Acute eosinophilic pneumonia following inhalation of turpentine oil: A case report

Abstract

Acute eosinophilic pneumonia (AEP) is an eosinophilic lung disease associated with environmental substances including smoking. Although the etiology of AEP has not been fully elucidated, it has been hypothesized that IL-33 plays a central role in the pathogenesis of AEP. Turpentine oil, from resins of pine trees, is not only used in paints, but also utilized in experimental animal models of inflammation because it leads to the production of inflammatory cytokines including IL-33. Here, we report the first case of AEP following turpentine oil inhalation. A 67-year-old woman reported using urushiol with turpentine oil to repair home goods. She had fever and persistent cough after turpentine inhalation over a very short period of time. The chest X-ray image showed consolidation in the upper right lung field. Laboratory findings indicated that there was no evidence of infection, collagen vascular diseases, and other allergic diseases that cause pneumonia, but analysis of the bronchoalveolar lavage fluid revealed 29% eosinophils with a small number of lipid-laden macrophages. With these findings, the diagnostic criteria of AEP was met. We rendered a diagnosis of AEP by inhalation of turpentine because no other cause for AEP was identified even with a structured questionnaire survey. The manifestations resolved immediately after steroid therapy. This is the first report of a case of AEP caused by the inhalation of turpentine oil.

Keywords: AEP, acute eosinophilic pneumonia; Acute eosinophilic pneumonia; BAL, bronchoalveolar lavage; BALF, bronchoalveolar lavage fluid; CRP, C-reactive protein; ELP, Exogenous lipoid pneumonia; GGO, ground-grass opacity; ILC2, Group2 innate lymphoid cells; Inhalation; Th2, T helper 2; Turpentine oil.

Fig. 1

Computed tomography of the chest at hospitalization. (A) Consolidation with ground-glass opacity (GGO) in posterior segment of right upper lobe. (B) Patchy GGO in segment 6 with slight pleural effusions.

Fig. 2

Giemsa stain of the bronchoalveolar lavage fluid. Representative image showing many eosinophils and lipid-laden macrophages. Original magnification, × 800.

Fig. 3

Response to corticosteroid treatment. Body temperature and CRP levels were measured daily for 9 days of corticosteroid treatment. Body temperature was stable in the normal range on day 10. Chest X-ray imaging was performed 1 month before onset, 1 month after onset, and on days 1 and 9 of corticosteroid treatment. BTmax, temperature maximum; CRP, C-reactive protein; MEP, methylprednisolone; PSL, prednisolone.