Abstract
Studies from Germany on the measurement of PM2.5 in urban air demonstrated that approximately 10% of fine particles are PM0.1. Experimental studies on hamsters reveled that inhaled ultrafine particles of metal fumes can penetrate Type I alvaolar epithelia and are deposited in the interstitium and lymphatic system or blood vessele of the lung. Quantitative animal studies show that ultrafine particles are more easily incorporated in the lung interstitium and hilar lymph nodes than fine particles. Ultrafine particles deposited in human lungs have been shown to contain several kinds of metals by analytical eletron microscopy, and SPMs from various souces can produce oxidants resulting in harmful effects to the lungs, depending on the metal species. Other reports, however, indicate toxic effects of ultrafine particles contained in Teflon fumes, a synthetic resin, which is ordinarily inert with human tissue. When ultrafine particles aggregate and become large conglomerates, toxic effects promptly disappear indicating that an important toxicity charac. teristic exists in ultrafine size particles, but not in the chemical composition, as in the case of Teflon particles. If PM2.5 is related to deaths from cardiopulmonary diseases as shown by epidemiological studies, ultrafine particles readily absorbed by the blood may explain one of the mechanisms of PM2.5 toxicity.
