Occupational lung disease

Occupational lung disease (OLDs) are interstitial lung diseases resulting from exposure to organic or inorganic substances such as asbestos, silica, beryllium, coal, animal allergens, talcum etc.

Inherently individuals who are exposed to such materials work in industries that have repetitive exposures to them, hence the term occupational lung diseases.

We will be focusing on pneumoconioses (silicosis, berylliosis, coal worker’s pneumoconiosis) and extrinsic allergic pneumonitis.

EXTRINSIC ALLERGIC ALVEOLITIS (EAA)/HYPERSENSITIVITY PNEUMONITIS

EAA or hypersensitivity pneumonitis is a non-IgE mediated inflammation of the alveoli and distal bronchioles as a result of immune activation after exposure to inhaled allergens.

Pathophysiology

Repetitive inhalation of low levels of organic dusts causes a type 3 hypersensitivity reaction where IgG forms immune complexes with foreign antigens. It may also involve cytotoxic T-cells (type 4 hypersensitivity).

Let’s look at some exposures:

1. Metalwork - most common cause (>50% of cases).
2. Avian antigens (from bird droppings) - causes bird fancier’s lung, pigeon breeder’s disease, budgerigar fancier’s disease.
3. Fungal antigens - most commonly spores of saccharopolyspora rectivirgula in mouldy hay (farmer’s lung).
4. Bacteria
1. Thermophilic actinomycetes - in mouldy sugar cane.
2. Mycobacterium - from hot tubs or humidifiers.
3. Aspergillus clavatus - malt worker’s lung.
5. Reactive chemicals - epoxy resin lung disease.
6. Drugs - nitrfurantoin, methotrexate, rituximab, amiodarone.

The inflammation of HP has a characteristic appearance: the infiltrates consists mainly of lymphocytes, plasma cells, neutrophils. There are also non-caseating granulomas and activated foamy macrophages.

The inflammation tends to be distributed around the bronchi or bronchioles, but later on it leads to interstitial fibrosis and irreversible lung damage.

🔢 Classification

• Non-fibrotic - solely inflammatory with absence of radiological/histopathological evidence of fibrosis.
• Fibrotic - presence of radiological/histopathological evidence of fibrosis.

😷 Presentation

Presentation can be divided into acute (4-8 hours after exposure) or chronic (weeks-months after exposure).

🔍 Investigations

A good history and high index of clinical suspicion are essential for diagnosis.

📷

Imaging:

1. CXR - patchy, nodular infiltrates, fibrosis (in fibrotic HP), ground glass opacity (usually in the upper or mid zones). It may be normal if not in an acute inflammatory state.
2. CT - more accurate than CXR as it can differentiate between fibrotic and non-fibrotic HP. Can be used for prognosis.

• Bronchoalveolar lavage (BAL) - may show lymphocytosis.
• Serologic assays for specific IgG antibodies - has a good negative predictive value. It is less useful between differentiating between HP and other ILDs.
• PFTs - spirometry may show a restrictive pattern (in inflammatory HP) or mixed pattern (in fibrotic HP). The vital capacity is generally lower than normal.
• Bloods - blood tests will show no eosinophilia as it is a non-IgE mediated disease.

🧰 Management

🥇 Avoidance of precipitating factor

• Consider oral glucocorticoids (prednisolone) - if persistent acute symptoms of HP persist despite avoidance.
• Pulmonary rehab programmes
• Oxygen therapy - if severely hypoxaemic.
• Smoking cessation for smokers.

PNEUMOCONIOSIS

Pneumoconiosis is the accumulation of dust in lungs and the body’s response to it. They are a group of interstitial lung diseases that are mostly due to occupational exposure to inorganic mineral or metal dusts (leading to interstitial fibrosis).

There are 4 main types which will be looked at:

1. Asbestosis
2. Coal worker’s pneumoconiosis
3. Silicosis
4. Berylliosis

Coal worker’s pneumoconiosis (CWP)

Coal worker’s pneumoconiosis, sometimes referred to black lung disease is an occupational lung disease caused by long-term exposure to coal dust particles. It is most commonly experienced by those involved in the coal mining industry. The severity is linked to the extent of exposure. Often there is a long lead time between first exposure and disease development.

🏘️ Epidemiology

• Higher in populations with high levels of exposure
• Male prevalence
• Usually 15-20 years after initial exposure

Pathophysiology

Coal dust which is (2-5um) is inhaled and enters the lungs. Normally the dust reaches the terminal bronchioles and is engulfed by the alveolar and interstitial macrophages. The macrophages move the dust particles via the mucociliary escalator and removed from the body as mucus. However, in coal miners, the chronic exposure overwhelms the system and macrophages begin to accumulate in the alveoli. This creates an inflammatory response that damages the lung tissue.

😷 Presentation

It can lead to 2 types of presentations:

1. Simple pneumoconiosis

This is the more common type. It is asymptomatic, but increases the risk of lung diseases, such as COPD and has the potential to deteriorate further into Progressive Massive Fibrosis (PMF).

2. Progressive Massive Fibrosis

Presents with round fibrotic masses in the upper lobes most commmonly.

• Dyspnoea on exertion
• Cough - may produce black sputum.
• Mixed obstructive/restrictive pattern on lung function testing

🔢 Classification

Simple pneumoconiosis can be divided into 3 based on its appearance on CXR based on the grading by International Labour Office:

1. Category 1 - some opacities and normal lung markings visible.
2. Category 2 - large number of opacities and normal lung markings visible.
3. Category 3 - large number of opacities but normal lung markings not visible.

🔍 Investigations

1. CXR - upper zone fibrosis.
2. PFT -spirometry may show restrictive pattern or mixed pattern.

🧰 Management

1. Avoid further exposure to coal dust and other respiratory irritants such as in smoking.
2. Symptomatic management

Patients may also be eligible for compensation with the Industrial Injuries Act.

Silicosis

Silicon (Si) is an element that when combined with oxygen forms silicon dioxide (SiO2) which is also known as silica. It is found in nature as quartz, a crystalline form of silica. In its crystalline form it is fibrogenic and may lead to interstitial fibrosis with prolonged exposure and inhalation.

Exposure occurs with mining and quarrying, ceramics manufacturing (e.g. sinks and toilet bowls), engineered countertop manufacturing and installation, abrasive blasting and cement cutting in construction.

Since mining increases risk exposure, coal miners are at increased risk once again.

Pathophysiology

Silica particles gain access to the alveoli and are ingested by macrophages which causes lysosomal damage and inflammatory activation → cellular apoptosis and subsequent lung fibrosis.

😷 Presentation

• Dyspnoea on exertion
• Dry cough - it may be productive if the patient has developed COPD as a complication.
• Normal chest examination findings

🧰 Management

The aims of management is symptomatic management.

• Avoidance of occupational exposure
• Smoking cessation
• Whole lung lavage - may be attempted but it isn’t common practice.

Annual flu vaccine is needed as well as the pneumococcal vaccine.

Berylliosis

Beryllium (Be) exposure occurs when manufacturing master alloy (98% copper and 2% beryllium) used in the metal industry. It can be used in electronic circuitry, heat-resistant ceramics, dental prostheses, metal products and nuclear weapons.

⚠️ Risk factors

• HLA-DP1 - largest risk factor for beryllium sensitisation and beryllium disease.

😷 Presentation

• Dyspnoea on exertion
• Dry cough - once again may be productive if the patient develops COPD as a complication.
• Normal chest examination findings

🧰 Management

The aims of management is symptomatic management.

• Avoidance of occupational exposure
• Oral glucocorticoids
• Prednisolone
• Smoking cessation

OCCUPATIONAL ASTHMA

Occupational asthma refers to asthma triggered by chemicals at work.

It is vital to take a good history as we may notice that the symptoms are worse during the week (when at work) or better on the weekends (when away from work).

⚠️ Risk factors

Some examples of chemicals that may induce occupational asthma include:

🔍 Investigations

1. Serial measurement of peak expiratory flow at work and away from work. If occupational asthma is suspected, specialist referral is warranted.

We will discuss asthma more here…

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