Lost workdays due to employee injuries were reduced 96% after Methodist Rehabilitation Center installed ceiling lifts to transfer patients. Credit: Methodist Rehabilitation Center Mississippi,U.S. Radiation Safety Technician at Mount Sinai Hospital checks for contamination after inpatient therapy procedure.

The purpose of a respirator is to prevent the inhalation of harmful airborne substances or to provide a source of respirable air when breathing in oxygen‐deficient atmospheres. For a physician to recommend the use of respirator, general background information on respiratory‐protective devices is required. The first part of this clinical practice review describes the general aspects of industrial hygiene, respirators and a respirator‐certification program. The second part addresses matters related to medical certification for respirator use. Medical certification for respirators is an important part of the activities of the occupational physician. To determine whether a worker is able to tolerate the added strain of a respiratory protective device is a complex process in which factors such as fitness for work, health of the individual, characteristics of the work itself, and the properties, type, and requirements of the respiratory protective device, have to be considered. Medical certification is of utmost importance for respirator use, and it should be viewed as an element in a comprehensive respiratory protection program. A comprehensive program is the key element in affording the workers' effective respiratory protection once the initial steps of the hierarchy of methods of hazard control have proved insufficient or infeasible. As a result, the need for the industrial hygiene/safety officer, the worker, the employer and the medical professional to work as a team is much more than in any other field of occupational medicine—a necessary requirement for making the right decision. Am. J. Ind. Med. 37:142–157, 2000. © 2000 Wiley‐Liss, Inc.

LA exposure can cause a non-malignant pleural disease that is more rapidly progressive and more severe than the usual asbestos-related disease.

Fibrosis, characterized by excessive collagen protein deposition, is a progressive disease that can fatally inhibit organ function. Prolonged exposure to pathogens or environmental toxicants such as asbestos can lead to chronic inflammatory responses associated with fibrosis. Significant exposure to amphibole asbestos has been reported in and around Libby, Montana due to local mining of asbestos-contaminated vermiculite. These exposures have been implicated in a unique disease etiology characterized predominantly by pleural disorders, including fibrosis. We recently reported the discovery of mesothelial cell autoantibodies (MCAAs) in the sera of Libby residents and demonstrated a positive and significant correlation with pleural disease; however, a mechanistic link was not determined. Here we demonstrate that MCAAs induce pleural mesothelial cells to produce a collagen matrix but do not affect production of the pro-inflammatory cytokine tumor growth factor-β. While autoantibodies commonly induce a pro-fibrotic state by inducing epithelial–mesenchymal transition (EMT) of target cells, we found no evidence supporting EMT in cells exposed to MCAA positive human sera. Although implicated in other models of pulmonary fibrosis, activity of the protein SPARC (secreted protein, acidic and rich in cysteine) did not affect MCAA-induced collagen deposition. However, matrix formation was dependent on matrix metalloproteinase (MMP) activity, and we noted increased expression of MMP-8 and -9 in supernatants of mesothelial cells incubated with MCAA positive sera compared to control. These data suggest a mechanism by which MCAA binding leads to increased collagen deposition through altering MMP expression and provides an important mechanistic link between MCAAs and asbestos-related, autoimmune-induced pleural fibrosis.

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