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Asbestos fiber length as related to potential pathogenicity: A critical review
Author(s) -
Dodson Ronald F.,
Atkinson Mark A.L.,
Levin Jeffrey L.
Publication year - 2003
Publication title -
american journal of industrial medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.7
H-Index - 104
eISSN - 1097-0274
pISSN - 0271-3586
DOI - 10.1002/ajim.10263
Subject(s) - medicine , asbestos , pathological , population , asbestos fibers , inhalation , pathology , fibrosis , disease , asbestosis , carcinogen , environmental health , lung , biology , anatomy , genetics , metallurgy , materials science
Background Asbestos inhalation is recognized as an exposure that increases the risk for the development of lung disease. It is unique among dusts in that it is both a carcinogen and capable of inducing extrapulmonary responses such as pleural thickening and fibrosis as well as malignancy. One feature of asbestos suggested as crucial in its pathological activity is its fibrous morphology. Long fibers that have been inhaled are cleared less readily and are thus more persistent in the body. Furthermore certain experimental models link fiber length to levels of risks for development of certain diseases. The present review will survey the data on this subject. Methods The review considers experimental models that have been used to assess the response to various lengths of fibers in animal models in addition to data obtained from studies of human materials. The review also emphasizes the importance in defining the method by which a sample is categorized. Results Data are offered which support the potential for longer fibers as well as shorter fibers to contribute to pathological responses. Conclusions The data presented argue that asbestos fibers of all lengths induce pathological responses and that caution should be exerted when attempting to exclude any population of inhaled fibers, based on their length, from being contributors to the potential for development of asbestos‐related diseases. Am. J. Ind. Med. 44:291–297, 2003. © 2003 Wiley‐Liss, Inc.