The diagnosis of paraffin-induced interstitial pulmonary disease was established by (1) evidence of massive exposure to aerosolized hot paraffin, (2) interstitial pulmonary disease with progressive constitution of restrictive syndrome, (3) CT scan demonstrating interstitial syndrome and hypodense mediastinal lymph nodes suggesting fat density, (4) light microscopy of open biopsy showing features consistent with lipoid pneumonia and fibrosis, and (5) demonstration of paraffin-laden AMs by electron microscopy.
Mineral oil is a well-known cause of lipoid pneumonia. Paraffin resists common hydrolysis and acts as a foreign body when aspirated during treatments with laxatives or nose drops. Lipoid pneumonia is usually restricted to exogenous causes; however, many pulmonary diseases are associated with lipid-laden AMs, in particular, obstructive cholesterol pneumonia, long-term amiodarone treatment, and lipid accumulation in the reticular endothelial system. generic cialis 20 mg
Pathologic findings in these diseases are almost similar to those of exogenous lipoid pneumonia. Many studies have suggested that electron microscopy or biochemistry of BAL and lung biopsy are useful tools for diagnosis. Thus, electron microscopy of mineral oil-laden vacuoles shows an “empty” appearance, as these vacuoles are not stained by osmic acid. In contrast, vegetable or animal oil-laden vacuoles are strongly stained by osmic acid, and lamellar mild osmiophilic vacuoles suggest amiodarone-induced pneumonia.
The diagnosis of paraffin-induced lipoid pneumonia requires both long-term exposure and suggestive histologic features. It has been suggested that BAL and transbronchial biopsy should be sufficient for diagnosis; however, a recent study found that lipid-laden AMs are not specific markers, as they are observed in non-lipoid pneumonia. On the other hand, open biopsy can establish the definitive diagnosis of lipoid pneumonia. Moreover, open biopsy is the only technique staging inflammation and assessing fibrosis.
Follow-up of this observation disclosed two clear-cut steps: alveolitis involving lymphocytes and AMs associated with hypoxemia and decrease in diffusing capacity followed by fibrosis, with marked restrictive syndrome and decrease in compliances and a switch from lymphocytes to PMNs in BAL. This suggests that alveolitis leads to fibrosis, despite withdrawal from exposure, and accords with recent concepts of the pathogenesis of interstitial pulmonary diseases.
Early observations suggested a possible relationship between occupational exposure to mineral oil and respiratory diseases; however, this relationship was not clearly demonstrated, and no recent observations confirmed it. The use of mineral oil in industry is prohibited by work legislation, which may explain why occupational pulmonary diseases induced by paraffin are exceptional. Moreover, paraffin inhalation may be underestimated, as it leads to insidious respiratory disorders without acute symptoms. This observation is the first in which a relationship between occupational paraffin exposure and interstitial pulmonary disease has been established by electron microscopy. The impairment of pulmonary function, despite treatment and withdrawal from exposure, emphasizes the importance of prevention for occupational pulmonary disease. canadian pharmacy cialis