Interstitial Pulmonary Disease Induced by Occupational Exposure to Paraffin

23 Mar

Interstitial Pulmonary

Paraffin, a mineral oil, can induce alveolitis and interstitial fibrosis, possibly related to the activation of oil-laden AMs. This lipoid pneumonia is usually related to repeated aspiration of paraffin-containing laxative or nasal drops. We report the first case of a workman suffering from an interstitial pulmonary disease related to occupational par­affin exposure.

Case Report

A 59-year-old workman, a mild smoker, was admitted to the hospital in July 1984 for exertional dyspnea. He had been well until May 1984. He had no previous medical or surgical history and had never received long-term treatment. He had no history of asbestos exposure. Five years ago, he started to work for an automobile dealer. From 1979 to May 1984, the patient was chronically exposed to paraffin in cleaning new cars protected by paraffin, using hot water generated by compressed air jets. This technique aerosolized hot paraffin from car surfaces in a closed workshop (80 m3) without any ventilation and led to massive inhalation. He never used a mask to reduce inhalation, whereas the French legislation requires the use of such protective devices. buy vardenafil online

FIGURE 1 . Computed tomographic scan shows diffuse interstitial

FIGURE 1. Computed tomographic scan shows diffuse interstitial process more pronounced in periphery of lower lobes.

The findings from physical examination, cardiac function, routine biologic analyses, and chest x-ray films were normal. A CT scan showed (1) a diffuse interstitial process more pronounced in the periphery of the lower lobes and (2) right paratracheal hypodense ( — 40 UH) lymph node enlargement (Fig 1).

Hypoxemia and a slight decrease in the DSS were found. In contrast, other pulmonary function tests, including plethysmo­graphy evaluation of compliances, were normal (Table 1).

Table 1-Follow-up Data ofPulmonary

A BAL was performed and showed an increase in total cell numbers and lymphocyte percentage. Light microscopy of a trans- bronchial biopsy showed mixed alveolitis involving both normal lymphocytes and AMs, some of them presenting unusual cytoplas­mic vacuoles. Diagnostic investigations failed to demonstrate any evidence of systemic disease, of infectious or hypersensitivity pneumonitis, and the patient did not present any evidence of endogenous dislipidosis or gastroesophagal reflux.

In March 1985, a surgical open biopsy of the right middle lobe was performed. Light microscopy following hematoxylin-eosin, PAS, and trichrome stainings disclosed a uniform interstitial pneumonitis with fibrosis. The alveoli were filled with extracellular lipoid droplets and large AMs containing lipid vacuoles. Some of them were multinucleated foam histiocytes (Touton giant cells). Lymphocytes were also involved in the alveolitis without granuloma organization. Some histiocytes were present in thickened interalveolar septum in which numerous collagen fibers were seen (Fig 2). Lipoid pneumonia was diagnosed.
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FIGURE 2. Open lung biopsy shows interstitial fibrosis with lymphocytic

FIGURE 2. Open lung biopsy shows interstitial fibrosis with lympho-cytic infiltrates. Alveoli are filled with macrophages which have appearance of foam cells; some of them are multinucleated (Touton giant cells; arrows). Numerous large extracellular cavities give “Swiss cheese” appearance (arrowhead) (trichrome stain, original magnification x 400).

A new BAL was performed after the open-lung biopsy. Electron microscopy of the AMs disclosed an aspect of foam cells with cytoplasmic vacuoles of various sizes unstained by osmic acid, a specific feature of mineral oil (Fig 3).

FIGURE 3. Cells from BAL show

FIGURE 3. Cells from BAL show alveolar macrophages with empty vacuoles. None of them are stained by osmic acid (original magni-fication x 20,000).

A daily dose of prednisolone (1.5 mg/kg) was begun in March 1985. Then dosage was slowly decreased until a daily maintenance dosage of 0.5 mg/kg was reached. In November 1985, corticosteroids were discontinued because of clinical impairment. An immunosup­pressive treatment by cyclophosphamide (2 mg/kg daily per os) was begun and maintained for four months. Cyclophosphamide induced neutropenia with digestive candidiasis. Despite therapy, dyspnea and pulmonary (unction became worse, and a restrictive syndrome occurred (Table 1). Diffusing capacity (49 percent) and static compliance (0.25 L/cm H20) decreased concomitantly. Serial cyto­logic studies of BAL fluid demonstrated the progressive decrease of total cells and lymphocyte counts, which returned to subnormal values, whereas PMNs increased (Table 1). As no clinical benefit justified farther active therapy, cyclophosphamide was discontin­ued, and only long-term oxygen therapy was maintained. Apcalis Oral Jelly