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)
