Occupational Lung Disease Flashcards
Background info
Caused by exposures in the workplace
17000/year new cases
12000lung disease deaths/year linked to past exposure in UK
Typically long latency
COPD, Malignant diseases (lung cancer, mesothelioma), occupational asthma, pneumoconioses (mineral dust - coal workers lung, asbestosis, silicosis)
Pneumoconioses
140 deaths/year
Uncomplicated CWP (coal workers pneumoconioses) - mild disease
Progressive massive fibrosis: activation of alveolar macrophages and progressive scarring causing stiff lungs
Treatment: prevent exposure, stop smoking, monitor lung function, symptomatic treatment
Silicosis
Slate workers, Potters, knife grinders, Hard rock miners, sand-blasting, foundry workers
10-20 deaths/year
Fibrotic lung disease: activation of macrophages, restrictive lung function deficit, eggshell calcification of lymph nodes
Risk factor for TB and lung cancer
Asbestos and the Lung
Benign - causes pleural plaques, benign pleural effusion, pleural thickening, asbestosis (interstitial lung disease-restrictive lung function, with reduction in FVC and reduced gas transfer)
Malignant - causes lung cancer (common in smokers), mesothelioma (malignancy of pleura and peritoneum, consider pleural plaques, chest pain, weight loss, brethlessness, unilateral pleural effusion)
Diagnosis of Occupational Asthma
Work aggravated - made worse by factors at work
Occupational asthma - caused by work
OA: personal factors - failure to respond to asthma Rx, other risk factors (atopy/rhinitis/smoking); workplace factors - high risk jobs, recent changes, preventative measures; other - lost job, seeking compensation?
Role of Challenge Testing
Confim diagnosis identify responsible agent confirm diagnosis with history and PEFR records Asthma should be stable Withhold bronchodilators Placebo exposure day is advisable
Allergic Occupational Asthma
High Molecular Weight: proteins, polysaccharides; 80-90% cases; sensitisation with latency period; IgE dependent; skin prick/allergy testing (flour, animals, latex, enzumes
Low Molecular Weight: mechanism poorly understood; usually independent of IgE; limited utility of skin prick/allergy testing (isocyantes, metals, dyes)
Irritant induced asthma (non-allergic)
Direct effect on airways - not immune mediate
Acute: reactive airways dysfunction syndrome (RADS) - develops within hours of a single high exposure to irritant, e.g. ammonia, fire/smoke, chlorine, tear gas, floor sealants
Subacute: insidous onset of asthma symptoms after multiple moderate exposure incidents
Susceptibility
Genetic Factors, e.g. protective effect of HbS against falciparum malaria
Co-morbidity/underlying disease that augment clinical impact of toxic load
Environmental factors - heat waves, cold snaps, smogs
Vehicle Exhaust Pollutants
Primary (from fossil fuel combustion) SO2, CO, Particulate matter, NO
NO: outdoor/indoor sources; associated with COPD and asthma related mortality
Secondary: from reactions between pollutants in the atmosphere
Health effects of ground level ozone
Decreased lung function
Pro-inflammatory effects: increased cytokines (IL6, IL8, GM-CSF) and neutrophilic bronchitis
Increased response to inhaled allergens
Increased respiratory morbidity
Particulate matter and Asthma
Rapid rise in prevalence of asthma in westernised countries
Cannot be explained by genetics alone
PM potentiates risk of airborne causing atopic sensitisation
OM affects airway structural elements (airway cilia, mucous production, oxidative stress to cell DNA, induction of epithelial apoptosis)
PM promotes airway inflammation and increased IgE production
Exposure Reduction
Occupational: FFP3 masks, ventilation/extraction
Environmental: air quality, remain indoors, close windows, minimise duration/intensity of outdoor activities
Recognise potential impact and contribution to disease in your patient
