ASBESTOS-RELATED PULMONARY DISEASES

Asbestos-related pulmonary diseases are a group of diseases that are associated with exposure to asbestos with subsequent development of a clinical condition attributed to the exposure. This document is an attempt to provide a brief overview of asbestos and the mechanism of its effects in humans, an overview of the more common asbestos-related pulmonary diseases, diagnostic considerations in individuals alleging asbestos-related pulmonary diseases, and application of the information to the Ohio Workers' Compensation System.


OVERVIEW OF ASBESTOS

Physical Properties and Effects in Humans


Asbestos is a term applied to a family of naturally occurring, flexible, silicate minerals that are resistant to heat and many chemicals.[1] The properties of relative heat and chemical resistance has lead to widespread use in the 20th Century of asbestos in many processes and products including insulation materials, building materials such as vinyl asbestos floor tile, linings of furnaces, filtration systems, asbestos cement products, and as spray products for acoustical, thermal, or fireproofing purposes. Therefore, asbestos is commonly found throughout the work and non-work environments. Identification of asbestos fibers in samples of lung tissue, lung lavage samples or sputum, documents past exposure, but not necessarily the source of the exposure or whether asbestos-related disease is present. While individuals with asbestos-related disease may have higher concentrations of fibers in tissue samples, there is considerable overlap and laboratory variation so that asbestos fiber count has limited usefulness.


Once inhaled, the body attempts to remove fibers by several pathways including mucociliary transport through the airways, the lymphatic system, or through degradation of the fibers by macrophages. The fundamental disease process is the induction of inflammation resulting in fibrosis and/or cancer of the lung and pleural space. The fibrosis process is the result of the inflammatory reaction and repair processes by the body’s defense system to remove asbestos fibers. These reactions lead to permanent scarring and fibrosis. The cancer processes are the result of damage to target cells with genetic mutations through a variety of molecular injuries.


The pathogenicity of asbestos fibers may be affected by the dose (concentration and duration of exposure), fiber type, fiber dimensions, durability of the fiber, and surface chemicals that may be present on the fiber. Several studies have shown that the toxicity of asbestos fibers is related to the fibrous nature of the mineral. Both fiber diameter and length are important. In general, fibers with diameters > 3mm in diameter and > 200mm in length do not penetrate the lower lung. Fibers shorter than approximately 3mm in length are usually phagocytosed by macrophages or removed by the lymphatic system. Therefore, fibers less than 3 mm in diameter and longer than 8 mm are more likely to penetrate the lower lung and are more difficult for host defense mechanisms to remove. Fibers of this size are more likely to initiate cellular and molecular events leading to fibrosis or carcinogenesis.

[1] Begin R, Samet GM, and Shaikh RA: “Asbestos” in Harber P, Schenker MB, and Balmes JR: Occupational and Environmental Respiratory Disease Mosby-Year Book, Inc., St. Louis, 1996, pp 293-321.



There is a latency period of several years between initial exposure and onset of clinical disease. The latency period is variable. Individuals who are no longer occupationally exposed to asbestos may develop asbestos-related diseases years after their removal from occupational exposure. Current OSHA regulations and industrial processes have tried to limit exposure by substitution of other materials, monitoring with limits on the concentration of fibers permitted per cc of air in the workplace, use of personal protective equipment when exposed to asbestos fibers in significant concentrations, and required periodic medical monitoring of exposed workers for asbestos-related diseases.


There is little doubt that the "dose" both in terms of concentration and duration of exposure is important with higher concentration and longer duration of exposure more likely to increase the probability of development of an asbestos-related disease. However, exact dose-response curves can not be reasonably determined due to variability among type of fibers, variability of host response systems, questionable exposure histories, and that the radiographic findings are not specific to asbestos-related disease



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