occupational lung disease Flashcards
what are occupational lung diseases
Range of lung diseases caused by exposures in the workplace – still relevant (often previous jobs) and prevalent
Typically long latency
what do occupational lung diseases contain
COPD
Malignant diseases (lung cancer, asbestos and non-asbestos related, mesothelioma)
Occupational asthma
Pneumoconiosis (mineral dust – coal workers lung, asbestosis, silicosis)
how should an occupational history be taken
Detailed history of exposure
Type of material, duration, intensity, temporal relationship to onset of symptoms
Symptoms – improvement away from workplace
what is pneumoconiosis
Coal workers pneumoconiosis – geography UK coalfields
Uncomplicated CWP – mild disease
Progressive massive fibrosis – activation of alveolar macrophages, progressive scarring leafing to stiff lungs
what is silicosis
Slate workers (wales) Potters (stoke on trent) Knife grinders (Sheffield) Hard rock miners (Canada etc) Sand blasting Foundry workers Fibrotic lung disease – activation of macrophages, restrictive lung function deficit, eggshell calcification of lymph nodes Risk factor for TB and lung cancer
how is pneumoconiosis treated
Prevent further exposures Stop smoking Monitor lung function Symptomatic treatment – cough, dyspnoea, cor pulmonale No specific treatment or cure
how does asbestos related lung disease occur
Mined in Canada, Australia, South Africa Imported via docks, esp Southampton Used widely in 1930s-70 – buildings, power stations, ship building, railways, cars (brake pads) Occupational history vital Risk of washing contaminated clothes
how does asbestos lead to benign disease
Pleural plaques (marker of exposure) Benign pleural effusion Pleural thickening (with subsequent restriction on lung function) Asbestosis – interstitial lung disease- restrictive lung function (FEV1/FVC >0.7)with reduction in forced vital capacity and reduced gas transfers
how does asbestos lead to malignant disease
Lung cancer (inc risk, esp smokers)
Mesothelioma (malignancy of pleura ans peritoneum by asbestos exposure, expected to have peaked in 2020)
Consider with history of asbestos exposure
Pleural plaques on previous CXRs, persistent unexplained chest pain, weight loss, breathless/unilateral pleural effusion
what is occupational asthma
Caused by workplace exposure or aggravated (pre-existing) by workplace
personal factors linking to occupational asthma
Asthma or COPD/HF/ILD
Consider with all adult onset asthma
Those failing to respond to asthma treatment
Other RFs like atopy, rhinitis, smoking
work factors linking to occupational asthma
Recognition of high risk job
Co-workers similarly affected
Recent changes (products used, tasks undertaken)
Prev measures (ventilation, masks etc)
other factors linking to occupational asthma
Lost job – difficulties proving diagnosis
Seeking compensation (time limits, financial motives)
Establishing causal link can be hard
what is challenge testing
Confirm diagnosis when new agent blamed
Identify responsible agent when multiple sensitisers in workplace
Confirm diagnosis when history and PEFR records equivocal
Rarely to exclude diagnosis in patient who otherwise lost their job
what must be ensured for challenge testing
Withhold bronchodilators
Placebo exposure free day
Equipment that delivers known conc of suspected agent
Monitor spirometry for several hours after each inc in exposure dosage
May take several days
what is HMW occupational asthma
Proteins or polysaccharideso 80-90% cases Sensitisation with latency period IgE dependant Skin prick (flour, animals, latex, enzymes)on k
what is LMW occupational asthma
Mechanism poorly understood
Usually independent of IgE
Limited utility of skin prick (isocyanates – printing/plastics, metals – welders, dyes)
what is Irritant-induced/non-allergic asthma
Direct effect on airways, non 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 mod/high exposure incidents
Causative agents of RADS
Caustic vapours, ammonia, fire/smoke, chlorine, tear gas, floor sealants
Airborne environmental factors
Toxins – naturally occurring poison produced in living cells or organisms (botulinum, ricin, snake venom)
Pollutant – any substance that contaminates the environment
what is exposure a function of
Conc, duration, intensity (exercise etc), route (skin vs inhaled), metabolism of toxin
Clinical impact varies with individual susceptibility/comorbidity
what determines susceptibility to lung disease
Genetic factors eg protective effect of HbS against malaria
Co-morbidity/underlying diseases that augment clinical impact of toxic load
Environmental factors – heat waves, cold snaps, smogs
what are vehicle exhaust pollutants
Primary pollutants
From fossil fuel combustion (NO, SO2, CO, particulate matter like fine particles of soot and metals forming smog)
Secondary pollutants – from reactions between pollutants in the atmosphere
Why does pollution matter
Deaths from outdoor air pollution – linked to cancer, asthma, stroke, heart disease, diabetes, obesity, dementia
Cost to healthcare and economy
Indoor pollution should also be considered
what are NO’s associated with
Associated with COPD and asthma related morbidity and mortality
Augments response to inhaled allergens
Increases likelihood that URTI will causes wheezing in children
what is ground level ozone
secondary pollution
heat + sunlight
volatile organic compounds - NO
Ground level ozone
what are the health effects of ground level ozone
Dec lung function
Pro-inflammatory effects (inc cytokines IL-6, IL-8, GM-CSF, neutrophilic bronchitis)
Inc response to inhaled allergens and respiratory morbidity
Particulate matter (PM) and asthma
Rise in prevalence of asthma in westernised countries
Not explained by genetics alone
Atopic sensitisation by allergens
Airway structural elements like cilia, mucous production, oxidative stress to cell DNA, induction of epithelial apoptosis
Promotes airway inflammation and inc IgE production
how is exposure to environmental pollutants reduced
Occupational – FFP3 marks, ventilation/extraction
Environmental – air quality warnings, remain indoors and close windows, minimise duration/intensity of outdoor activities
Recognises potential impact and contribution to disease
