CASE

An 82-year-old African-American male presented to the emergency department (ED) with a complaint of fever for 3 days and a history of previous abnormal findings on chest radiograph. As part of the patient's evaluation, a CBC, electrolytes, and coagulation panel were ordered and a plain chest radiograph was obtained. The patient's medical history was significant for benign prostatic hypertrophy (BPH) and hypertension. He smoked as a young man from age 21 to 30 years, with a packper- day habit. He had no complaints of cough, shortness of breath, or chest pain. His family history was significant for hypertension and heart disease; his occupational history was not immediately available. Review of systems was positive for fever and headache. At present, the patient lived with his immediate family and denied any recent travel or sick contacts.

On physical examination, vital signs were normal with the exception of a temperature of 101ºF. The patient was not in distress. No lymphadenopathy was found. The lungs were clear to auscultation. The cardiac examination revealed a regular heart rate and rhythm without murmurs. Abdominal examination findings were benign with positive bowel sounds in all four quadrants. The patient's neurologic state was without appreciable abnormalities. No rashes were noted.

Figure 1: Chest radiographLaboratory tests results were WBC count, 12,000/ L with normal differential; sodium, 140 mmol/L; potassium, 4.0 mmol/L; BUN, 21 mg/dL; and creatinine, 1.2 mg/dL. Pulse oximetry was 98% on 2 L oxygen via nasal cannula. The chest radiograph taken in the ED demonstrated diffuse bilateral, rounded, calcified pleural plaques (see Figure 1). These nonspecific findings were relayed to the house officer, whereupon CT was ordered to evaluate parenchyma and pleurae of the lungs. CT demonstrated bilateral pleural thickening and extensive calcified pleural plaques in both lungs (see Figure 2). Noncalcified pleural plaques were also noted. The patient's occupational history revealed that he had been a laborer on railroad construction in the 1940s and had a documented history of asbestos exposure. He was informed of the chronic changes on radiography in 1998. The last radiographic evaluation was performed more than 10 years ago, and the patient denied having symptoms from his asbestos-related condition.

DISCUSSION

Figure 2: Pleural plaquesThe generic term asbestos is used to describe a group of minerals that break into fibers when crushed. The term refers to well-developed, hairlike, longfibered varieties of certain minerals that satisfy particular industrial needs. Asbestos fibers have great tensile strength, heat resistance, and acid resistance; some varieties are also flexible. On the basis of these characteristics, asbestos has been broadly used in insulation, brake linings, flooring, cement, paint, textiles, and many other products. Commercial use of asbestos has declined substantially in more recent years, however. Asbestos and asbestiform minerals may occur as a natural accessory mineral in other industrial mineral deposits or rocks.

The spectrum of pulmonary disorders associated with asbestos exposure includes asbestosis, pleural disease (focal and diffuse benign pleural plaques), and malignancies (non-small cell and small cell carcinoma of the lung as well as malignant mesothelioma).1 Pleural involvement is a hallmark of asbestosrelated disease, whereas it is unusual in other interstitial lung disorders. Pleural plaques are frequently documented on plain chest radiographs, but CT is more sensitive for their detection. The presence of plaques is associated with a greater risk of mesothelioma and lung cancer compared with persons with comparable histories of asbestos exposure who do not have plaques. Slow progression of plaques is typical. Approximately 85% of heavily exposed workers showed pleural thickening (predominantly plaques) on plain film more than 40 years after their first exposure, as did up to 17% of environmentally exposed populations.2 Most patients are asymptomatic for at least 20 to 30 years after the initial exposure; the latency period between exposure and onset of symptoms is inversely proportional to the intensity of asbestos exposure. The earliest symptom of asbestosis is usually the insidious onset of breathlessness with exertion.

Our patient was evaluated for a 3-day history of fever and abnormal findings on the chest radiograph. The source of fever was determined to be a urinary tract infection related to his history of BPH. The chest radiograph and CT findings and their significance were described to the patient. Pulmonary function testing and further follow-up with the pulmonary team were scheduled to monitor the progression of asbestos-related pleural disease.

Asbestosis currently does not have a specific treatment. Smoking cessation, early detection, and regular follow-up care are recommended. Risk of bronchogenic carcinoma increases manyfold in smokers with a history of exposure to asbestos. Asbestos is still a hazard for an estimated 1.3 million workers in the construction industry in the United States and for workers involved in building and equipment maintenance.3 Most asbestos in the United States is found in building and machinery insulation and in older appliances and other insulated products that may be available for resale.

A comprehensive occupational and environmental history is essential when asbestos-related disease is suspected. The occupational history should emphasize occupational and environmental opportunities for exposure that may have occurred about 15 years or more before presentation.4 The diagnosis of asbestosis is ideally based on an accurate exposure history obtained directly from the patient. The history should define the duration, intensity, time of onset, and setting of exposure. Evaluation of persons with suspected asbestos-related disease should include spirometry, all lung volumes, and the carbon monoxide diffusing capacity. JAAPA

Alex Shalshin works in the Department of Pulmonary & Critical Care Medicine, Winthrop University Hospital, Mineola, New York. He has indicated no relationships to disclose relating to the content of this article.


Julie Vajnar, PA-C, RT, department editor

REFERENCES

1. American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 2004;170(6):691-715.

2. van Loon AJ, Kant IJ, Swaen GM, et al. Occupational exposure to carcinogens and risk of lung cancer: results from The Netherlands cohort study. 1997;54(11):817-824.

3. Centers for Disease Control and Prevention (CDC). Changing patterns of pneumoconiosis mortality—United States, 1968- 2000. MMWR Morb Mortal Wkly Rep. 2004;53(28):627-632.

4. Selikoff IJ. Historical developments and perspectives in inorganic fiber toxicity in man. Environ Health Perspect. 1990;88:269-276.