History and exam
Key diagnostic factors
common
presence of risk factors
Occupational exposure to silica, coal, or beryllium is a strongly associated risk factor for pneumoconiosis. In the case of chronic silicosis and coal workers' pneumoconiosis, exposure should have occurred with sufficient latency (at least 10 and usually 20 or more years prior to radiographic changes).[30][31]
Other factors strongly associated with pneumoconiosis include high cumulative dose of inhaled silica or coal (i.e., the more silica or coal inhaled, the greater the risk of developing silicosis or coal workers' pneumoconiosis).[30][31]
Cigarette smoking is strongly associated with the development of obstructive pulmonary changes on pulmonary function testing in people exposed to coal and silica.[25][26]
The presence of glutamic acid at position 69 of the HLA-DP1 beta chain is strongly associated with chronic beryllium disease.
Other diagnostic factors
common
dyspnoea on exertion
Typically the first sign of pneumoconiosis.
Increases with progression of disease. May be absent in patients with early pneumoconiosis.
An acute form of berylliosis may present as pneumonitis, with acute wheezing, chest tightness, and shortness of breath. This is a rare presentation in the US, but may be more common in developing countries.
cough
Dry, non-productive; frequency increases with progression.
May be absent in patients with early pneumoconiosis.
A productive cough may be seen if the patient has also developed COPD as a complication.
normal chest examination
Chest auscultation will be normal early in these diseases.
uncommon
crackles on chest auscultation
May be heard in people with chronic beryllium disease.
Chest auscultation will be normal early in these diseases.
chest tightness and/or wheezing
May be present in silica- and coal-exposed workers who have developed COPD.
An acute form of berylliosis may present as pneumonitis, with acute wheezing, chest tightness, and shortness of breath. This is a rare presentation in the US, but may be more common in developing countries.
prolonged expiration and wheezing on chest auscultation
May be present in silica- and coal-exposed workers who have also developed COPD. Chest auscultation will be normal early in these diseases.
areas of dullness on chest percussion
May occur with progressive massive fibrosis (in coal- or silica-exposed people).
cyanosis
As with other respiratory diseases, as the disease progresses the patient may be cyanotic, develop a barrel chest, and have weight loss.
Oxygen saturation may be checked during physical examination, and may help to define the degree of impairment.
barrel chest
As with other respiratory diseases, as the disease progresses the patient may be cyanotic, develop a barrel chest, and have weight loss.
haemoptysis, fever, or night sweats
Symptoms of pulmonary TB, which is a complication of silica exposure, and may be the presenting condition.
Haemoptysis with or without weight loss may be the presenting symptoms of lung cancer.
clubbing of fingers and toes
Only found in advanced pneumoconiosis.
Not specific to pneumoconiosis.
weight loss
As with other respiratory diseases, as the disease progresses the patient may be cyanotic, develop a barrel chest, and have weight loss.
In developed countries, the severity of presentation has reduced so this feature is less commonly seen.
May occur with pulmonary TB, which may occur in silica-exposed workers, or lung cancer, which may occur in beryllium-exposed workers.
signs of rheumatoid arthritis or scleroderma
Rheumatoid arthritis and scleroderma may be complications of silica or coal exposure.
Symptoms and signs of these conditions (e.g., Raynaud's phenomenon, joint tenderness and swelling, skin changes, sclerodactyly [with scleroderma] ) may be presenting features.[Figure caption and citation for the preceding image starts]: Hands demonstrating Raynaud's phenomenonFrom the collection of Maureen D. Mayes, University of Texas [Citation ends].
[Figure caption and citation for the preceding image starts]: Fingers demonstrating sclerodactyly with finger curling, shiny skin at the fingers, and telangiectasiasFrom the collection of Maureen D. Mayes, University of Texas [Citation ends].
signs of renal failure (e.g., weight gain, oedema, hypertension)
The complication of renal failure may be the presenting condition.
Risk factors
strong
occupational exposure to silica
Occurs with mining and quarrying; at foundries; with manufacture of toilet bowls, sinks, and ceramics; with abrasive blasting, and cement cutting in construction; with manufacture and installation of engineered stone countertops; and with hydraulic fracking while drilling for gas and oil.[11][23][24]
Artificial stone silicosis (e.g., in kitchen benchtop production) appears to differ from silicosis associated with other occupational settings, having a shorter latency and rapid progression.[11]
occupational exposure to coal
Occurs when working in underground coal mines. Exposures to workers are significantly less in open-pit mines.
occupational exposure to beryllium
Occurs in the manufacture of master alloy (98% copper and 2% beryllium) used in electronic circuitry and the manufacture of heat-resistant ceramics, dental prostheses, metal products, and nuclear weapons.[13]
Historically, exposure occurred in the manufacture of fluorescent light bulbs.
high cumulative dose of inhaled silica or coal
The best predictor for the development of silicosis or coal workers' pneumoconiosis is the total amount of silica or coal inhaled. The risk for advancing to more severe disease is related to the cumulative dose inhaled. Cumulative dose is also a risk factor for chronic obstructive pulmonary disease (COPD) and progressive lung function loss.[25]
The risk of developing acute, accelerated silicosis is based on more immediate high levels of exposure.
cigarette smoking
Strongly associated with an increased risk of obstructive changes, found on pulmonary function testing, in silica- and coal-exposed workers.[25][26]
Weakly associated with an increased risk of the interstitial changes in silicosis.[26]
No risk has been noted for developing beryllium-related lung disease.
glutamic acid at position 69 of the B1 chain of the HLA-DP molecule (chronic beryllium disease)
The risk of chronic beryllium disease or sensitisation after exposure to beryllium is markedly increased with this polymorphism.[21] However, people who do not have this polymorphism may develop chronic beryllium disease and sensitisation, and many who have the polymorphism do not develop chronic beryllium disease or sensitisation.[18][27]
weak
high cumulative dose of inhaled beryllium
Beryllium is immunologically mediated with a strong genetic component, so that the typical dose response demonstrated with the other pneumoconioses is not seen.
With high enough exposure, acute beryllium disease may occur, which may progress to chronic beryllium disease.[27]
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