Silicosis is a permanent disease with no cure. Treatment options currently available focus on alleviating the symptoms and preventing any further progress of the condition. These include:

- Stopping further exposure to airborne silica, silica dust and other lung irritants, including tobacco smoking.

- Cough suppressants.

- Antibiotics for bacterial lung infection.

- TB prophylaxis for those with positive tuberculin skin test or IGRA blood test.

- Prolonged anti-tuberculosis (multi-drug regimen) for those with active TB.

- Chest physiotherapy to help the bronchial drainage of mucus.

- Oxygen administration to treat hypoxemia, if present.

- Bronchodilators to facilitate breathing.

- Lung transplantation to replace the damaged lung tissue is the most effective treatment, but is associated with severe risks of its own.

- For acute silicosis, bronchoalveolar lavage may alleviate symptoms, but does not decrease overall mortality.

Experimental treatments include:

- Inhalation of powdered aluminium, d-penicillamine and polyvinyl pyridine-N-oxide.

- Corticosteroid therapy.

- Chinese Herbal Kombucha

- The herbal extract tetrandrine may slow progression of silicosis.

The best way to prevent silicosis is to identify work-place activities that produce respirable crystalline silica dust and then to eliminate or control the dust ("primary prevention"). Water spray is often used where dust emanates. Dust can also be controlled through dry air filtering.

Following observations on industry workers in Lucknow (India), experiments on rats found that jaggery (a traditional sugar) had a preventive action against silicosis.

Pulmonary fibrosis creates scar tissue. The scarring is permanent once it has developed. Slowing the progression and prevention depends on the underlying cause:

- Treatment options for idiopathic pulmonary fibrosis are very limited. Though research trials are ongoing, there is no evidence that any medications can significantly help this condition. Lung transplantation is the only therapeutic option available in severe cases. Since some types of lung fibrosis can respond to corticosteroids (such as prednisone) and/or other medications that suppress the body's immune system, these types of drugs are sometimes prescribed in an attempt to slow the processes that lead to fibrosis.

- Two pharmacological agents intended to prevent scarring in mild idiopathic fibrosis are pirfenidone, which reduced reductions in the 1-year rate of decline in FVC. Pirfenidone also reduced the decline in distances on the 6-minute walk test, but had no effect on respiratory symptoms. The second agent is nintedanib, which acts as antifibrotic, mediated through the inhibition of a variety of tyrosine kinase receptors (including platelet-derived growth factor, fibroblast growth factor, and vascular endothelial growth factor). A randomized clinical trial showed it reduced lung-function decline and acute exacerbations.

- Anti-inflammatory agents have only limited success in reducing the fibrotic progress. Some of the other types of fibrosis, such as non-specific interstitial pneumonia, may respond to immunosuppressive therapy such as corticosteroids. However, only a minority of patients respond to corticosteroids alone, so additional immunosuppressants, such as cyclophosphamide, azathioprine, methotrexate, penicillamine, and cyclosporine may be used. Colchicine has also been used with limited success. There are ongoing trials with newer drugs such as IFN-γ and mycophenolate mofetil..

- Hypersensitivity pneumonitis, a less severe form of pulmonary fibrosis, is prevented from becoming aggravated by avoiding contact with the causative material.

- Oxygen supplementation improves the quality of life and exercise capacity. Lung transplantation may be considered for some patients.

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.

Patients with single aspergillomas generally do well with surgery to remove the aspergilloma, and are best given pre-and post-operative antifungal drugs. Often, no treatment is necessary. However, if a patient coughs up blood (haemoptysis), treatment may be required (usually angiography and embolisation, surgery or taking tranexamic acid). Angiography (injection of dye into the blood vessels) may be used to find the site of bleeding which may be stopped by shooting tiny pellets into the bleeding vessel.

For chronic cavitary pulmonary aspergillosis and chronic fibrosing pulmonary aspergillosis, lifelong use of antifungal drugs is usual. Itraconazole and voriconazole are first and second-line anti fungal agents respectively. Posaconazole can be used as third-line agent, for patients who are intolerant of or developed resistance to the first and second-line agents. Regular chest X-rays, serological and mycological parameters as well as quality of life questionnaires are used to monitor treatment progress. It is important to monitor the blood levels of antifungals to ensure optimal dosing as individuals vary in their absorption levels of these drugs.

Hypoxia caused by pulmonary fibrosis can lead to pulmonary hypertension, which, in turn, can lead to heart failure of the right ventricle. Hypoxia can be prevented with oxygen supplementation.

Pulmonary fibrosis may also result in an increased risk for pulmonary emboli, which can be prevented by anticoagulants.

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.

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.

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.

Regardless of cause, UIP is relentlessly progressive, usually leading to respiratory failure and death without a lung transplant. Some patients do well for a prolonged period of time, but then deteriorate rapidly because of a superimposed acute illness (so-called "accelerated UIP"). The outlook for long-term survival is poor. In most studies, the median survival is 3 to 4 years. Patients with UIP in the setting of rheumatoid arthritis have a slightly better prognosis than UIP without a known cause (IPF).

Pulmonary talcosis, less specifically referred to as talcosis, is a pulmonary disorder caused by talc.

It has been related to silicosis resulting from inhalation of talc and silicates. It is also tied to heroin use where talc might be used as an adulterant to increase weight and street value. It is one of several noted associations and possible risks of street heroin use. Talcosis can also arise from the injection of drugs intended for oral administration, as talc is present in many tablets and capsules that are used intravenously, such as benzodiazepines, dextroamphetamine, and prescription opioids.

Coal ash, also known as coal combustion residuals (CCRs), is the particulate residue that remains from burning coal. Depending on the chemical composition of the coal burned, this residue may contain toxic substances and pose a health risk to workers in coal-fired power plants.

Prevention measures include avoidance of the irritant through its removal from the workplace or through technical shielding by the use of potent irritants in closed systems or automation, irritant replacement or removal and personal protection of the workers.

In order to better prevent and control occupational disease, most countries revise and update their related laws, most of them greatly increasing the penalties in case of breaches of the occupational disease laws. Occupational disease prevention, in general legally regulated, is part of good supply chain management and enables companies to design and ensure supply chain social compliance schemes as well as monitor their implementation to identify and prevent occupational disease hazards.

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

Usual interstitial pneumonia (UIP) is a form of lung disease characterized by progressive scarring of both lungs. The scarring (fibrosis) involves the supporting framework (interstitium) of the lung. UIP is thus classified as a form of interstitial lung disease. The term "usual" refers to the fact that UIP is the most common form of interstitial fibrosis. "Pneumonia" indicates "lung abnormality", which includes fibrosis and inflammation. A term previously used for UIP in the British literature is cryptogenic fibrosing alveolitis, a term that has fallen out of favor since the basic underlying pathology is now thought to be fibrosis, not inflammation.

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.

Lead: The exposure of lead in coal ash can cause major damage to the nervous system. Lead exposure can lead to kidney disease, hearing impairment, high blood pressure, delays in development, swelling of the brain, hemoglobin damage, and male reproductive problems. Both low levels and high levels of lead exposure can cause harm to the human body.

Cadmium: When coal ash dust is inhaled, high levels of cadmium is absorbed into the body. More specifically, the lungs directly absorb cadmium into the bloodstream. When humans are exposed to cadmium over a long period of time, kidney disease and lung disease can occur. In addition, cadmium exposure can be associated with hypertension. Lastly, chronic exposure of cadmium can cause bone weakness which increases the risk of bone fractures and osteoporosis.

Chromium: The exposure of chromium (IV) in coal ash can cause lung cancer and asthma when inhaled. When coal ash waste pollutes drinking water, chromium (IV) can cause ulcers in the small intestine and stomach when ingested. Lastly, skin ulcers can also occur when the exposure chromium (IV) in coal ash comes in contact with the skin.

Arsenic: When high amounts of arsenic is inhaled or ingested through coal ash waste, diseases such as bladder cancer, skin cancer, kidney cancer and lung cancer can develop. Ultimately, exposure of arsenic over a long period of time can cause mortality. Furthermore, low levels of arsenic exposure can cause irregular heartbeats, nausea, diarrhea, vomiting, peripheral neuropathy and vision impairment.

Mercury: Chronic exposure of mercury from coal ash can cause harm to the nervous system. When mercury is inhaled or ingested various health effects can occur such as vision impairment, seizures, numbness, memory loss and sleeplessness.

Boron: When coal ash dust is inhaled, the exposure of boron can cause discomfort in the throat, nose and eye. Moreover, when coal ash waste is ingested, boron exposure can be associated with kidney, liver, brain, and intestine impairment.

Molybdenum: When molybdenum is inhaled from coal ash dust, discomfort of the nose, throat, skin and eye can occur. As a result, short-term molybdenum exposure can cause an increase of wheezing and coughing. Furthermore, chronic exposure of molybdenum can cause loss of appetite, tiredness, headaches and muscle soreness.

Thallium: The exposure of thallium in coal ash dust can cause peripheral neuropathy when inhaled. Furthermore, when coal ash is ingested, thallium exposure can cause diarrhea and vomiting. In addition, thallium exposure is also associated with heart, liver, lung and kidney complications.

Silica: When silica is inhaled from coal ash dust, fetal lung disease or silicosis can develop. Furthermore, chronic exposure of silica can cause lung cancer. In addition, exposure to silica over a period of time can cause loss of appetite, poor oxygen circulation, breathing complications and fever.

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.

Aspergillosis is an infection caused by the fungus "Aspergillus". Aspergillosis describes a large number of diseases involving both infection and growth of fungus as well as allergic responses. Aspergillosis can occur in a variety of organs, both in humans and animals.

The most common sites of infection are the respiratory apparatus (lungs, sinuses) and these infections can be:

- Invasive (e.g. – IPA)

- Non-invasive (e.g. Allergic Pulmonary Aspergillosis - ABPA)

- Chronic pulmonary and aspergilloma (e.g. chronic cavitary, semi-invasive)

- Severe asthma with fungal sensitisation (SAFS)

Chronic pulmonary aspergillosis (CPA) is a long-term aspergillus infection of the lung and "Aspergillus fumigatus" is almost always the species responsible for this illness. Patients fall into several groups as listed below.

- Those with an aspergilloma which is a ball of fungus found in a single lung cavity - which may improve or disappear, or change very little over a few years.

- Aspergillus nodule

- Chronic cavitary pulmonary aspergillosis (CCPA) where cavities are present in the lungs, but not necessarily with a fungal ball (aspergilloma).

- Chronic fibrosing pulmonary aspergillosis this may develop where pulmonary aspergillosis remains untreated and chronic scarring of the lungs occurs. Unfortunately scarring of the lungs does not improve.

Most patients with CPA have or have had an underlying lung disease. The most common diseases include tuberculosis, atypical mycobacterium infection, stage III fibrocystic pulmonary sarcoidosis, ABPA, lung cancer, COPD and emphysema, asthma and silicosis.

Occupational skin diseases are ranked among the top five occupational diseases in many countries.

Occupational skin diseases and conditions are generally caused by chemicals and having wet hands for long periods while at work. Eczema is by far the most common, but urticaria, sunburn and skin cancer are also of concern.

Contact dermatitis due to irritation is inflammation of the skin which results from a contact with an irritant. It has been observed that this type of dermatitis does not require prior sensitization of the immune system. There have been studies to support that past or present atopic dermatitis is a risk factor for this type of dermatitis. Common irritants include detergents, acids, alkalies, oils, organic solvents and reducing agents.

The acute form of this dermatitis develops on exposure of the skin to a strong irritant or caustic chemical. This exposure can occur as a result of accident at a workplace. The irritant reaction starts to increase in its intensity within minutes to hours of exposure to the irritant and reaches its peak quickly. After the reaction has reached its peak level, it starts to heal. This process is known as decrescendo phenomenon. The most frequent potent irritants leading to this type of dermatitis are acids and alkaline solutions. The symptoms include redness and swelling of the skin along with the formation of blisters.

The chronic form occurs as a result of repeated exposure of the skin to weak irritants over long periods of time.

Clinical manifestations of the contact dermatitis are also modified by external factors such as environmental factors (mechanical pressure, temperature, and humidity) and predisposing characteristics of the individual (age, sex, ethnic origin, preexisting skin disease, atopic skin diathesis, and anatomic region exposed.

Another occupational skin disease is Glove related hand urticaria. It has been reported as an occupational problem among the health care workers. This type of hand urticaria is believed to be caused by repeated wearing and removal of the gloves. The reaction is caused by the latex or the nitrile present in the gloves.

High-risk occupations include:

- Hairdressing

- Catering

- Healthcare

- Printing

- Metal machining

- Motor vehicle repair

- Construction