History
A comprehensive history of exposure to tobacco mold and leaves should be obtained. Workers who do not use masks during their working period are 5 times more likely to develop this disease, [12] and longer duration of work is associated with an increased risk of disease. In one study, those working with tobacco for more than 10 years were twice as likely to develop the disease than those who worked in the field for less than 5 years. [12]
Tobacco worker’s lung, as with most hypersensitivity pneumonitis syndromes, has acute, subacute, and chronic presentations. In acute presentations, patients develop abrupt onset of fever, cough, chills, myalgias, headache, and malaise about 4-6 hours after exposure to tobacco plants and molds. These symptoms are self-limited, resolving in 12 hours to several days once the patient avoids the inciting agent. The symptoms may recur with reexposure.
Patients who have had long-term exposure to tobacco plantations usually have insidious onset of cough, exertional dyspnea, fatigue, and weight loss. Disabling and irreversible respiratory findings due to pulmonary fibrosis may occur late in the course of the disease. Removing patients from tobacco exposure results in only partial improvement.
Physical
Physical examination reveals the following:
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Tachypnea
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Diffuse fine rales
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Wheezing
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Weight loss
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Digital clubbing
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Fever
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Evidence of cor pulmonale
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High-resolution CT scan of lungs shows ground-glass opacification seen in an acute phase of tobacco worker's lung.
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Giant cells are a characteristic feature of acute tobacco worker's lung, which is a form of hypersensitivity pneumonitis.
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High-resolution CT (HRCT) scan shows a ground-glass appearance and reticulonodular opacities in subacute phase of hypersensitivity pneumonitis (HP) secondary to moldy hay.
