Typical levels of beryllium that industries may release into the air are of the order of , averaged over a 30-day period, or of workroom air for an 8-hour work shift. Compliance with the current U.S. Occupational Safety and Health Administration (OSHA) permissible exposure limit for beryllium of has been determined to be inadequate to protect workers from developing beryllium sensitization and CBD. The American Conference of Governmental Industrial Hygienists (ACGIH), which is an independent organization of experts in the field of occupational health, has proposed a threshold limit value (TLV) of in a 2006 Notice of Intended Change (NIC). This TLV is 40 times lower than the current OSHA permissible exposure limit, reflecting the ACGIH analysis of best available peer-reviewed research data concerning how little airborne beryllium is required to cause sensitization and CBD.

Because it can be difficult to control industrial exposures to beryllium, it is advisable to use any methods possible to reduce airborne and surface contamination by beryllium, to minimize the use of beryllium and beryllium-containing alloys whenever possible, and to educate people about the potential hazards if they are likely to encounter beryllium dust or fumes. It is important to damp wipe meallographic preparation equipment to prevent accumulation of dry particles. Sectioning, grinding, and polishing must be performed under sufficiently vented hoods equipped with special filters.

On 29 January 2009, the Los Alamos National Laboratory announced it was notifying nearly 2,000 current and former employees and visitors that they may have been exposed to beryllium in the lab and may be at risk of disease. Concern over possible exposure to the material was first raised in November 2008, when a box containing beryllium was received at the laboratory's short-term storage facility.

There is no cure for berylliosis; the goals of treatment are to reduce symptoms and slow the progression of disease.

Although the evidence that stopping exposure to beryllium decreases progression of the disease, it is still considered to be an accepted approach to treatment in any stage of disease.

People with early stages of disease, without lung function abnormalities or clinical symptoms, are periodically monitored with physical exams, pulmonary function testing and radiography.

Once clinical symptoms or significant abnormalities in pulmonary function testing appear, treatments include oxygen and oral corticosteroids and whatever supportive therapy is required.

Therapy is supportive and includes removal from further beryllium exposure. For very severe cases mechanical ventilation may be required.

Acute beryllium poisoning is an occupational disease. Relevant occupations are those where beryllium is mined, processed or converted into metal alloys, or where machining of metals containing beryllium or recycling of scrap alloys occurs.

Beryllium is regarded extraordinarily hazardous to health upon enough amounts of dust, mists, or fumes consisting fragments little enough to inhale (typically 10µm or less). Metallographic preparation equipment and laboratory work surfaces must be damp wiped occasionally to inhibit buildup of particles. Cutting, grinding, and polishing procedures which manufacture dusts or fumes must be handled within sufficiently vented coverings supplied with particular filters.

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.

In 2013 pneumoconiosis 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.

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.

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.

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.

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.

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.

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

Beryllium poisoning is poisoning by the toxic effects of beryllium, or more usually its compounds. It takes two forms:

- Acute beryllium poisoning, usually as a result of exposure to soluble beryllium salts

- Chronic beryllium disease (CBD) or berylliosis, usually as a result of long-term exposure to beryllium oxide usually caused by inhalation.

The following are causes of BHL:

- Sarcoidosis

- Infection

- Tuberculosis

- Fungal infection

- Mycoplasma

- Intestinal Lipodystrophy (Whipple's disease)

- Malignancy

- Lymphoma

- Carcinoma

- Mediastinal tumors

- Inorganic dust disease

- Silicosis

- Berylliosis

- Extrinsic allergic alveolitis

- Such as bird fancier's lung

- Less common causes also exist:

- Eosinophilic granulomatosis with polyangiitis

- Human immunodeficiency virus

- Extrinsic allergic alveolitis

- Adult-onset Still's disease

Bilateral hilar lymphadenopathy is a bilateral enlargement of the lymph nodes of pulmonary hila. It is a radiographic term that describes the enlargement of mediastinal lymph nodes and is most commonly identified by a chest x-ray.

Granuloma is an inflammation found in many diseases. It is a collection of immune cells known as histiocytes (macrophages). Granulomas form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate. Such substances include infectious organisms including bacteria and fungi, as well as other materials such as keratin and suture fragments.

Certain inflammatory diseases are characterised by a combination of granulomatous inflammation and vasculitis (inflammation of the blood vessels). Both the granulomas as well as the vasculitis tend to occur in association with necrosis. Classic examples of such diseases include granulomatosis with polyangiitis (GPA; previously referred to by the eponym Wegener's granulomatosis) and eosinophilic granulomatosis with polyangiitis (EGPA; formerly known as Churg-Strauss syndrome).