Opinion ID: 1973725
Heading Depth: 1
Heading Rank: 3

Heading: asbestos related disease:

Text: The parties in the present case have stipulated to a summary of medical evidence they would introduce if they were to present evidence at a full medical hearing. Included in the stipulation is the testimony of John Edward Craighead, a clinical pathologist who for many years has studied pneumoconiosis and asbestos related disease. He defines injury as a process which alters structure, and applies the term regardless of whether he is referring to a cell, a tissue, an organ, or the body itself. Disease is defined as occurring when there is an injury and a response to that injury. The presence of asbestos in the lungs stimulates a wide range of reactions, which Dr. Craighead divides into three responses. The first response, characterized as direct injury, occurs when asbestos fibers in the respiratory tract interact with the membranes of the tracheal lining cells causing the release of enzymes and superoxides which either damage or kill the individual cells. If sufficient cells are damaged, tissue, which is simply the accumulation of cells, is damaged or destroyed. This injury process occurs within one hour of introduction of the asbestos fiber to the cell. The second response occurs when the presence of asbestos fibers stimulates macrophages to accumulate. Macrophages are scavenger cells which attempt to engorge foreign particles. As the macrophages attempt to ingest the fibers there is a release of enzymes which have a damaging effect on tissue. There is also a chemical reaction which stimulates the production of fibrous tissue. Which, in turn, creates a scar in the injured tissue. The accumulation of the scar tissue in the respiratory system prevents the lung from performing its normal oxygen/carbon-dioxide gas exchange. This accumulative process of macrophages, referred to as the indirect injury by Dr. Craighead, has been seen to occur within the first month of exposure, and it is indicated that it starts even earlier than that. The third response in the asbestosis process is the change in the nature of the cells lining the bronchial tree. The normal lining, designed to move dust particles out of the body, is replaced by cells lacking cilia, resulting in the tendency toward accumulation of asbestos particles. Dr. Craighead would also testify that, although there had previously been general acceptance among medical authorities that there existed a clinical progression of asbestosis post exposure, there was substantial doubt developing among leading authorities that this was indeed true. The emerging view theorizes that disease progression may be attributable to the eventual, and inevitable, decrease in the respiratory function involved in the aging process, and also to other factors such as cigarette smoking or infection. Less is known about mesothelioma, a cancer causally linked to asbestos. However, it seems undisputed that it is linked directly to asbestos exposure to the pleural cavity upon which non-malignant lesions develop which then become malignant. The tumor grows and pushes the lung aside adversely affecting respiratory function. Mesothelioma has a lengthy latent residency period, often manifesting twenty or more years after exposure to asbestos.