Occupational Lung Disease Flashcards
Diseases encompassed
Occupational asthma
COPD
Pneumoconioses (mineral dust)
- Coal Workers’ Lung
- Asbestosis
- Silicosis
Malignant diseases
Lung cancer, Mesothelioma
Occupational history
Detailed history of exposure Type of material Duration Intensity Temporal relationship to onset of symptoms
Symptoms - Improvement away from workplace
Pneumoconioses
Coal-workers’ pneumoconiosis
140 deaths/yr
Geography UK coalfields
Uncomplicated CWP – mild disease
Progressive Massive Fibrosis
Activation of alveolar macrophages
Progressive scarring causing stiff lungs
Silicosis
10-20 deaths/yr
Fibrotic lung disease
- Activation of macrophages - Restrictive lung function deficit - Eggshell calcification of lymph nodes
Risk factor for TB & lung cancer
Treatment of Pneumoconioses
Prevent further exposure
Stop smoking
Monitor lung function
Symptomatic treatment
Cough, dyspnoea, cor pulmonale
No cure
Asbestos - Benign
Pleural plaques (marker of exposure)
Benign pleural effusion
Pleural thickening & restriction
Asbestosis (fibrosis)
Asbestos - Malignant
Lung cancer In asbestosis RR of lung cancer: 7x in non-smokers 93x in smokers Mesothelioma Malignancy of pleura and peritoneum Expected to peak in 2020
Diagnosis of Occupational Asthma (OA
Occupational asthma that is caused by workplace exposures
OR
Work-aggravated asthma in which pre-existing cases are made worse by factors in the workplace
Workplace factors
Recognition of high risk job Co-workers similarly affected Recent changes Products used, tasks undertaken Preventative measures Ventilation, masks etc
Importance of Challenge Testing
Confirm diagnosis when new agent blamed
Identify responsible agent when multiple sensitisers in workplace
Confirm diagnosis when history & PEFR records are equivocal
(rarely) to exclude diagnosis in patient who will otherwise lose their job
Challenge Testing
Asthma should be stable
Withhold bronchodilators
A placebo exposure day is advisable
Equipment that delivers known concentration of suspected agent
Monitor spirometry for several hours after each increase in exposure dose
May take several days
Allergic OA - High Molecular Weight
Proteins, polysaccharides
80-90% cases
Sensitisation with latency period (weeks-years)
IgE-dependent
Skin prick/allergy testing Flour (bakers) Animals (farmers) Latex Enzymes (eg detergents)
Allergic OA - Low Molecular Weight
Mechanism poorly understood
Usually independent of IgE
Limited utility of skin prick/allergy testing
Isocyanates (printing, plastics)
Metals (welders)
Dyes (hairdressers)
Irritant-Induced/Non-Allergic Asthma
Direct effect on airways, not immune-mediated, occurs without pre-existing asthma
Acute
Reactive Airways Dysfunction Syndrome (RADS)
Develops within hours of a single, very high exposure to an irritant
Subacute
Insidious onset of asthma symptoms after multiple moderate/high exposure incidents
RADS: some causative agents
Caustic vapours Ammonia Fire/Smoke Chlorine Tear Gas Floor Sealants
