ALOK SINHADepartment of Medicine

Manipal College of Medical SciencesPokhara, Nepal

Occupational lung disease (Pneumoconiosis) permanent alteration of lung structure caused by inhalation of a mineral dust and the reaction of the lung tissue to this dust

Substances known to cause lung disease • coal dust• Silica• Asbestos • Berillium

Mineral dust

Disease Examples of exposure

Coaldust

I. Simple pneumoconiosis

II. Progressive massive Fibrosis

III. Caplan's syndrome

Coal mining, especially hard coal

Silica I. Silicosis Foundry work, sandblasting, stonecutting,hard rock mining

Asbestos I. AsbestosisII. Benign asbestos-

related pleural disease

III. MesotheliomaIV. Lung cancer

Mining, milling, and fabrication.Installation and removal ofinsulation

Beryllim I. Acute berylliosisII. Beryllium granulomatosis

Mining, fabrication of electrical and electronic equipment, workers in nuclearand aerospace industry.

Iron oxide Siderosis Welding

Bariumsulphate

Baritosis Mining

Tin oxide Stannosis Mining

Aluminium Like silicosis (bauxite worker's lung, Shaver's disease)

Mining, firework, painting, and armament manufacture

Pneumoconiosesnon-neoplastic pulmonary diseases caused by the reaction of the lung to the inhalation of mainly mineral

Inhaled particles of dust size < 5 µm reach the terminal airways and alveoli and settle on the epithelial lining

slowly cleared by macrophages or alveolar cells. They may pass into the

• lymphatic system• be cleared via the airway• or remain in the alveolus

lead to an inflammatory reaction within the lung, depending on their physical and chemical properties

causes characteristic alterations in pulmonary structure and radiological abnormalities

barium, tin, and iron – no fibrosis silica - nodular fibrosis asbestos - diffuse fibrosis coal dust - Macule formation with focal

emphysema beryllium- systemic response and induce

a granulomatous reaction in the lungs

Pneumoconioses can appear and progress

after the exposure has ceased

Coal-workers' pneumoconiosis

Open cast mines

deposition of coal dust within the lung and its associated inflammatory reaction

Coal workers pneumoconiosis is of two types-

Simple pneumoconiosis which can progress to

Complicated pneumoconiosis - also known as progressive massive fibrosis (PMF)–Related to degree of exposure to coal

dust

Healthy lung

progressive massive fibrosisprogressive massive fibrosis

Simple pneumoconiosis

Coal dust inhaled into the alveolus &

engulfed by macrophages

form a black stellate lesion - the coal macule

coal macule

Dilated terminal

bronchiole with

Peribronchiolar

Coal ladened

macrophages

coal macules are found throughout the lung, especially in the upper zones of the upper and lower lobes

associated with surrounding bronchiolar dilatation

leading to focal emphysema

cytokine release and subsequent inflammatory cell recruitment, leading to fibroblast activation Progression of the disease

P.M.F. PMF occurs on this background

with aggregation of the fibrotic nodules to form larger lesions – 2 to10 cm diameter

central area of nodules- necrotic

outer rim - firm and collagenous

distort the adjacent lung and cause emphysma

lesions continue to progress out of the work environment

Larger lesions may have • cavitation and necrosis• areas of calcification

Clinical featuresSimple pneumoconiosis asymptomatic with no associated

clinical signsProgressive massive fibrosis Cough with mucoid or blackened

sputum breathlessness on exertion may lead to the development of

c o r p u l m o n a l e

Simple pneumoconiosis asymptomatic with no associated

clinical signsProgressive massive fibrosis Cough with mucoid or blackened

sputum breathlessness on exertion may lead to the development of

c o r p u l m o n a l e

CXRIn simple pneumoconiosis

nodular shadowing of varying size- up to 10 mm in the upper and middle zones

graded according to the number of different sized nodules p = < 1.5 mm

q = 1.5-3 mm r = 3-10 mm

PMF

diagnosed when one or more opacities of > 1 cm diameter are present, on the background of simple pneumoconiosis

located in the upper lobes and enlarge, becoming increasingly radio dense and clearly demarcated

simple pneumoconiosis

PMF

PFTs Simple pneumoconiosis:

• FEV1 and FVC are normal • TLCO may be slightly decreased

PMF: Mixed feature

• airway obstruction due to emphysema

• restriction due to loss of lung volumes

• TLCO is reduced

Management Minimization of dust exposure with

• improved mine ventilation • respirator provision • monitoring of dust levels

Periodic CXR every 4 years moved to less dusty work if they show signs

of pneumoconiosis, to prevent development of PMF

Miners with signs of coal workers' pneumoconiosis are entitled to industrial injury benefits

Caplan's syndrome Miners with seropositive rheumatoid

arthritis can develop large well-defined nodules

occur on a background of simple pneumo coniosis and with a relatively low coal dust exposure

multiple and may cavitate Cause no significant functional

impairment and have no malignant potential

Has to be considered in the D/D of T.B. malignency etc

http://upload.wikimedia.org/wikipedia/commons/2/23/Dimension_Stone_QuarryUSGOV.jpg

chronic nodular densely fibrosing pneumoconiosis, caused by the prolonged inhalation of silica particles.

Long lag time of decades between exposure and clinical disease

Insidious onset & progressive

Larger radiological opacities than those seen in coal-workers' pneumoconiosis, and more rapid progression

The pattern of disease depends on the level and duration of the silicone dust exposure

quartzquartz

Silica is present as crystalline quartz

mined and quarried

used in industries

ceramics, brick-making, and stone masonry

Pathology Dust particles in the alveoli are phagocytosed

by macrophages removed to the lymphatics cause diffuse inflammatory change Layers of collagen are deposited around the

dust particle. Nodules are found within the secondary pulmonary lobule

types of silicosis

Acute silicosis

Subacute silicosis & chronic silicosis

Silicotuberculosis

Acute silicosisintense exposure to fine dusts produced by sand blasting

apparent in workers within a few months to a year of starting work

Rapid deterioration over 1- 2 years, with treatment being ineffective.

Clinically• dry cough • shortness of breath• feeling of tightness on breathing deeply

Rapid deterioration over a few weeks • Fine crepitations over the lower zones

bilaterally • Leads to respiratory failure

• CXR Patchy bilateral lower air space consolidation, which may look like pulmonary oedema

Subacute silicosis

Dry cough

gradual onset of s o b

Chronic silicosisoccurs with lower dust concentrations

PFTs- Slow decline

mild restrictive pattern obstructive or mixed picture

(Due to emphysema)

Silicotuberculosis Increased likelihood of active TB infection in

people with silicosis, most likely due to the reactivation of quiescent lesions.

tuberculosis is three times greater than that of age-matched controls. Those with acute and accelerated silicosis have the highest incidence of mycobacterial disease.

individuals with silicosis or long-term exposure to crystalline silica should receive a tuberculin skin test. If the reaction is 10 mm or greater tuberculosis chemoprophylaxis should be administered even in absence of evidence of active tuberculosis

T.B. suspected whenCavitationHaemoptysis fevernew soft CXR opacities

CXR A few upper and mid-zone nodules

occur, which become calcified after 10 years or so. no associated parenchymal distortion

may be associated hilar lymphadenopathy with egg shell calcification

disease may progress on further silica exposure with coalescence of nodules

widespread nodules measuring 2-5 mm in diameter, with a predominance in the middle and upper lung zones.

Management

Prevention

by monitoring and minimizing dust levels with adequate ventilation

Masks useful for short-term use

Stop smoking

http://en.wikipedia.org/wiki/Image:Leuchtstofflampen-chtaube050409.jpg

I. Acute berylliosis

II. Beryllium granulomatosis (Subacute and chronic berylliosis)

Acute Berylliosis

Acute alveolitis due to the direct effects of high-dose inhaled beryllium fumes

• widespread airway and pulmonary oedema causes • Dyspnoea• Cyanosis• widespread inspiratory crepitations

• CXR shows pulmonary oedema

• self-limiting if mild

• severe is usually fatal

• Corticosteroids may prevent progression, but the patient is often left with residual pulmonary impairment

Subacute and chronic berylliosis

hypersensitivity-type disease that occurs long time after beryllium exposure in a minority of individuals

clinically indistinguishable from sarcoidosis seen in

•wives of beryllium workers • who live near beryllium refineries

• cell-mediated immune response, with production of numerous inflammatory cytokines granulomatous inflammation.

• Following a long latent period up to

10 years + after exposure, non-caseating granulomatous tissue reactions occur in • lungs or • on the skin Similar to

granuloma – ball-like collection of immune cells which forms when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate

granuloma is a special type of inflammatory reaction that can occur in a wide variety of diseases, both infectious and non-infectious

Such substances include

– infectious organisms bacteria & fungi as well as

– other materials such as mineral dust keratin suture fragments and vegetable particles

Clinical features

Symptoms Coughdyspnoea Macular skin lesions, which do not

resolve

Signs clubbing & crepitations with

established fibrosis Hepato/splenomegaly and macular

skin lesions

Skin lesions in berryliosis

Skin lesions in berryliosis

CXRFine reticulonodular appearance

throughout both lungs. Finer nodules than sarcoidosis.

Progression to irregular interstitial fibrosis, with irregular linear opacities seen in the lung bases.

Hilar lymphadenopathy can occur, but always in association with interstitial lung disease

BAL- High levels of T-lymphocytes

PFTs Restrictive defect, with decreased KCO

No single test to distinguish berylliosis from sarcoidosis

Management

Corticosteroids prevent disease progression. Continue indefinitely as few patients gain complete resolution of symptoms

Annual screening of beryllium-exposed workers with CXR

breathlessness or skin rashes- an indication to start oral steroids to delay progression to interstitial fibrosis

Prognosis

with very low exposure who develop CXR changes may resolve

Granulomata do not spontaneously resolve

can be excised if causing problems, such as troublesome lesions on the skin

Interstitial fibrosis occurs in the lungs- progressive and leads to cyanosis and death. complications includePneumothoraxHypercalcaemia & hypercalciuriaNephrocalcinosis