Asthma is a respiratory disease that can begin or worsen due to exposure at work and is characterized by episodic narrowing of the respiratory tract. Occupational asthma has a variety of causes, including sensitization to a specific substance, causing an allergic response; or a reaction to an irritant that is inhaled in the workplace. Exposure to various substances can also worsen pre-existing asthma. People who work in isocyanate manufacturing, who use latex gloves, or who work in an indoor office environment are at higher risk for occupational asthma than the average US worker. Approximately 2 million people in the US have occupational asthma.

According to a recent study, the main risk factors for RA-ILD are advancing age, male sex, greater RA disease activity, rheumatoid factor (RF) positivity, and elevated titers of anticitrullinated protein antibodies such as anticyclic citrullinated peptide. Cigarette smoking also appears to increase risk of RA-ILD, especially in patients with human leukocyte antigen DRB1.

A recently published retrospective study by a team from Beijing Chao-Yang Hospital in Beijing, China, supported three of the risk factors listed for RA-ILD and identified an additional risk factor. In that study of 550 RA patients, logistic regression analysis of data collected on the 237 (43%) with ILD revealed that age, smoking, RF positivity, and elevated lactate dehydrogenase closely correlated with ILD.

Recent studies have identified risk factors for disease progression and mortality. A retrospective study of 167 patients with RA-ILD determined that the usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography (HRCT) was a risk factor for progression, as were severe disease upon diagnosis and rate of change in pulmonary function test results in the first 6 months after diagnosis.

A study of 59 RA-ILD patients found no median survival difference between those with the UIP pattern and those without it. But the UIP group had more deaths, hospital admissions, need for supplemental oxygen, and decline in lung function.

Chronic obstructive pulmonary disease is a respiratory disease that can encompass chronic bronchitis and/or emphysema. 15% of the cases of COPD in the United States can be attributed to occupational exposure, including exposure to silica and coal dust. People who work in mining, construction, manufacturing (specifically textiles, rubber, plastic, and leather), building, and utilities are at higher risk for COPD than the average US worker.

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.

Silicosis resulted in 46,000 deaths in 2013 down from 55,000 deaths in 1990.

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

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.

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.

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.

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.

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 presence of rheumatoid arthritis alters how a person's immune system responds to foreign materials, such as dust from a coal mine. When a person with rheumatoid arthritis is exposed to such offensive materials, they are at an increased risk of developing pneumoconiosis.

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.

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.

Caplan syndrome occurs only in patients with both RA and pneumoconiosis related to mining dust (coal, asbestos, silica). The condition occurs in miners (especially those working in anthracite coal-mines), asbestosis, silicosis and other pneumoconioses. There is probably also a genetic predisposition, and smoking is thought to be an aggravating factor.

Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, 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 goes awry 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 term ILD is used to distinguish these diseases from obstructive airways diseases.

In children, several unique forms of ILD exist which are specific for the young age groups. The acronym chILD is used for this group of diseases and is derived from the English name, Children’s Interstitial Lung Diseases – chILD.

Prolonged ILD may result in pulmonary fibrosis, but this is not always the case. Idiopathic pulmonary fibrosis is interstitial lung disease for which no obvious cause can be identified (idiopathic), and is associated with typical findings both radiographic (basal and pleural based fibrosis with honeycombing) and pathologic (temporally and spatially heterogeneous fibrosis, histopathologic honeycombing and fibroblastic foci).

In 2013 interstitial lung disease affected 595,000 people globally. This resulted in 471,000 deaths.

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.

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.

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.

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.

Smoking has a supra-additive effect in increasing the risk of lung cancer in those exposed to asbestos. Studies have shown an increased risk of lung cancer among smokers who are exposed to asbestos compared to nonsmokers.

Pregnancy has been reported to exacerbate LAM in some cases. However, the risk has not been rigorously studied. In a survey of 318 patients who indicated that they had had at least one pregnancy, 163 responded to a second survey focusing on lung collapse. A total of 38 patients reported a pneumothorax with pregnancy, consistent with an incidence of pneumothorax in pregnancy of at least 10% (38 of 318). In one third of patients, the pneumothorax during pregnancy led to the LAM diagnosis. Pneumothoraces were almost twice as frequent on the right as on the left, and four women presented with bilateral spontaneous pneumothorax. Most pneumothoraces took place during the second and third trimesters. This study and others suggest that pregnancy is associated with pleural complications in LAM patients. Few women with a known LAM diagnosis choose to become pregnant and patients in whom LAM is diagnosed during pregnancy rarely have baseline pulmonary function tests available, complicating resolution of this question.

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

Patients may develop pneumothorax (collapsed lung).

The annual age-adjusted incidence rate (AAIR) of PSP is thought to be three to six times as high in males as in females. Fishman cites AAIR's of 7.4 and 1.2 cases per 100,000 person-years in males and females, respectively. Significantly above-average height is also associated with increased risk of PSP – in people who are at least 76 inches (1.93 meters) tall, the AAIR is about 200 cases per 100,000 person-years. Slim build also seems to increase the risk of PSP.

The risk of contracting a first spontaneous pneumothorax is elevated among male and female smokers by factors of approximately 22 and 9, respectively, compared to matched non-smokers of the same sex. Individuals who smoke at higher intensity are at higher risk, with a "greater-than-linear" effect; men who smoke 10 cigarettes per day have an approximate 20-fold increased risk over comparable non-smokers, while smokers consuming 20 cigarettes per day show an estimated 100-fold increase in risk.

In secondary spontaneous pneumothorax, the estimated annual AAIR is 6.3 and 2.0 cases per 100,000 person-years for males and females, respectively, with the risk of recurrence depending on the presence and severity of any underlying lung disease. Once a second episode has occurred, there is a high likelihood of subsequent further episodes. The incidence in children has not been well studied, but is estimated to be between 5 and 10 cases per 100,000 person-years.

Death from pneumothorax is very uncommon (except in tension pneumothoraces). British statistics show an annual mortality rate of 1.26 and 0.62 deaths per million person-years in men and women, respectively. A significantly increased risk of death is seen in older victims and in those with secondary pneumothoraces.

Working with asbestos is the most common risk factor for mesothelioma. However, mesothelioma has been reported in some individuals without any known exposure to asbestos.