Occupational lung diseases

-Saniya Waghmare
 The term 'pneumoconiosis' includes those
occupational lung diseases which are due to exposure
to inorganic or mineral dust that is retained in the
lung parenchyma and incites fibrosis.
 Other occupational lung diseases which occur due to
organic dust are not associated with such
accumulation of particles within the lungs and are
believed to have an immunologic pathogenesis.
Pneumoconioses and Asbestosis

 Pneumoconioses are diseases caused by inhalation of mineral

dusts.
 Asbestos related diseases of lungs and pleura-
 The main types of asbestos are white asbestos (chrysotile),
blue asbestos (crocidolite) and brown asbestos (amosite). All
fibre types have the potential to cause asbestos-related
diseases.
 Occupational exposure is highest with mining and milling of
asbestos, manufacturing processes involving asbestos and
demolition and shipyard workers. It can also occur in
automobile and railroad workers and those involved in
electrical wire insulation.
 There are six asbestos-related diseases:
• Benign pleural plaques
• Benign pleural effusion
• Asbestosis (progressive pulmonary fibrosis)
• Bronchial carcinoma
• Mesothelioma of pleura
• Mesothelioma of peritoneum (rare).
• Of all asbestos-related effects, highest dose is required to
cause asbestosis.
 Benign Pleural Plaques

• These are localised or diffuse areas of pleural thickening

which are often calcified.
• Common sites are diaphragm and anterolateral pleural
surfaces.
• Clinically, the patients are asymptomatic. The disease is
usually identified on a routine chest radiograph.
• May lead to a significant decrease in total lung capacity,
forced expiratory volume in 1 second and forced vital
capacity (restrictive pattern)
 Benign Pleural Effusion

• Benign (non-malignant) and self-limiting disease; may

be bilateral.
• Associated with pleuritic pain, fever and leucocytosis.
• Pleural fluid is often haemorrhagic.
• Common complication is pleural fibrosis.
• Exclude pleural mesothelioma by thoracoscopy and
biopsy.
• Moderate to severe exposure for at least 10 years.
• Pathologically characterised by progressive pulmonary
fibrosis.
• Clinically characterised by progressive exertional
breathlessness, finger clubbing and end-inspiratory
crepitations over lung bases.
• Radiologically (chest X-ray and HR.CT) characterised by
mottled shadows with some streaky opacities and sometimes
"honeycombing" in the mid and lower zones. On plain chest
radiograph, many do not manifest pleural disease; however,
CT picks up pleural disease in more than 90% of cases.
• Pulmonary function tests show reduced carbon
monoxide transfer factor, decreased lung volumes and
a restrictive ventilatory defect.
• Lung biopsy may show asbestos bodies.
• Complications of asbestosis include respiratory
failure, right ventricular failure and bronchial carcinoma.
 Bronchial Carcinoma

• Either squamous cell carcinoma or adenocarcinoma.

• Minimum lapse of 15-20 years between exposure and
development of carcinoma.
• Multiplicative effect of smoking
 Mesothelioma

 Mesothelioma is a primary malignant tumour of pleura, most

commonly caused by blue asbestos.
 In contrast to bronchial carcinoma, development of mesothelioma is
not related to smoking.
 Relatively short period of exposure (even 1-2 years) that occurred
more than 20-30 years ago, is required.
 Clinically, the patient presents with chest pain, breathlessness and
haemorrhagic pleural effusion.
 Although approximately 50% of mesotheliomas metastasise, the
tumour is locally invasive and death usually occurs due to local
invasion.
 On chest radiograph, the mediastinum is either not shifted or shifted
to the same side.
Coal workers pneumoconiosis/Caplan’s
syndrome

 Coal-worker's pneumoconiosis (CWP) is seen in coal

miners with a prolonged history of inhalation of coal
dust. More common in anthracite coal miners.
 Chronic obstructive pulmonary disease is often
associated with CWP.
 CWP is subdivided into two:
 1. Simple CWP
 2. Progressive massive fibrosis (PMF).
Simple Coal-Worker's Pneumoconiosis

 Develops after prolonged exposure (15-20 years) to coal dust.

 Does not progress if the miner leaves the industry.
 Depending on the site and extent of the nodulation, simple
CWP is radiologically divided into three categories:
1. Category 1: Few small round opacities.
2. Category 2: Numerous small round opacities but normal lung
markings still visible.
3. Category 3: Numerous small round opacities and the normal
lung markings partly or fully obscured.
 Progressive Massive Fibrosis (PMF)
 This condition progresses even after the miner leaves the
industry.
 Characterised by single or multiple nodules (> 1 cm in size to
large dense masses in the upper lobes, which may cavitate).
 Clinically characterised by cough with blackish expectoration
(melanoptysis) and progressive breathlessness.
 Complications of PMF include pulmonary tuberculosis,
respiratory failure, right ventricular failure and Caplan's
syndrome.
 Treatment of latent TB infection should be considered
for coal workers.
 Smoking cessation
 Management of chronic bronchitis and emphysema
 Silicosis

 Silicosis is caused by inhalation of silica dust or quartz particles.

 Occupations with high risk include mining, quarrying, dressing
of sandstone and granite, pottery and ceramics industry, boiler
scaling, sandblasting, etc.
 Tuberculosis commonly complicates silicosis (silicotuberculosis).
 Silica exposure increases the risk for developing lung cancer,
chronic renal insufficiency and autoimmune diseases,
particularly scleroderma, rheumatoid arthritis and Wegener's
granulomatosis. It can also produce chronic airway obstruction
similar to COPD.
 Chronic or Simple Silicosis

 It is the most common form of silicosis which occurs after many decades
of exposure to relatively low levels of silica.
 This form of silicosis is characterised by gradually progressive dyspnoea
and dry cough. It is often compatible with normal life.
 The radiological features of silicosis are variable and range from diffuse
fine rounded regular nodulation resembling miliary tuberculosis through
coarse irregular nodules to extensive fi0brosis resembling PMF.
 In early stages, upper zones of the lungs are more commonly involved as
compared to the lower zones.
 Pulmonary function tests typically reveal a mixed pattern of obstruction
and restriction with a reduced diffusion capacity.
 May lead to PMF.
 Management and control

 Change in occupation to an environment free of silica

containing dust
 Lung lavage to remove silica from the lung
 Rx of all forms of silicosis should be directed toward
control of mycobacterial disease.
 Smoking cessation
 Acute and accelerated silicosis- lung transplant
Sarcoidosis/ Lofgren’s syndrome

 Definition
 Sarcoidosis is a multisystem, chronic granulomatous
inflammatory disorder of unknown aetiology. It is
characterised by the accumulation of T lymphocytes
and mononuclear phagocytes and non-caseating
epithelioid granulomas in the affected organs
 Aetiology

 Aetiology of sarcoidosis is unknown.

 The disease probably results from an exaggerated
cellular immune response to an infectious or non-
infectious environmental agent in a person
genetically susceptible to develop sarcoidosis.
 Probable infectious agents include Propionibacterium
acnes, atypical mycobacteria and a M. tuberculosis
protein. Non-infectious agents include insecticides
and molds.
 Sarcoidosis can affect any part of the body. The most
frequently involved organ is lung. The other organs
commonly involved are lymph nodes, eyes, skin, parotid
glands, liver, spleen and kidneys.
 Clinical features:
 Sarcoidosis can manifest in three forms:
 1. Asymptomatic form (30-45%).
 2. Acute or subacute form (10-15%).
 3. Chronic form ( 40-60% ).
 Asymptomatic form is usually detected incidentally on a routine
chest film.
 Acute or subacute form develops abruptly over a period of few
weeks. Patients have constitutional symptoms like fever, fatigue,
malaise, anorexia and weight loss. Respiratory symptoms are
cough, dyspnoea and retrosternal chest discomfort.
 Chronic form develops over months, characterised by
respiratory complaints without significant constitutional
symptoms. Clubbing and haemoptysis are uncommon. The
disease keeps waxing and waning over many years with nearly
60% recovering spontaneously over 10 years.
 Physiotherapy management

 PT Rx:
 PT to change the breathing pattern is not helpful because of the
rapid shallow breathing reduces the effect of excessive lung recoil.
 Patient may find relieve by deep breathing,
 Patient may respond to some measure to reduce WOB by use of
non invasive ventilation
 Twice encouragement helps to maintain function act within the
limits of dyspnoea, desaturation and fatigue
 Positioning given in later stages forward lean posture should be
avoided.