Occupational lung disease Flashcards
Occupational lung disease
Disease caused by exposure in the workplace- has a typically long latency.
Examples:
Occupational asthma
COPD
Pneumoconioses
Malignant disease
Coal workers’ pneumoconiosis
Caused by high exposure to inhaling fine coal dust.
Associated with individuals that used to work in coal fields.
Can be uncomplicated if exposure to coal is small- causes mild disease.
If exposure is large- leads to progressive massive fibrosis.
Progressive massive fibrosis
Severe consequence of pneumoconiosis.
Inhalation of fine mineral particles causes alveolar macrophages to be activated.
This stimulates excessive inflammation that leads to progressive scarring.
Silicosis
Pneumoconiosis due to inhalation of fine silica particles.
Common workers associated with this disease:
Slate workers
Potters
Knife grinders
Hard rock miners
Sand-blasting
Foundry workers (metal castings)
Pathophysiology of silicosis
Inhalation of fine silica causes activation of alveolar macrophage.
Stimulates inflammation and scarring.
Causes restrictive lung function.
Observation of eggshell calcification of lymph nodes
Increases risk factor for TB and lung cancer.
Treatment of pneumoconiosis
Further exposure to pathological substance must be prevented.
Smoking cessation
Monitor lung function
Treat symptoms: cough, dyspnoea, cor pulmonale
Asbestosis
Pneumoconiosis caused by inhaling fine asbestos.
Associated with those who worked with asbestos: Buildings Power stations Ship-buildings Railways Brake pads washing contaminated clothes.
Pathophysiology of asbestosis
Asbestos can have benign effects:
Pleural plaque
Pleural effusion
Pleural thickening and restriction
Fibrosis.
Can progress into malignancy:
Lung cancer
Mesothelioma
Occupational asthma
Asthma where:
It is caused by workplace exposures- occupational
OR
It is pre-existing asthma made worse by factors in the workplace- work aggravated
Personal factors to consider when diagnosing occupational asthma
- Consider if it is actually asthma or another condition: COPD, heart failure, anxiety.
- When did asthma present? Especially consider if it occurred in adult life.
- Consider OA if they fail to respond to asthma treatment.
- Assess other risk factors: atopy, rhinitis, smoking.
Workplace factors to consider when diagnosing occupational asthma
- Recognise if the patient’s work is high risk.
- Assess if co-workers are similarly affected.
- Consider there were any recent changes in the workplace.
- Assess if there any preventative measures used: ventilation, masks. etc.
Challenge test
This is carried out to assess if the new agent blamed for OA is responsible.
The agent is identified and assessed using history and PEFR at work.
Conditions:
- Asthma must be stable
- No bronchodilators used.
- Placebo exposure day.
- Equipment that delivers known concentration of known agent must be used.
- Spirometry must be monitored for several hours.
Allergic occupational asthma
Condition that arises due to agent that triggers allergic reaction in the patient.
Two classifications:
High molecular weight
Low molecular weight.
High molecular weight allergic occupation asthma
OA caused by allergic reaction to proteins and polysaccharides.
Ig-E dependant mechanism.
Shows sensitisation with latency period last weeks to years.
Skin prick testing for allergy to done to confirm: Flour Animals Latex Enzymes (in detergent for examples)
Low molecular weight allergic occupation asthma
OA caused by allergic agents that trigger a mechanism poorly understood.
This mechanism is IgE independent.
Skin prick testing is limited but allergy to these agents are related:
Isocyanates (printing and plastics)
Metals (welders)
Dyes (hairdressers)
Non-allergic/ Irritant-induced asthma
Caused by when agents have a direct effect on the airways and does not stimulate an immune response.
This occurs without pre-existing asthma.
Can be acute or subacute.
Acute non-allergic asthma
Reactive airways dysfunction syndrome (RADS)
Asthmatic reaction that develops within hours of a single and very high exposure to an irritant.
Causative agents: Caustic vapours Ammonia Fire/smoke Chlorine Tear gas Floor sealent
Subacute non-allergic asthma
Asthmatic reaction to multiple moderate/high exposures to certain agents.
Causes an insidious onset of asthma symptoms.
Toxin
A naturally occurring poison produced within living cells or organism
Includes:
Botulinum
Ricin
Snake venom
Pollutant
Any substance that contaminates the environment.
Can be a toxin.
Susceptibility to toxins
Dependent on individual factors in patient making them more/less affected by toxins:
- Genetic factors
I.e HbS is protective against falciparum malaria. - Comorbidity
- Environmental factor: heat waves, cold snaps, smogs.
Primary vehicle exhaust pollutants
Created from fossil fuel combustion:
NO
SO- from diesel combustion
CO
Particulate matter
Secondary vehicle exhaust pollutants
Created from reactions between pollutants in the atmosphere.
Heat and sunlight causes volatile organic compounds to produce NO in the ground level ozone
Health effects of ground level ozone pollution
Decreases lung function
Increases pro-inflammatory effects
Increases response to inhaled allergens
Increases respiratory morbidity.
