There is no cure available for asbestosis. Oxygen therapy at home is often necessary to relieve the shortness of breath and correct underlying low blood oxygen levels. Supportive treatment of symptoms includes respiratory physiotherapy to remove secretions from the lungs by postural drainage, chest percussion, and vibration. Nebulized medications may be prescribed in order to loosen secretions or treat underlying chronic obstructive pulmonary disease. Immunization against pneumococcal pneumonia and annual influenza vaccination is administered due to increased sensitivity to the diseases. Those with asbestosis are at increased risk for certain cancers. If the person smokes, quitting the habit reduces further damage. Periodic pulmonary function tests, chest x-rays, and clinical evaluations, including cancer screening/evaluations, are given to detect additional hazards.

Once tuberculosis has been excluded, treatment is with steroids. All exposure to coal dust must be stopped, and smoking cessation should be attempted. Rheumatoid arthritis should be treated normally with early use of DMARDs.

ILD is not a single disease, but encompasses many different pathological processes. Hence treatment is different for each disease.

If a specific occupational exposure cause is found, the person should avoid that environment. If a drug cause is suspected, that drug should be discontinued.

Many cases due to unknown or connective tissue-based causes are treated with corticosteroids, such as prednisolone. Some people respond to immunosuppressant treatment. Patients with a low level of oxygen in the blood may be given supplemental oxygen.

Pulmonary rehabilitation appears to be useful. Lung transplantation is an option if the ILD progresses despite therapy in appropriately selected patients with no other contraindications.

On October 16, 2014, the Food and Drug Administration approved a new drug for the treatment of Idiopathic Pulmonary Fibrosis (IPF). This drug, Ofev (nintedanib), is marketed by Boehringer Ingelheim Pharmaceuticals, Inc. This drug has been shown to slow the decline of lung function although the drug has not been shown to reduce mortality or improve lung function. The estimated cost of the drug per year is approximately $94,000.

Many people with this condition have no symptoms. Treatment is aimed at the health problems causing the lung problem and the complications caused by the disorder.

Fast-acting drugs for RA include aspirin and corticosteroids, which alleviate pain and reduce inflammation. Slow-acting drugs termed disease modifying antirheumatic drugs (DMARDs), include gold, methotrexate and hydroxychloroquine (Plaquenil), which promote disease remission and prevent progressive joint destruction. In patients with less severe RA, pain relievers, anti-inflammatory drugs and physical rest are sufficient to improve quality of life. In patients with joint deformity, surgery is the only alternative for recovering articular function.

Prognosis is related to the underlying disorder and the type and severity of lung disease. In severe cases, lung transplantation can be considered. This is more common in cases of bronchiolitis obliterans, pulmonary fibrosis, or pulmonary hypertension. Most complications are not fatal, but does reduce life expectancy to an estimated 5 to 10 years.

Coal workers' pneumoconiosis (CWP), also known as black lung disease or black lung, is caused by long exposure to coal dust. It is common in coal miners and others who work with coal. It is similar to both silicosis from inhaling silica dust and to the long-term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and cannot be removed by the body; this leads to inflammation, fibrosis, and in worse cases, necrosis.

Coal workers' pneumoconiosis, severe state, develops after the initial, milder form of the disease known as anthracosis ("anthrac" — coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, "simple coal workers' pneumoconiosis" and "complicated coal workers' pneumoconiosis" (or progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis, clinically defined as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In nonsmokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% to 17% incidence of industrial bronchitis.

In 2013 CWP resulted in 25,000 deaths down from 29,000 deaths in 1990.

Asbestosis is a fibrosing interstitial lung disease caused by exposure to forms of the mineral asbestos.

Occupational lung diseases are occupational diseases affecting the respiratory system, including occupational asthma, black lung disease (coalworker's pneumoconiosis), chronic obstructive pulmonary disease (COPD), mesothelioma, and silicosis. Infectious lung diseases can also be acquired in an occupational context. Exposure to substances like flock and silica can cause fibrosing lung disease, whereas exposure to carcinogens like asbestos and beryllium can cause lung cancer. 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.

Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines and from agriculture.

In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis.

Positive indications on patient assessment:

- Shortness of breath

- Chest X-ray may show a characteristic patchy, subpleural, bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing.

Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.

The exact cause of rheumatoid lung disease is unknown. However, associated factors could be due largely to smoking. Sometimes, the medicines used to treat rheumatoid arthritis, especially methotrexate, may result in lung disease.

Prevention's:

- Stop smoking: Chemicals found in cigarettes can irritate already delicate lung tissue, leading to further complications.

- Having regular checkups: The doctor could listen to lungs and monitor breathing, because lung problems that are detected early can be easier to treat.

Asbestosis is long term inflammation and scarring of the lungs due to asbestos. Symptoms may include shortness of breath, cough, wheezing, and chest pain. Complications may include lung cancer, mesothelioma, and pulmonary heart disease.

Asbestosis is caused by breathing in asbestos fibers. Generally it required a relatively large exposure over a long period of time. Such levels of exposure typically only occur in those who work with the material. All types of asbestos fibers are associated with concerns. It is generally recommended that currently existing asbestos be left undisturbed. Diagnosis is based upon a history of exposure together with medical imaging. It is a type of interstitial pulmonary fibrosis.

There is no specific treatment. Recommendations may include stopping smoking, influenza vaccination, pneumococcal vaccination, or oxygen therapy. Asbestosis affected about 157,000 people and resulted in 3,600 deaths in 2015. Asbestos use has been banned in a number of countries in an effort to prevent disease.

Mineral dust airway disease is due to inhaled mineral dust causing fibrosis and narrowing of primarily the respiratory bronchioles. It is distinct from pneumoconiosis which is due to lung tissue fibrosis but shares the same cause.

The nodules may pre-date the appearance of rheumatoid arthritis by several years. Otherwise prognosis is as for RA; lung disease may remit spontaneously, but pulmonary fibrosis may also progress.

Coal dust is not as fibrogenic as in silica dust. Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Coal dust provides a sufficient stimulus for the macrophage to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors, which are important in the inflammation and fibrosis of CWP. Aggregations of carbon-laden macrophages can be visualized under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centers of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung.

ILD may be classified according to the cause. One method of classification is as follows:

1. Inhaled substances

- Inorganic

- Silicosis

- Asbestosis

- Berylliosis

- printing workers (eg. carbon bblack, ink mist)

- Organic

- Hypersensitivity pneumonitis

2. Drug-induced

- Antibiotics

- Chemotherapeutic drugs

- Antiarrhythmic agents

3. Connective tissue and Autoimmune diseases

- Rheumatoid arthritis

- Systemic lupus erythematosus

- Systemic sclerosis

- Polymyositis

- Dermatomyositis

4. Infection

- Atypical pneumonia

- Pneumocystis pneumonia (PCP)

- Tuberculosis

- "Chlamydia" trachomatis

- Respiratory Syncytial Virus

5. Idiopathic

- Sarcoidosis

- Idiopathic pulmonary fibrosis

- Hamman-Rich syndrome

- Antisynthetase syndrome

6. Malignancy

- Lymphangitic carcinomatosis

7. Predominantly in children

- Diffuse developmental disorders

- Growth abnormalities deficient alveolarisation

- Infant conditions of undefined cause

- ILD related to alveolar surfactant region

Progressive Massive Fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis (usually in the upper lung zones), 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 paracitricial emphysema.

The disease arises firstly through the deposition of silica or coal dust (or other dust) within the lung, and then through the body's immunological reactions to the dust.

The pathogenesis of PMF is complicated, but involves two main routes - an immunological route, and a mechanical route.

Immunologically, disease is caused primarily through the activity of lung macrophages, which phagocytose dust particles after their deposition. These macrophages seek to eliminate the dust particle through either the mucociliary mechanism, or through lymphatic vessels which drain the lungs. Macrophages also produce an inflammatory mediator known as interleukin-1 (IL-1), which is part of the immune systems first line defenses against infecting particles. IL-1 is responsible for 'activation' of local vasculature, causing endothelial cells to express certain cell adhesion molecules, which help the cells of the bodies immune system to migrate into tissues. Macrophages exposed to dust have been shown to have markedly decreased chemotaxis. Production of inflammatory mediators - and the tissue damage that ensues as an effect of this, as well as reduced motility of cells, is fundamental to the pathogenesis of pneumoconiosis and the accompanying inflammation, fibrosis, and emphysema.

There are also some mechanical factors involved in the pathogenesis of Complex Pneumoconiosis that should be considered. The most notable indications are the fact that the disease tends to develop in the upper lobe of the lung - especially on the right, and its common occurrence in taller individuals.

Initially, the disease appears as alveolitis, and then progresses to emphysema.

Patients may develop pneumothorax (collapsed lung).

The barium particles can be seen as opaque shadows on the chest X-rays of people with baritosis. However, being a benign condition, it neither interferes with lung function nor causes symptoms other than a mild cough.

After exposure to barium dust ceases, the X-ray abnormalities gradually resolve.

Bauxite pneumoconiosis, also known as Shaver's disease, corundum smelter's lung, bauxite lung or bauxite smelters' disease, is a progressive form of pneumoconiosis usually caused by occupational exposure to bauxite fumes which contain aluminium and silica particulates.

It is typically seen in workers involved in the smelting of bauxite to produce corundum.

Since the mechanism behind chylothorax is not well understood, treatment options are limited. Drainage of the fluid out of the pleural space is essential to obviate damage to organs, especially the inhibition of lung function by the counter pressure of the chyle. Another treatment option is pleuroperitoneal shunting (creating a communication channel between pleural space and peritoneal cavity). By this surgical technique loss of essential triglycerides that escape the thoracic duct can be prevented. Omitting fat (in particular FFA) from the diet is essential. Either surgical or chemical pleurodesis are options: the leaking of lymphatic fluids is stopped by irritating the lungs and chest wall, resulting in a sterile inflammation. This causes the lung and the chest wall to be fused together which prevents the leaking of lymphatic fluids into the pleural space. The medication octreotide has been shown to be beneficial and in some cases will stop the chylothorax after a few weeks.

In animals, the most effective form of treatment until recently has been surgical ligation of the thoracic duct combined with partial pericardectomy. There is at least one case report (in a cat) of clinical response to treatment with rutin.

Baritosis is a benign type of pneumoconiosis, which is caused by long-term exposure to barium dust.

Barium has a high radio-opacity and the disease may develop after few months of exposure. Extremely dense, discrete small opacities of 2–4 mm diameter, sometimes of a star-like configuration, are seen on the radiograph. Their distribution is uniform. When they are very numerous, superimposition may give the impression of confluency, but this does not seem to occur in reality. The hilar lymph nodes can be very opaque but not enlarged. After cessation of exposure, there is a gradual clearing of the opacities.

Chalicosis (Greek, χάλιξ, gravel), sometimes called flint disease, is a form of pneumoconiosis affecting the lungs or bronchioles, found chiefly among stonecutters.

The disease is caused by the inhalation of fine particles of stone.

People may be exposed to toxic chemicals or similar dangerous substances from pharmaceutical products, consumer products, the environment, or in the home or at work. Many toxic tort cases arise either from the use of medications, or through exposure at work.

Pharmaceutical injuries can occur when a person is injured by a dangerous, defective or contaminated medication. Many pharmaceutical toxic injury cases are mass tort cases, as most medications are consumed by thousands of people. The cases are often litigated against drug manufacturers and distributors, and potentially against prescribing physicians. When prosecuted against drug manufacturers and distributors, pharmaceutical toxic tort cases differ from medical malpractice suits in that pharmaceutical toxic tort cases are essentially product liability cases, the defective product being the drug.