PNEUMOCONIOSES: OCCUPATIONAL LUNG DISEASES
ASBESTOSIS
ANTHRACOSIS
BYSSINOSIS
BAGASOSIS
SILICOSIS
ALUMINOSIS
BERYLLIOSIS
As you can see from the above, occupational diseases of the lungs have very unusual names; names that are not easy to remember. You’ve probably heard of Asbestosis because of the frequent commercials sponsored by law firms guaranteeing you a big dollar settlement if you were exposed to asbestos 40-50 years ago. And you may have heard of Black Lung Disease (Anthracosis) so common among coal miners. But Bagasosis, Byssinosis, Berylliosis, and Silicosis are not household names. I had never heard of these diseases, either, until I read about them in my Pathology textbook in my second year of medical school.
The name used for classifying occupational lung diseases is Pneumoconiosis. The plural for the category is Pneumoconioses. These diseases are not terribly common because they occur only in areas where the offending substances are mined, refined, manufactured, or used in construction, and only occur in the people who work in those industries; eg. Anthracosis occurs in miners exposed to coal dust stirred up by the mining of coal. Because these diseases take many years of exposure before symptoms occur, a lot of workers suffered lung damage, or died, before the harm they cause was acknowledged. A direct correlation between these diseases and occupational exposure is well-established, today.
Numerous occupations involve exposure to mineral particles cast into the air. Everyone is exposed to small concentrations of mineral dust in the course of normal life activities, but individuals who work in mines, machine shops, factories, or smelting and manufacturing areas containing high concentrations of mineral dust are susceptible to the lung diseases they cause. The name of the occupational lung disease is determined by the type of mineral dust inhaled. Each mineral compound has its own long term effect, some worse than others.
Industrial mineral dust particles small enough to be inhaled into the terminal branches of the bronchial tree, make their way into air sacs (alveoli) in the lungs. They initially cause an inflammatory response which spills into the space between the air sacs (the interstitium). That reaction progresses over time into fibrosis (scarring) causing the lungs to stiffen and the passage of oxygen into the blood stream to be affected.
Air filtration systems, filtering masks, and other mechanisms to limit exposure to mineral dust, have reduced the incidence of pneumoconioses. However, cases do still occur. But “the clinical picture of the classic pneumoconioses and their complications has not changed substantially.” That means in spite of major precautions, some miners still get Anthracosis, some metallurgists still get berylliosis, and workers exposed to asbestos in past years still have alarmingly high rates of asbestosis and mesotheliomata.
Anthracosis develops from inhaling coal dust. It is also called Black Lung or Coal Workers Pneumoconiosis. It takes several years of exposure to develop Anthracosis, but when it does it causes cough, shortness of breath, and excessive phlegm. Prolonged exposure results in emphysema, chronic lung disease, and far too frequently, lung cancer. Examination of the lungs of patients with black lung at autopsy shows exactly what the name describes. The lungs are black or dark gray, rather than pink, and collections coal dust particles are found throughout.
Coal particles form fibrous nodules in the lungs which become non-functional scar tissue. The spaces between the air sacs are filled with inflammatory cells and develop fibrous (scar) tissue over time. When this has happened, the part of the lung involved is unable to perform oxygenation of the blood.
Asbestosis is the most well-known of the pneumoconioses. It is caused by the inhalation asbestos, a fire retardant material used by plumbers, installers, and construction workers in the building of homes and businesses. Water pipes, heating and air conditioning systems, ceiling and flooring materials, and insulation contained asbestos for many years. Finally, when astute clinicians correlated asbestos with the development of chronic lung disease, the government issued a ban of the use of asbestos. Asbestosis sufferers were developing pulmonary fibrosis, inflammatory plaques of the pleura (the membrane covering the outer surface of the lungs and inner surface of the chest wall). Many years after these changes developed, asbestosis patients were developing malignancies of the pleural lining. These cancers were called mesotheliomata, and their discovery sparked a monumental lawsuit against the manufacturers of asbestos on behalf of the millions of people afflicted with these problems. Since the banning of asbestos in the 1970’s, doctors have begun to see fewer new cases of asbestosis.
Byssinosis is a rare disorder caused by inhaling hemp, flax, and cotton dust particles, and symptom-wise is much like asthma. In fact, it has been called occupational asthma as well as brown lung. Long term it can have permanent effects on lung function causing reduced exercise capacity and chronic cough and shortness of breath.
Bagassosis is also a rare disorder caused by inhaling a fibrous cane-sugar residue called bagasse. It is largely composed of cellulose, proteins, ash, and plant materials. Long term exposure results in pulmonary fibrosis, a consequence of most pneumoconioses.
Silicosis, a lung disorder like all the rest, results from the industrial inhalation of silica, a crystalline dust by-product of crushed stone, rock, sand, and clay. As with all pneumoconioses it causes cough, shortness of breath, and reduced lung function because it causes pulmonary fibrosis. A ”rapidly progressive form of silicosis can occur after short periods of intense exposure.”
Aluminosis, as the name implies, is a chronic lung disease from the inhalation of aluminum-bearing dust. Pulmonary fibrosis is a long term result. Like all pneumoconioses, aluminosis is irreversible. It does help early in the term of exposure to remove oneself from that environment, but once damage to the lungs has occurred, the condition cannot be eliminated or reversed. Pulmonary fibrosis causes significant limitation in exercise capacity and limits physical activity.
Berylliosis is caused by inhaling beryllium. Beryllium is used in making copper and nickel alloys used in gyroscopes, electrodes, and electrical contacts. Beryllium increases electrical conductivity. Unfortunately, beryllium does horrible things to the lungs, as can be seen by the chest X-ray at the beginning of this article. Cough, fever, night sweats, and fatigue are symptoms of berylliosis.
Two other very rare pneumoconioses are Bird Fancier’s Lung and Popcorn Lung. Bird fanciers are exposed to an “avian antigen” and develop a “hypersensitivity pneumonitis”, an inflammatory condition of the lung. Popcorn manufacturers suffer damage to their small airways from a food additive that “simulates butter flavor in microwave popcorn.” Both are diseases resulting from inhalation of a foreign, irritating substance.
Diagnosing a pneumoconiosis requires a thorough detailed occupational history and information on what industrial materials have been encountered, and for how long. Chest X-ray, CT Imaging of the lungs, and breathing function tests also help in determining the specific cause and functional status. Some pneumoconioses have X-ray or CT changes that are diagnostic of the specific disease, ie. Berylliosis. These findings, coupled with a detailed history of exposure, are all that’s needed to determine the diagnosis.
Once the patient becomes symptomatic and/or has X-ray or CT findings, it’s too late. The damage done to the lungs is irreversible so prevention and protection of the worker are the most effective approaches to reduction of disease incidence. The action of banning asbestos in the 1970’s has, and will, affect the number of cases of asbestosis and mesothelioma 20-40 years from now. Ideally, the ban of asbestos and replacement of asbestos-containing items, will eliminate the disease altogether. Nothing is 100% effective, however.
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De Vuyst P, Camus P. The past and present of pneumoconioses. Curr Opin Pulm Med 2000 Mar;6(2):151-156.
HTTPS:/www.cdc.gov/niosh/topics/pneumoconioses/default.html
Hula JT, Cool CD, Green FHY. Pathology and Mineralogy of the Pneumoconioses. Semin Respir Crit Care Med 2023 June;44(3):327-339.
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