occupational lung disease Flashcards

1
Q

what are occupational lung diseases

A

Range of lung diseases caused by exposures in the workplace – still relevant (often previous jobs) and prevalent
Typically long latency

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2
Q

what do occupational lung diseases contain

A

COPD
Malignant diseases (lung cancer, asbestos and non-asbestos related, mesothelioma)
Occupational asthma
Pneumoconiosis (mineral dust – coal workers lung, asbestosis, silicosis)

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3
Q

how should an occupational history be taken

A

Detailed history of exposure
Type of material, duration, intensity, temporal relationship to onset of symptoms
Symptoms – improvement away from workplace

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4
Q

what is pneumoconiosis

A

Coal workers pneumoconiosis – geography UK coalfields
Uncomplicated CWP – mild disease
Progressive massive fibrosis – activation of alveolar macrophages, progressive scarring leafing to stiff lungs

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5
Q

what is silicosis

A
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
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6
Q

how is pneumoconiosis treated

A
Prevent further exposures
Stop smoking 
Monitor lung function
Symptomatic treatment – cough, dyspnoea, cor pulmonale
No specific treatment or cure
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7
Q

how does asbestos related lung disease occur

A
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
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8
Q

how does asbestos lead to benign disease

A
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
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9
Q

how does asbestos lead to malignant disease

A

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

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10
Q

what is occupational asthma

A

Caused by workplace exposure or aggravated (pre-existing) by workplace

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11
Q

personal factors linking to occupational asthma

A

Asthma or COPD/HF/ILD
Consider with all adult onset asthma
Those failing to respond to asthma treatment
Other RFs like atopy, rhinitis, smoking

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12
Q

work factors linking to occupational asthma

A

Recognition of high risk job
Co-workers similarly affected
Recent changes (products used, tasks undertaken)
Prev measures (ventilation, masks etc)

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13
Q

other factors linking to occupational asthma

A

Lost job – difficulties proving diagnosis
Seeking compensation (time limits, financial motives)
Establishing causal link can be hard

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14
Q

what is challenge testing

A

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

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15
Q

what must be ensured for challenge testing

A

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

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16
Q

what is HMW occupational asthma

A
Proteins or polysaccharideso
80-90% cases
Sensitisation with latency period
IgE dependant
Skin prick (flour, animals, latex, enzymes)on k
17
Q

what is LMW occupational asthma

A

Mechanism poorly understood
Usually independent of IgE
Limited utility of skin prick (isocyanates – printing/plastics, metals – welders, dyes)

18
Q

what is Irritant-induced/non-allergic asthma

A

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

19
Q

Causative agents of RADS

A

Caustic vapours, ammonia, fire/smoke, chlorine, tear gas, floor sealants

20
Q

Airborne environmental factors

A

Toxins – naturally occurring poison produced in living cells or organisms (botulinum, ricin, snake venom)
Pollutant – any substance that contaminates the environment

21
Q

what is exposure a function of

A

Conc, duration, intensity (exercise etc), route (skin vs inhaled), metabolism of toxin
Clinical impact varies with individual susceptibility/comorbidity

22
Q

what determines susceptibility to lung disease

A

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

23
Q

what are vehicle exhaust pollutants

A

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

24
Q

Why does pollution matter

A

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

25
Q

what are NO’s associated with

A

Associated with COPD and asthma related morbidity and mortality
Augments response to inhaled allergens
Increases likelihood that URTI will causes wheezing in children

26
Q

what is ground level ozone

A

secondary pollution
heat + sunlight
volatile organic compounds - NO
Ground level ozone

27
Q

what are the health effects of ground level ozone

A

Dec lung function
Pro-inflammatory effects (inc cytokines IL-6, IL-8, GM-CSF, neutrophilic bronchitis)
Inc response to inhaled allergens and respiratory morbidity

28
Q

Particulate matter (PM) and asthma

A

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

29
Q

how is exposure to environmental pollutants reduced

A

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