respiratory system: pneumoconiosis
TRANSCRIPT
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