RESPIRATORY SYSTEM: PNEUMOCONIOSIS

PNEUMOCONIOSIS

Dr Vijay Shankar S

28TH APRIL

WORLD DAY FOR SAFETY & HEALTH AT WORK

is an annual international campaign to promote safe, healthy and decent work. Has been observed by the International

Labor Organization (ILO) since 2003.

Theme-2014

“Safety and health in the use of chemicals at work“

Theme-2015

• “Join in building a culture of prevention on Occupational Safety and Health”

PNEUMOCONIOSIS

Introduction

Coined from the Greek (pneumo = lung, konis =dust) & introduced in the 19th century to describe lung diseases due to the inhalation of mineral dust

May have been first described by Hipprocrates in a metal digger’s difficulty in breathing

PATHOGENESIS- GENERAL ASPECTS

• The development of a pneumoconiosis depends on 1. the amount of dust retained in the lung and

airways; 2. the size, shape, and therefore buoyancy of the

particles; 3. particle solubility and physiochemical reactivity;

and4. the possible additional effects of other irritants

(e.g., concomitant tobacco smoking).

• In general, only a small percentage of exposed people develop occupational respiratory diseases,

implying

a genetic predisposition to their development!!

COAL WORKERS PNEUMOCONIOSIS

THE SPECTRUMAsymptomatic anthracosis

Simple CWP with little to no pulmonary dysfunction

Complicated CWP, or progressive massive fibrosis (PMF), in which lung function is compromised

SILICOSIS

Silicosis Has been recognized for hundreds of

years as occupational hazard of stonecutters

Silica comprises some 25% of earth’s crust

Degree of exposure varies considerably with the type of rock mined– Sandstone consist of 100% silica

High Risk Occupations

Foundry worker Sand blasting

Hard rock miningStone cutting

SILICA

CRYSTALLINE AMORPHOUSQuartz, crystobalite, and tridymite

Silicosis Silicosis refers to the lung disease

attributed to the inhalation of crystalline silicon dioxide (silica)

Most common occupational lung disease worldwide

Estimated 1 million workers are exposed to high levels of silica

PATHOGENESISInhalation of crystalline silica

Interact with epithelial cells & macrophages

Release of mediators

fibrosis

IL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines

Pathology

Pathology of silicosis is based on chronicity, incubation time & level

of exposure

Classification

Chronic or Classic Silicosis Accelerated Silicosis Acute Silicosis

Chronic Silicosis

Most common form Exposure 20-40 yrs Hallmark of chronic form

is the silicotic nodule or islet

Silicotic islet develops in the hilar lymph nodes & calcify

Disease progress to fibrosis of the upper lobe

Accelerated Silicosis

Similar to chronic silicosis but exposure is shorter & heavier (<10yrs)

Acute Silicosis

Intense exposure to high silica dust occurs over months

Acute silicosis may show features similar to pulmonary alveolar proteinosis with silica particles identified in proteinaceous material

Rarely seen in the US

Clinical Features

Dyspnea-initially with exercise Cough with or without sputum Wheezing or chest tightness which can

lead to respiratory failure

Chest X-ray of Uncomplicated Silicosis

Enlargement of hilar nodes may precede parenchymal disease

Uncomplicated silicosis has small round opacities

Egg-shell calcification of the hilum is suggestive of silicosis

Occasional can calcify

morphology

Complication of Silicosis

M. tuberculosis/ Atypical mycobacterium Rates of TB range

from 5-43% Factors that may

influence is the stage & type of disease (acute silicosis high risk for TB)

Complications of Silicosis

Cor pulmonale Spontaneous

pneumothorax Collagen vascular

disease (scleroderma) Lung Cancer

ASBESTOSIS

MillingMetal fabrication

Building insulation Electrical insulation

ASBESTOSAmphiboleSerpentine

Most commonly used

Chrysotile

More flexible and curved

Likely to be impacted in upper respiratory passages

Less commonly used

Amosite, Crocidolite, anthophyllite, tremolite

Stiff and short

Likely to delivered deeper into the lungs

Asbestos related lung diseases

• Produces 4 major categories of human disease– Pulmonary fibrosis (asbestosis)

– Benign asbestos-related pleural response

– Bronchogenic carcinoma

– Mesothelioma

Pathogenesis

PATHOGENESISInhalation of asbestos

Interact with epithelial cells & macrophages and penetrate the

alveoli

Release of mediators

INTERSTITIAL fibrosis

IL-1, TNF, fibronectin, lipid mediators, oxygen-derived free radicals, and fibrogenic cytokines

ALSO ACT AS TUMOR INITIATOR AND PROMOTER

CARCINOGENESIS

Pathologic features

• Begin in lower lobes and sub pleura• Early stages – minimal fibrosis• Late stages- extensive fibrosis- destroys the

architecture-dilated/cystic air spaces- honeycombed appeareance

Microscopy

Asbestos bodies: asbestos fibres coated with a film of proteins rich in iron.

Golden brown, fusiform or beaded rods. coating is thickest at ends - Dumbell shape form when macrophages phagocytose asbestos, iron derived from

phagocyte ferritin.

• Ferrugious bodies : other inorganic particles/fibres coated with similar protein iron complex

Clinical Diagnosis of Asbestosis

Earliest symptom is insidious onset of breathlessness with exertion

Clubbing of digits (32-42%), râles(32-64%) Cough, wheezing & sputum production are

unusual; if present can be attributed to cigarette smoking

Pleural Disease Associated with Asbestosis

Pleural Plaques Pleural Thickening Pleural Effusion Mesothelioma

Pleural Plaques

Smooth white raised lesions located on the posterolateral aspect of the parietal pleura or diaphragm

Plaques vary in size & shape Asymptomatic in pts without parenchymal disease Presence of plaques is associated with likelihood of

developing parenchymal disease Rarely seen before 20yrs after exposure

Pleural Thickening

Diffuse or focal Pleural thickening are

often associated with parenchymal disease

Asbestos bodies can be found in visceral pleura

Can cause symptoms

Pleural Effusions

May persist for months-years Symptoms - chest tightness, pleuritic chest

pain, fever, dyspnea May reoccur on same side or opposite side

after yrs of exposure Effusions maybe bloody

Mesothelioma

Arise in the pleura & peritoneum

80% occur in men exposed to asbestos in the workplace or living near the mines

Smoking does not enhance prevalence of disease

Lung Cancer & Asbestos

First recognized in 1930

Average latency period 20-30 yrs

Association of lung cancer with smokers & asbestos exposure is multiplicative

Adenocarcinoma & squamous cell carcinoma

Summary

Coal workers pneumoconiosis. Know the difference between Asbestosis &

Silicosis.

Thank you