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
Pollutant
Any substance that contaminates the environment
Toxin
A naturally occurring poison produced within living cells or organisms
Botulinum, Ricin, Snake venom
Exposure & Toxins
Exposure is a function of:
- Concentration of toxin/pollutant
- Duration
- Intensity (exercise etc)
- Route (skin vs inhaled)
- Metabolism of toxin
Clinical impact varies with individual susceptibility / comorbidity
Toxin susceptibility
Genetic factors
eg protective effect of HbS against falciparum malaria
Co-morbidity / underlying diseases that augment clinical impact of toxic load
Environmental factors
Heat waves, cold snaps, smogs
Vehicle Exhaust Pollutants
Primary pollutants From fossil fuel combustion Nitrogen oxide Sulphur dioxide (diesel) Carbon monoxide Particulate matter Fine particles of soot and metals forming smog
Secondary pollutants
From reactions between pollutants in the astmosphere
NO
No effect on lung function in normals
Augments response to inhaled allergens
Increases likelihood that URTI will cause wheezing in children
NO2 and infection
87 volunteers exposure to 1-2 ppm, 2h/d, 3 days intranasal challenge with influenza A virus on day 2 91% infection in those exposed to NO2 71% in control subjects
Health Effects of Ground Level Ozone
Decrease lung function
pro-inflammatory effects
- Increase cytokines (IL-6, IL-8, GM-CSF)
- neutrophilic bronchitis
Increase response to inhaled allergens
Increase respiratory morbidity
Particulate Matter (PM) & Asthma
PM potentiates risk of airborne allergens causing atopic sensitisation
PM affects airway structural elements Airway cilia Mucous production Oxidative stress to cell DNA Induction of epithelial apoptosis
PM promotes airway inflammation and ↑ IgE production
Exposure reduction
Occupational
FFP masks
ventilation
Environmental Air quality warnings Remain indoors, close windows Minimise duration/intensity of outdoor activities ?anti-oxidants