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ASBESTOS HAZARDTEXT ® - Hazard Management Page 2 of 2

E. Transforming growth factor (TGF)-alpha was also upregulated in the lungs of rats as a result of a single 5-hour exposure to asbestos. Increases in TGF-alpha mRNA and peptide were seen as early as 24 hours after the acute exposure and persisted for at least 2 weeks. These results support the idea that TGF-alpha is involved in the mechanism of asbestos-induced proliferation of epithelial and mesenchymal cells in the lung (Liu et al, 1996).

3.3 CHRONIC CLINICAL EFFECTS

A. Occupational exposure to asbestos dust is associated with chronic laryngitis, chronic bronchitis, chronic obstructive pulmonary disease, chronic inflammation of the lungs, pleural effusions, pleural plaques, and cancer (ACGIH, 1991; Harbison, 1998; ILO, 1998). The primary determinant seems to be fiber length (Clayton & Clayton, 1993). Fibers less than 5 micrometers in length are considered not pathogenic (ACGIH, 1991). 1. Among insulation workers, 7 percent developed asbestosis, an interstitial fibrosis caused by inhaling fibers less than about 3 microns in diameter and 200 microns in length. In these same workers, 8 percent developed mesothelioma of the pleura and peritoneum, and 21 percent developed carcinoma of the lung (Stich, 1985). B. Asbestosis is pneumoconiosis resulting from asbestos exposure (ILO, 1998). Symptoms of asbestosis include shortness of breath and difficulty breathing, chest tightness, an initially non­ productive then productive cough, and cyanosis (ILO, 1998; Zenz, 1994). Fibrosis decreases lung compliance, which increases the energy required to breath; decreased gas diffusion increases breathlessness (ACGIH, 1991). C. Signs of asbestosis include granular changes on chest X-ray, restrictive pulmonary function, rales and clubbing of fingers (Hathaway et al, 1991). Parietal pleura can undergo severe thickening, forming pleural hyaline plaques, which can become impregnated with calcium salts and opaque to X-ray even in the absence of asbestosis (ACGIH, 1991). Rheumatoid factor and anti-nuclear antibodies have also been found in patients with asbestosis (Lange, 1980). D. The unambiguous diagnosis of asbestosis is sometimes difficult. In one study of 176 exposed persons, nine had clinical signs of asbestosis, but no asbestos bodies were seen in the lung tissues (Gaensler et al, 1991). Diagnosis should be based on a history of known exposure and presence of diffuse interstitial pulmonary fibrosis, but when the exposure is difficult to ascertain, diagnosis must be based on pathological findings (Jones, 1991). E. Most of the literature on asbestos is concerned with its ability to cause various forms of cancer (see CARCINOGENIC EFFECTS section below). 1. Mesothelioma is associated with asbestos exposure. The primary symptom is chest pain, then breathlessness, pleuritic pain, cough, weight loss and fatigue. Pleural effusions develop, with pleural thickening and densities seen on chest X-ray (Harbison, 1998). 2. Studies have shown an increased risk of laryngeal cancer after occupational exposure to asbestos (lARC, 1998). Workers exposed to asbestos who develop hoarseness or pain or sore throat should be referred for examination for laryngeal cancer (HSDB, 2001). F. Consistent with the previous observation is the finding that humoral immunity was elevated in patients with asbestosis (Lange, 1980), although cellular immunity can be depressed (Deshazo et al, 1982). Cellular immunity is thought to be involved in host defense mechanisms against cancer cells.

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