Document K6NDxB03Le8k2XMM8g0MbjxMx
measuring both coated and uncoated fibers, is needed to define a gradient of accumulated fibers for correlation with incidence of disease, on the one hand, and history of environmental exposure, on the other.
Although there appears no doubt that asbestos fibers are pre sent in many human lungs, there are sources of airborne fibers other than asbestos. Some are probably derived from the burning of leaves and plant products, such as paper, wood and coal. Man made (mostly vitreous) fibers have also been identified in the sediment isolated from human lungs. Talc, often used generously as a dusting powder, may contain a significant amount of trenolite asbestos fibers.
Information is sparse concerning possible increase of fibers " in lungs with increasing use of asbestos and concerning the exis tence of significant differences between urban and rural populations. Selikoff and Hammond compared lung tissues obtained in 1934 and 1967 and found no significant increase in the proportion containing ferruginous bodies. This suggested that, despite increasing use cf asbestos in New York City between 1934 and 1967, fibers of a type producing ferruginous bodies had not been increasing at a correspond ing rate. Other cormer.tators, however, have noted an increase over each decade in asbestos bodies in samples cf lungs from per sons who died in London in 1936, 1946, 195*6 and 1966.
A review of the literature related to pleural calcification and asbestos exposure strongly suggests ar. association"between pleural calcification and nonoccupatior.al exposures to asbestos. See Nat'l. Acad., Ex. 19, c. 14.
Industrial experience has showrvthat prolonged inhalation of .asbestos can increase the risk of neoplastic (tuner producing) disease. Examination of lung tissue has made it apparent that a much larger proportion of the general public nas inhaled and retained asbestos fibers than had formerly been realized; in fact, most urban dwellers have some such fibers in their lungs. The basic issue is whether the general public, as well as persons working near occupa tional sources, living in the households cf asbestos workers, living in the neighborhoods of asbestos plants, or having occasional random exposures, have a detectably increased risk of malignancy or other disease because of airborne asbestos.' What information there is to answer these questions comes either from direct epidemio logic studies of groups with various levels of nonoccupational expo sure or by extrapolation from the experience of industrial populations with direct or indirect asbestos exposures.
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