SYNOPSIS OF ASBESTOS-RELATED DISEASES



ASBESTOS-RELATED PULMONARY DISEASES

Asbestos-related pulmonary diseases are a group of diseases that are associated with exposure to asbestos with subsequent development of a clinical condition attributed to the exposure. This document is an attempt to provide a brief overview of asbestos and the mechanism of its effects in humans, an overview of the more common asbestos-related pulmonary diseases, diagnostic considerations in individuals alleging asbestos-related pulmonary diseases, and application of the information to the Ohio Workers' Compensation System.

OVERVIEW OF ASBESTOS

Physical Properties and Effects in Humans

Asbestos is a term applied to a family of naturally occurring, flexible, silicate minerals that are resistant to heat and many chemicals.[1] The properties of relative heat and chemical resistance has lead to widespread use in the 20th Century of asbestos in many processes and products including insulation materials, building materials such as vinyl asbestos floor tile, linings of furnaces, filtration systems, asbestos cement products, and as spray products for acoustical, thermal, or fireproofing purposes. Therefore, asbestos is commonly found throughout the work and non-work environments. Identification of asbestos fibers in samples of lung tissue, lung lavage samples or sputum, documents past exposure, but not necessarily the source of the exposure or whether asbestos-related disease is present. While individuals with asbestos-related disease may have higher concentrations of fibers in tissue samples, there is considerable overlap and laboratory variation so that asbestos fiber count has limited usefulness.

Once inhaled, the body attempts to remove fibers by several pathways including mucociliary transport through the airways, the lymphatic system, or through degradation of the fibers by macrophages. The fundamental disease process is the induction of inflammation resulting in fibrosis and/or cancer of the lung and pleural space. The fibrosis process is the result of the inflammatory reaction and repair processes by the body’s defense system to remove asbestos fibers. These reactions lead to permanent scarring and fibrosis. The cancer processes are the result of damage to target cells with genetic mutations through a variety of molecular injuries.

The pathogenicity of asbestos fibers may be affected by the dose (concentration and duration of exposure), fiber type, fiber dimensions, durability of the fiber, and surface chemicals that may be present on the fiber. Several studies have shown that the toxicity of asbestos fibers is related to the fibrous nature of the mineral. Both fiber diameter and length are important. In general, fibers with diameters > 3(m in diameter and > 200(m in length do not penetrate the lower lung. Fibers shorter than approximately 3(m in length are usually phagocytosed by macrophages or removed by the lymphatic system. Therefore, fibers less than 3 (m in diameter and longer than 8 (m are more likely to penetrate the lower lung and are more difficult for host defense mechanisms to remove. Fibers of this size are more likely to initiate cellular and molecular events leading to fibrosis or carcinogenesis.

There is a latency period of several years between initial exposure and onset of clinical disease. The latency period is variable. Individuals who are no longer occupationally exposed to asbestos may develop asbestos-related diseases years after their removal from occupational exposure. Current OSHA regulations and industrial processes have tried to limit exposure by substitution of other materials, monitoring with limits on the concentration of fibers permitted per cc of air in the workplace, use of personal protective equipment when exposed to asbestos fibers in significant concentrations, and required periodic medical monitoring of exposed workers for asbestos-related diseases.

There is little doubt that the "dose" both in terms of concentration and duration of exposure is important with higher concentration and longer duration of exposure more likely to increase the probability of development of an asbestos-related disease. However, exact dose-response curves can not be reasonably determined due to variability among type of fibers, variability of host response systems, questionable exposure histories, and that the radiographic findings are not specific to asbestos-related disease.

ASBESTOS-RELATED DISEASES

The following conditions are generally considered to be asbestos-related diseases:

• Asbestosis which is an interstitial fibrosis of the lung

• Benign asbestos pleurisy or benign pleural effusion which is a transient inflammation of the pleura

• Pleural plaques which are accumulations of collagen fibers forming hyalin masses usually on the parietal pleura (internal lining of chest wall).

• Pleural thickening which are accumulations of collagen fibers forming hyalin masses that affect the parietal and visceral pleura.

• Bronchogenic carcinoma of the lung

• Malignant mesothelioma which is rapidly invading tumor of the mesothelium of the pleura typically fatal within 12 to 24 months after diagnosis.

Asbestosis

Asbestosis is interstitial fibrosis of the lung caused by inhalation of asbestos fiber. Once the asbestos fibers reach lung tissue, macrophages respond to try to degrade or remove the fiber by phagocytosis. This results in the release of a variety of chemical mediators including those stimulating fibrosis. These processes lead to local damage and collagen deposition. This ongoing process leads to increase in the tissue mass and fibrosis of the lung tissue. Since the fibers persist even after removal of the individual from the exposure source, the process will continue after termination of exposure (employment). The latency period for development of asbestosis is believed to be at least 15 years. It is not possible to predict which individuals with clinical disease will progress significantly in the future or what other related conditions may develop.

While pathological (tissue) diagnosis showing interstitial fibrosis with asbestosis bodies would be ideal, many times this is not possible. For one thing, the pathologic diagnosis is dependent on tissue or fluid specimen from the individual. Even if a specimen is submitted, the pathological diagnosis of asbestosis may be difficult for several reasons.[2] These include the following:

• there are numerous other causes interstitial fibrosis.

• the distribution of interstitial fibrosis in the lung may be irregular and any sampling of lung tissue may fail to sample an adequate amount of tissue.

• asbestos bodies or fibers may not always be found because many fibers are cleared from the lungs or undergo degradation over time.

• not everyone who inhales asbestos fibers develops even microscopic asbestosis due to the lung’s ability to remove the fibers and the individual's response to exposure.

As stated above, the presence of asbestos fibers or asbestos bodies indicate a prior exposure. There are no pathognomic findings unique to asbestosis. The American Thoracic Society also has stated “open biopsy is rarely indicated in the assessment of workers for compensation purposes. The benefit of the doubt should be given whenever the clinical features and occupational exposure data are compatible with the diagnosis.” Therefore, in most cases it is necessary to base the diagnosis of asbestosis on clinical information.

The clinical features of asbestosis are similar to those of other interstitial lung fibroses. The major complaint in most individuals is shortness of breath or dyspnea on physical exertion. Cough, if present, is usually not or only minimally productive of sputum. The primary physical finding is basilar crackles (rales) that occur bilaterally and fail to clear with deep coughing. These rales can be heard at the lateral and posterior lung bases at the end or during peak inspiration early in the disease process. With progression of the disease process, the crackles may be heard earlier in inspiration and further up from the lung bases. Clubbing of the fingers is not common early in the disease process and is also seen in other disease processes. These factors limit the usefulness of clubbing when it is present.

On pulmonary function testing, characteristic findings include patterns consistent with restrictive lung disease. This includes a reduction in lung volumes primarily affecting inspiratory capacity and vital capacity. This results in a decrease in pulmonary compliance. The diffusing capacity is also usually impaired, particularly during exercise.

The chest x-ray is the most commonly used diagnostic study. Interpretation and description of findings and the extent of lung involvement noted on the x-ray is based on the method described by the International Labour Office (ILO-1980 Classification) that is used for pneumoconioses. This method relies on use of a certified reviewer, “B-reader”, providing interpretation on a standardized form. This method of classification as applied to asbestosis uses the letters “s”, “t”, and “u” to described respectively fine, medium, and coarse irregular opacifications seen on x-ray typically in the lower lung fields. The number of abnormalities in a given area of chest film is called their “profusion”. The profusion is graded 0 for none, 1 for slight, 2 for moderate, and 3 for severe. Due to difficulty in specific grading of profusion, a two-step review of the chest x-ray was introduced to reduce observer variability. This review process requires the observer to view the x-ray and indicate the profusion most likely. Later, the same review re-examines the x-ray and indicates a second profusion value that he/she might also consider. The profusion then is reported as 0/1, 1/0/, 1/1, 1/2, etc with the first number being the reading most likely. This report also requires a description of abnormalities of the pleura if present which indicate other conditions that may be asbestos-related. Despite its use, the chest x-ray was found to be normal. (profusion 0/0) in 10% of symptomatic individuals who had biopsy proven interstitial lung disease.

High Resolution Computerized Tomographic Scan (HRCT scan) in the supine and prone positions has been used more recently to diagnose or confirm interstitial lung disease. Reportedly, this procedure can detect early interstitial lung disease in 10% to 20% of symptomatic asbestos workers with normal chest x-rays. It also may assist with the evaluation of pleural disease. Its use is not recommended in screening, but it appears to be indicated in the clinical investigation of individuals with symptoms and suspected pleural or interstitial disease with a normal chest x-ray. Any findings noted on HRCT can not be attributed to asbestosis without a history of significant exposure to asbestosis.

Since there are no pathognomomic clinical, physiological, or radiological features, it is necessary to establish a credible history of exposure to asbestos and physical and diagnostic findings consistent with interstitial fibrosis. According to the American Thoracic Society[3], a diagnosis of asbestosis in the absence of lung tissue demonstrating asbestos bodies and interstitial fibrosis (pathologic diagnosis), will need to be made by clinical judgement based on consideration of:

1. A reliable history of exposure.

2. An appropriate time interval between exposure and detection.

3. Chest x-ray with “s”, “t”, or “u” small irregular opacifications with a profusion of 1/1 or greater.

4. A restrictive pattern of lung impairment with a forced vital capacity below the lower limit of normal.

5. A diffusing capacity below the lower limit of normal.

6. Bilateral late or pan inspiratory crackles at the posterior lung bases not cleared by cough.

In regard to these, the American Thoracic Society and most authors indicate that a history of occupational exposure and radiographic findings are most important and other considerations are confirmatory.

The clinical course of asbestosis depends on development of other diseases such as carcinoma, development of complications such as infection, other medical conditions and continuation of cigarette smoking if present, and the stage at which the asbestosis is diagnosed. It estimated that 20% to 40% of individuals will have progression of their disease once exposure is terminated. The disease process may progress with development of hypoxia and right heart failure ultimately leading to death. There is no documented treatment other than cessation of exposure, stopping cigarette smoking, and treatment of complications.

Benign Pleural Effusion or Pleurisy

This may be an early manifestation of asbestos exposure when it occurs. It also is caused by many other medical conditions. Pleural effusion secondary to asbestos is usually unilateral, may recur, and may be blood stained with variable numbers of red blood cells, macrophages, lymphocytes, and mesothelial cells. It is diagnosed by chest x-ray. The individuals are usually asymptomatic, but can have chest pain and shortness of breath. It is one of the first manifestations of asbestos-related diseases and the latency period is usually less than 20 years. When detected, the physician must consider malignant neoplasms such as mesothelioma as a cause of the effusion.

Pleural Plaques

These typically occur as lesions on the posterolateral aspect of the lower parietal pleura or diaphragm. These are frequently diagnosed by chest x-ray in asymptomatic individuals. They are considered the most frequent manifestation of asbestos exposure and asbestos is the most frequent cause of pleural plaques. The latency time is 20 to 30 years. They are believed to be from mechanical irritation of asbestos fibers in the lung surface and have limited progression. They can be seen in the absence of asbestosis. Diagnosis is by chest x-ray though CT scan may detect plaques much earlier. Pleural plaques themselves may be significant only in indicating the exposure and typically have not been thought to contribute to any physiologic impairment. This position has been questioned recently though the more recently described impairment may be related to early fibrosis rather than to the plaques themselves.

Pleural Thickening or Fibrosis

This process affects the visceral (lung) pleura causing a focal or diffuse thickening resulting in restriction of lung expansion. It frequently follows pleural effusions. It is frequently associated with diffuse interstitial fibrosis and can extend to the interlobar or interlobular spaces. Occasionally the pleural fibrosis will cause a retracted fibrotic mass, a pseudotumor, with a pleural bases (or rounded atelectasis). It may cause symptoms of shortness of breath and cause abnormalities of pulmonary function (spirometry). This condition may be seen secondary to other inflammatory conditions such as tuberculosis, surgery, trauma, or drug reaction which should be excluded as a cause. It may be seen on chest x-ray typically in the posterior and posterolateral region of the lower lung. CT scan facilitates the diagnosis. CT scan also facilitates in the diagnosis and management of “rounded atelectasis” or “pseudotumor”. It may cause restrictive pattern on spirometry.

Bronchogenic Carcinoma

It is unknown whether asbestos is a tumor promoter or initiator and there is controversy over the risk of cancer in asbestos workers who have smoked and do not have asbestosis. Pathologic reviews of lung cancer in asbestos workers have shown that all individuals had demonstrable fibrosis on the pathologic specimen. It has been shown that there is increased risk of cancer in smokers (10 times likelihood) and in individuals with pulmonary asbestosis (5 times likelihood). In those who are smokers and with pulmonary asbestosis, the risk of cancer is multiplied (50 times likelihood). Other potential risk factors also seem to increase the likelihood such as exposure to ionizing radiation and certain chemicals.

Pathological studies have failed to identify an increase in cell type, location, or other characteristics unique to asbestos-related cancer of the lung. The distribution of cell type is similar to the population with lung cancer not exposed to asbestos. These observations are complicated because most individuals with lung cancer with asbestos exposure also have a history of cigarette smoking.

The clinical aspects of asbestos-related lung cancer is indistinguishable from symptoms caused by other carcinogens unless there is the influence of coexisting asbestosis. Typical symptoms depending on location, extent, and metastasis include cough, chest pain, shortness of breath, recurrent bouts of pneumonia, hemoptysis, or weight loss. Most are diagnosed by chest x-ray and have no specific manifestation differentiating these tumors from other lung tumors.

Malignant Mesothelioma

This is a relatively rare type of cancer which has no association with cigarette smoke exposure. It is noted to have an incidence five to 20 times background incidence in those exposed to asbestos. Alternatively, 90% of individuals diagnosed with mesothelioma have had asbestos exposure. The cancer appears to have a latency period of 20 to 50 years and can follow relative short exposure. The typical symptoms are chest pain that is dull, achy, and frequently worse with breathing. Cough and shortness of breath are frequent with weight loss, fever, and general malaise present later with spread of the tumor. It is diagnosed by chest x-ray showing pleural abnormalities, nodules, and pleural effusion. The diagnosis is confirmed by tissue diagnosis, either by open surgery or biopsy. Survival for 24 months post diagnosis is unusual.

OHIO WORKERS' COMPENSATION LAWS AND RULES

Ohio Industrial Commission policy R96-1-01, "Referral of Dust Claims for Medical Specialist Examination" provides the minimum evidence that must be submitted by the claimant prior to referral of the claimant for an examination by a qualified medical specialist. This policy requires the claimant to submit prior to the claimant being referred for examination the following:

• A written interpretation of x-rays by a certified "B reader".

• Pulmonary function studies and interpretation by a licensed physician.

• An opinion of causal relationship by a licensed physician.

Ohio Revised Code 4123.68 states: "Before awarding compensation for disability or death due to silicosis, asbestosis, or coal miners' pneumoconiosis, the administrator shall refer the claim to a qualified medical specialist for examination and recommendation with regard to the diagnosis, the extent of disability, the cause of death, and other medical questions connected with the claim. An employee shall submit to such examinations, including clinical and x-ray examinations, as the administrator requires. In the event that an employee refuses to submit to examinations, including clinical and x-ray examinations, after notice from the administrator, or in the event that a claimant for compensation for death due to silicosis, asbestosis, or coal workers’ pneumoconiosis fails to produce necessary consents and permits, after notice from the commission, so that such autopsy examination and tests may be performed, then all rights for compensation are forfeited."

These two citations provide the basis for BWC authority to perform a clinical evaluation and the Industrial Commission policy provides the evidence that is expected to be submitted to support a claim. By interpreting the "causal relationship by a licensed physician" to include history and physical examination findings supporting a diagnosis of asbestosis and an adequate exposure to asbestos with an appropriate time interval between exposure sufficient to establish asbestos as a probable cause for the diagnosis, the required evidence described are similar to the criteria listed by the American Thoracic Society for the diagnosis of clinical asbestosis.

As described above, for each of the asbestos-related diseases, the chest x-ray is the primary study for detection. Therefore, use of chest x-ray in the evaluation should provide adequate evaluation for each of these conditions.

BIBLIOGRAPHY

Harber P, Schenker MB, and Balmes JR: Occupational and Environmental Respiratory Disease, Mosby-Year Book, Inc., St. Louis, 1996.

Parkes WR: Occupational Lung Disorders, Third Edition, Butterworth-Heinemann Ltd, Oxford, 1994.

2000 Ohio Industrial Commission and Bureau of Workers' Compensation Laws, Anderson Publishing Company, Cincinnati, 2000.

2000 Ohio Industrial Commission and Bureau of Workers' Compensation Rules, Anderson Publishing Company, Cincinnati, 2000.

"R96-1-01: Referral of Dust Claims for Medical Specialist Examination", Policy of The Industrial Commission of Ohio, February 26, 1996.

American Thoracic Society: "The Diagnosis of Nonmalignant Diseases Related to Asbestos", American Review of Respiratory Disease 134:363-368, 1986.

American Thoracic Society: "Standardization of Spirometry - 1994 update", American Journal of Respiratory and Critical Care Medicine 152:1107-1136, 1995.

American Thoracic Society: "Lung Function Testing: Selection of Reference Values and Interpretative Strategies", American Review of Respiratory Disease 144:1202-1218, 1991.

International Labour Office, "International Classification of Radiographs of Pneumoconiosis", 1980.

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[1] Begin R, Samet GM, and Shaikh RA: “Asbestos” in Harber P, Schenker MB, and Balmes JR: Occupational and Environmental Respiratory Disease Mosby-Year Book, Inc., St. Louis, 1996, pp 293-321.

[2]American Thoracic Society: “The Diagnosis of Nonmalignant Diseases Related to Asbestos”, American Review of Respiratory Disease 134:363-368, 1986.

[3]American Thoracic Society: “The Diagnosis of Nonmalignant Diseases Related to Asbestos”, American Review of Respiratory Disease 134:363-368, 1986.

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