Abstract: Case Reports |


Gilbert Seda, MD*; John Perri, DO
Author and Funding Information

Naval Medical Center, San Diego, CA


Chest. 2008;134(4_MeetingAbstracts):c41001. doi:10.1378/chest.134.4_MeetingAbstracts.c41001
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INTRODUCTION: Hypersensitivity pneumonitis (HP) also called extrinsic allergic alveolitis, refers to a constellation of lung diseases resulting from immunologic reactions to a wide variety of inhaled antigens. Although little is known about the true incidence and prevalence of HP, rates appear to be low relative to more common lung diseases due in part to under recognition and misdiagnosis. The wide range of specific antigens causing HP can be grouped into three general categories: microbial agents, animal and plant proteins, and low-molecular weight chemicals. We present a case of HP induced by occupational exposure to DOT 5 silicone brake fluid.

CASE PRESENTATION: A previously healthy 47-year old man was involved in an occupational accident exposing him to DOT 5 silicone brake fluid vapor in an enclosed space. He reported no acute symptoms or irritation of his mucous membranes after the event. Over the next two weeks, he complained of dyspnea with exertion, chest discomfort, and occasional cough. On physical exam, he was hypertensive with no tachypnea and pulse oximetry of 94% on room air. Pulmonary and cardiovascular exam were normal with no clubbing, cyanosis or edema. Pulmonary function testing revealed a proportionate reduction in forced vital capacity and forced expiratory volume over 1 second (FEV1) with a borderline low FEV1%. Total lung capacity (TLC) was mildly reduced and diffusion of carbon monoxide (DLCO) was moderately reduced. He required supplemental oxygen with exertion due to oxygen desaturation. Chest radiograph revealed micronodular changes suggestive of pneumonitis. Computed tomography of the chest revealed diffuse bilateral ground glass attenuating opacities with focal areas of air trapping. Bronchoalveolar lavage revealed a neutrophil predominant cell count without eosinophils, and transbronchial lung biopsy revealed poorly formed noncaseating granulomatous within the alveolar spaces. Special stains for acid fast bacili and fungal organisms were negative. The patient was treated with Prednisone. After two weeks, he no longer required supplemental oxygen and was feeling better. Repeat chest computed tomography revealed interval improvement in the bilateral, diffuse ground glass opacities.

DISCUSSIONS: We describe the first case of HP associated with DOT 5 silicone brake fluid. DOT 5 silicone brake fluid is composed of 3% di-ethylhexyl sebacate, 95% dimethyl polysiloxane, and 2% tributyl phosphate. Tributyl phosphate (TBP) is regulated by the Occupational Safety and Health Association. Although HP is typically associated with animal/plant proteins or microbial antigens, chemicals such as toluene diisocyanate and diphenylmethane diisocyanate have been associated with chemical HP. The pathogenesis of HP involves antigen exposure, immunologic sensitization of the host to the antigen, and immune-mediated damage to the lung. The immune inflammation results in a lymphocytic alveolitis and granulomatous pneumonitis involving a combination of immune complex-mediated, humoral, and cell-mediated or delayed (type IV) immune reactions. A study that specifically investigated the pneumotoxic effects of TPB in rats found elevated lipid peroxidation and a reduction in superoxide dismutase, glutathione peroxidase, and glutathione reductase. The depression of antioxidant enzymes in the setting of immune mediate lung injury are probably important mechanisms of HP.

CONCLUSION: Occupational exposure to DOT 5 silicone brake fluid can cause a chemical HP. TBP appears to be the pneumotoxin which suppresses key antioxidant enzymes in animal studies.

DISCLOSURE: Gilbert Seda, No Financial Disclosure Information; No Product/Research Disclosure Information

Tuesday, October 28, 2008

4:15 PM - 5:45 PM




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