Environmental Lung Diseases
Environmental lung diseases result from exposure to specific airborne agents, most occupational, but can also be linked to air pollution in industrial or urban areas. A well-done occupational history is neccesary to diagnose environmental disease.
Pathophysiology
Alveolitis depends on particle facotrs, individual susceptibility, smoking history, and prior lung disease.
Amount of particles retained in the lungs: concentration in the air, duration of exposure, and effective of clearance mechanisms affect the amount of particles retained in the lungs.
The small pool of macrophages can get overwhelmed by large dust burdens.
Size and shape of particles: the most dangerous range from 1-5 um in diameter, as they can reach the alveolar sacs and settle there.
Solubility and cytotoxicity: some particles cause formation of free radicals or triggering of macrophages to release inflammatory contents. Further macrophage recruitment magnifies this effect.
Particles which reach lymph nodes can activate exaggerated immune responses.
Possible additional effects of other irritants, ie smoking.
Occupational asthma
The most common cause of occupational airway disease, occupational asthma is variable airflow limitation caused by sensitization to a substance at work. The diagnosis requires some period of latency, with subsequent sensitization.
Over 300 causative substances have been identified.
For high molecular weight substances, the vast majority of the condition is IgE mediated:
- animal products (rats)
- birds
- shellfish (10% of crabmeat processors get occupational asthma)
- insects
- plants
- enzymes, ie pepsin
- vegetable gums
For low molecular weight substances, atopy is not as involved:
- diisocyanates (paints)
- anhydrides (eopxy)
- wood dust (especially cedar)
- metals, ie platinum
- fluxes
- drugs
- chemicals such as formalin
Occupational asthma is diagnosed with:
- history
- objective evidence of asthma or atopy: exam, serology, skin tests, lung function tests
- evidence of work-symptom relationship
- ***airway reactivity can be tested using methylcholine/histamine and then measure peak flow
- response to therapy
- patients can take their own peak flow meters home and measure over time
It is very difficult to predict who will develop occupational asthma. Prevention can be difficult without respirator use. Once people develop occupational asthma, they almost always are removed permanently from that job. There is no liability issues, as it is unpredictable and not really the emplyer's fault.
The Worker's Compensation Board considers FEV1 reversibility, bronchial hyperresonsiveness, and medications.
reactive airway disease syndrome: asthma develops immediately and acutely after exposure.
pneumoconiosis
inhalation of minerals or respirable inorganic particles, leading to fibrosis and/or aggregation of dust particles.
type, size, amount, mixture
Asbestosis
Asbestos is a naturally occurring flexible, industructible, heat resistant fibre, and there are many many uses of it. One of the biggest risks nowadays is DIU home improvement. Amphibole is the most dangerosis form. Phagocytic attempts by macrophages results in their skewering.
Asbestos-related symptoms do not show up until at least 10 years after exposure. Pleurisy is a common early manifestation, with painful, bloody pleural effusion.
Asbestosis is chronic progressive interstitial pulmonary fibrosis, with preferential lower lobe involvement. Disease extent depends on dose, fibre type, host susceptibility, and smoking history.
Other diseases, such as rounded atelectasis, lung carcinoma, and mesothelioma, can follow asbestos exposure. Asymptomatic or more serious plaques can be found on the parietal pleura.
Silicosis
Silica (sand; SiO2) is ubiquitous. Exposure is most common in mining, sandblasting, pottery making.
Simple silicosis usually occurs as bilateral, multiple nodules, with central collagen and peripheral macrophages. Complicated silicosis occurs as massive fibrosis, with conglomerations of nodules in the upper lobe
CXR: lots and lots of little dots, often with lymph node enlargement.
Coal Workers Pneumoconiosis
Anthracosis is the most common (and innocuous) pulmonary problem seen in 5-10% coal miners, and is found in virtually all city dwellers and smokers. 1-2 um black carbon particles are found in macrophages, with no fibrosis.
Coal workers pneumonoconiosis can range from asymptomatic to leading to congestive heart failure. Simple CWP is asymptomatic and non progressive. Complicated disease results in a mass of fibrosis. Diffuse interstitial pulmonary fibrosis can occur.
Resources and References
Dockery DW et al, Air Pollution and mortality, NEJM 1993
Menzies R et al, Sick Building syndrome, NEJM 1993
No Great Mischief. Alistair MacLeod.
- novel about NS coal miners