Pneumoconiosis | |
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Micrograph of asbestosis (with ferruginous bodies), a type of pneumoconiosis. H&E stain. | |
Specialty | Pulmonology |
Pneumoconiosis is the general term for a class of interstitial lung disease where inhalation of dust (for example, ash dust, lead particles, pollen grains etc) has caused interstitial fibrosis. [1] [2] The three most common types are asbestosis, silicosis, and coal miner's lung. [3] Pneumoconiosis often causes restrictive impairment, [4] although diagnosable pneumoconiosis can occur without measurable impairment of lung function. [1] [2] Depending on extent and severity, it may cause death within months or years, or it may never produce symptoms. It is usually an occupational lung disease, typically from years of dust exposure during work in mining; [5] textile milling; shipbuilding, ship repairing, and/or shipbreaking; sandblasting; industrial tasks; rock drilling (subways or building pilings); [6] or agriculture. [7] [8] It is one of the most common occupational diseases in the world. [9]
Depending upon the type of dust, the disease is given different names:
The reaction of the lung to mineral dusts depends on many variables, including size, shape, solubility, and reactivity of the particles. [13] For example, particles greater than 5 to 10 μm are unlikely to reach distal airways, whereas particles smaller than 0.5 μm move into and out of alveoli, often without substantial deposition and injury. [14] Particles that are 1 to 5 μm in diameter are the most dangerous, because they lodge at the bifurcation of the distal airways. Coal dust is relatively inert, and large amounts must be deposited in the lungs before lung disease is clinically detectable. Silica, asbestos, and beryllium are more reactive than coal dust, resulting in fibrotic reactions at lower concentrations. Most inhaled dust is entrapped in the mucus blanket and rapidly removed from the lung by ciliary movement. However, some of the particles become stuck at alveolar duct bifurcations, where macrophages accumulate and engulf the trapped particulates. The pulmonary alveolar macrophage is a key cellular element in the initiation and perpetuation of lung injury and fibrosis. Many particles activate the inflammasome and induce IL-1 production. The more reactive particles trigger the macrophages to release a number of products that mediate an inflammatory response and initiate fibroblast proliferation and collagen deposition. Some of the inhaled particles may reach the lymphatics either by direct drainage or within migrating macrophages and thereby initiate an immune response to components of the particulates and/or to self-proteins that are modified by the particles. This then leads to an amplification and extension of the local reaction. Tobacco smoking worsens the effects of all inhaled mineral dusts, more so with asbestos than with any other particle. [7]
Typical indications on patient assessment include: [15]
Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome. [20] [21]
The prevalence as of 2021 of pneumoconiosis is around 527,500 cases, with over 60,000 new patients reported globally in 2017. Prevalence has trended somewhat downward since 2015. [2] The mortality of pneumoconiosis patients remained at a high level in recent years, with over 21,000 deaths each year since 2015. [2] It is likely that pneumoconiosis is under-diagnosed and under-reported, especially in countries without highly developed healthcare systems. [2]
Lung damage due to pneumoconiosis cannot be reversed. [22] However, some steps can slow down disease progression and relieve symptoms. These include the prescription of medications and breathing treatments to open airways and reduce inflammation. [22] Pulmonary rehabilitation and supplemental oxygen may also be recommended. [22] A lung transplant may be needed in cases of serious diseases. If the patient smokes, smoking cessation is also important. [22] Regular testing, such as X-rays or lung function tests, may be indicated to monitor disease progression.
To reduce the likelihood of developing pneumoconiosis, individuals working in affected industries should wear a mask, wash skin that comes in contact with dust, remove dust from clothing and wash the face and hands before eating or drinking. [22] In addition, governments often regulate industry, especially mines, to limit how much dust is in the air. [23] In the United States, coal miners injured by pneumoconiosis and their families may receive monthly payments and medical benefits under the Black Lung Benefits Act. [24]
Asbestosis is long-term inflammation and scarring of the lungs due to asbestos fibers. Symptoms may include shortness of breath, cough, wheezing, and chest tightness. Complications may include lung cancer, mesothelioma, and pulmonary heart disease.
Silicosis is a form of occupational lung disease caused by inhalation of crystalline silica dust. It is marked by inflammation and scarring in the form of nodular lesions in the upper lobes of the lungs. It is a type of pneumoconiosis. Silicosis, particularly the acute form, is characterized by shortness of breath, cough, fever, and cyanosis. It may often be misdiagnosed as pulmonary edema, pneumonia, or tuberculosis. Using workplace controls, silicosis is almost always a preventable disease.
Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of respiratory diseases affecting the interstitium and space around the alveoli of the lungs. It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, and perivascular and perilymphatic tissues. It may occur when an injury to the lungs triggers an abnormal healing response. Ordinarily, the body generates just the right amount of tissue to repair damage, but in interstitial lung disease, the repair process is disrupted, and the tissue around the air sacs (alveoli) becomes scarred and thickened. This makes it more difficult for oxygen to pass into the bloodstream. The disease presents itself with the following symptoms: shortness of breath, nonproductive coughing, fatigue, and weight loss, which tend to develop slowly, over several months. The average rate of survival for someone with this disease is between three and five years. The term ILD is used to distinguish these diseases from obstructive airways diseases.
A chest radiograph, called a chest X-ray (CXR), or chest film, is a projection radiograph of the chest used to diagnose conditions affecting the chest, its contents, and nearby structures. Chest radiographs are the most common film taken in medicine.
Pulmonary fibrosis is a condition in which the lungs become scarred over time. Symptoms include shortness of breath, a dry cough, feeling tired, weight loss, and nail clubbing. Complications may include pulmonary hypertension, respiratory failure, pneumothorax, and lung cancer.
Pneumonitis describes general inflammation of lung tissue. Possible causative agents include radiation therapy of the chest, exposure to medications used during chemo-therapy, the inhalation of debris, aspiration, herbicides or fluorocarbons and some systemic diseases. If unresolved, continued inflammation can result in irreparable damage such as pulmonary fibrosis.
Siderosis is the deposition of excess iron in body tissue. When used without qualification, it usually refers to an environmental disease of the lung, also known more specifically as pulmonary siderosis or Welder's disease, which is a form of pneumoconiosis.
Black lung disease (BLD), also known as coal-mine dust lung disease, or simply black lung, is an occupational type of pneumoconiosis caused by long-term inhalation and deposition of coal dust in the lungs and the consequent lung tissue's reaction to its presence. It is common in coal miners and others who work with coal. It is similar to both silicosis from inhaling silica dust and asbestosis from inhaling asbestos dust. Inhaled coal dust progressively builds up in the lungs and leads to inflammation, fibrosis, and in worse cases, necrosis.
Progressive massive fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis, can complicate silicosis and coal worker's pneumoconiosis. Conglomerate masses may also occur in other pneumoconioses, such as talcosis, berylliosis (CBD), kaolin pneumoconiosis, and pneumoconiosis from carbon compounds, such as carbon black, graphite, and oil shale. Conglomerate masses can also develop in sarcoidosis, but usually near the hilae and with surrounding paracicatricial emphysema.
Occupational lung diseases comprise a broad group of diseases, including occupational asthma, industrial bronchitis, chronic obstructive pulmonary disease (COPD), bronchiolitis obliterans, inhalation injury, interstitial lung diseases, infections, lung cancer and mesothelioma. These can be caused directly or due to immunological response to an exposure to a variety of dusts, chemicals, proteins or organisms. Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.
Caplan's syndrome is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogeneous and well-defined on chest X-ray.
Usual interstitial pneumonia (UIP) is a form of lung disease characterized by progressive scarring of both lungs. The scarring (fibrosis) involves the pulmonary interstitium. UIP is thus classified as a form of interstitial lung disease.
Restrictive lung diseases are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.
Rheumatoid lung disease is a disease of the lung associated with RA, rheumatoid arthritis. Rheumatoid lung disease is characterized by pleural effusion, pulmonary fibrosis, lung nodules and pulmonary hypertension. Common symptoms associated with the disease include shortness of breath, cough, chest pain and fever. It is estimated that about one quarter of people with rheumatoid arthritis develop this disease, which are more likely to develop among elderly men with a history of smoking.
Mineral dust airway disease is a general term used to describe complications due to inhaled mineral dust causing fibrosis and narrowing of primarily the respiratory bronchioles. It is a part of a group of disorders known as pneumoconioses which is characterized by inhaled mineral dust and the effects on the lungs.
Asbestos-related diseases are disorders of the lung and pleura caused by the inhalation of asbestos fibres. Asbestos-related diseases include non-malignant disorders such as asbestosis, diffuse pleural thickening, pleural plaques, pleural effusion, rounded atelectasis and malignancies such as lung cancer and malignant mesothelioma.
Stannosis is an occupational, non-fibrotic pneumoconiosis caused by chronic exposure and inhalation of tin. Pneumoconiosis is essentially when inorganic dust is found on the lung tissue; in this case, caused by tin oxide minerals. Dust particles and fumes from tin industries, stannous oxide (SnO) and stannic oxide (SnO2), are specific to stannosis diagnoses. Hazardous occupations such as, tinning, tin-working, and smelting are where most cases of stannosis are documented. When melted tin ions are inhaled as a fume, the tin oxides deposit onto the lung nodules and immune response cells. If a worker is exposed to tin oxides over multiple events for an extended time, they are at risk of developing stannosis.
Indium lung is a rare occupational lung disease caused by exposure to respirable indium in the form of indium tin oxide. It is classified as an interstitial lung disease.
Emphysema is any air-filled enlargement in the body's tissues. Most commonly emphysema refers to the enlargement of air spaces (alveoli) in the lungs, and is also known as pulmonary emphysema.
William N. Rom is the Sol and Judith Bergstein Professor of Medicine and Environmental Medicine, Emeritus at New York University School of Medicine and former Director of the Division of Pulmonary, Critical Care and Sleep Medicine at New York University and Chief of the Chest Service at Bellevue Hospital Center, 1989–2014. He is Research Scientist at the School of Global Public Health at New York University and Adjunct Professor at the NYU Robert F. Wagner Graduate School of Public Service. He teaches Climate Change and Global Public Health and Environmental Health in a Global World.
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