold below which PM effects disappear.
There is also a considerable support for the importance of metals in the proinflammatory effects of PM10. Transition metals are known to redox-cycle by Fenton chemistry, generating hydroxyl radicals capable of inducing oxidative stress and damage within biological systems.
Further studies in humans will no doubt help to elucidate the relevant mechanisms of air fine particles, and experimental use of defined mixtures will allow investigation of their potential additive or synergistic properties .
BAL: Bronchoalveolar lavage
FEV1: Forced expiratory volume at first second
PEF: Peak expiratory flow
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Dr. Nicola Verna is an allergist and clinical immunologist with a Ph.D. in metabolic diseases. He worked as research fellow at the Trauma Center of Brigham and Women's Hospital in Boston, Massachusetts. He collaborated on the organization of international meetings focused on occupational medicine and environmental medicine.
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The human body And Todays chemical infested world. Here is a news flash You are not allergic to pollen, pet dander, or whatever it is that makes your body revolt Rather, your body just can not handle that one thing, what ever it is, anymore, due to the massive barrage of toxic chemicals you and everyone else are ingesting every single day.