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ASBESTOS HAZARDTEXT ® - Hazard Management Page 1 of 2

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ASBESTOS HAZARDTEXT ® - Hazard Management

3.0 CLINICAL EFFECTS 3.1 GENERAL CLINICAL EFFECTS

A. No well-documented fatalities have been reported as a result of acute exposure. Fulminant pulmonary asbestosis following massive short-term industrial exposure is now only of historical interest. Asbestos toxicity is usually manifested after a long latent period. The respiratory tract is the usual target organ. There are two main categories of asbestos diseases. 1. Fibrosis/effusions of the lungs and pleura (asbestosis). 2. Asbestos-related cancers, primarily mesothelioma of the pleura and peritoneum and bronchogenic carcinoma. B. Cor pulmonale is secondary to fibrosis and increased resistance to pulmonary capillary blood flow. C. Autoimmune disorders may be more common in patients with overt asbestosis. D. ERG2000 INFORMATION- 1. HEALTH HAZARDS - ERG2000 (SUBSTANCES (LOW TO MODERATE HAZARD)) - GUIDE 171 a. Inhalation of material may be harmful. b. Contact may cause bums to skin and eyes. c. Inhalation of Asbestos dust may have a damaging effect on the lungs. d. Fire may produce irritating, corrosive and/or toxic gases. e. Runoff from fire control may cause pollution. f. Reference: ERG, 2000.

3.2 ACUTE CLINICAL EFFECTS

A. There is no evidence of any acute systemic effect from exposure to asbestos (Clayton & Clayton, 1993). Nearly all of the toxicologic literature on asbestos is concerned with its activity as a human carcinogen with chronic exposure. B. Asbestos is not acutely toxic, except for possible irritation of the eyes, skin, and respiratory tract due to mechanical action of the fibers. Skin irritation with com formation can result from penetration of the skin by asbestos spicules (HSDB, 2000). C. The dose-response relationship for induction cancer from exposure to asbestos is not well understood for low-level exposures. It has been suggested that even a single, high-dose acute exposure might be sufficient to induce cancer (Stich, 1985). D. Asbestos fibers can stimulate the production of interleukin (IL)-8 in cultured lung cells. The mechanism of this induction involves redox changes and phosphorylation by means of staurosporine-sensitive and tyrosine kinase(s), activation of transcription factors that bind to the NF-kappaB/NF-IL-6 binding site of the IL-8 promoter, and upregulation of the IL-8 gene (Simeonova & Luster, 1996).

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