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Poster Presentations: Wednesday, November 3, 2010 |

Short-term Passive Smoking May Cause Acute Eosinophilic Pneumonia: An Evidence of Very High Urinary Cotinine and Nicotine Levels FREE TO VIEW

Shunsuke Akashi, MD; Shinji Teramoto; Kosaku Komiya, MD; Masahiro Kawashima, MD; Shunsuke Shoji, MD; Akira Hebisawa, MD
Author and Funding Information

Tokyo National Hospital, Kiyose-shi, Japan



Chest. 2010;138(4_MeetingAbstracts):538A. doi:10.1378/chest.10639
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Abstract

PURPOSE: Acute eosinophilic pneumonia (AEP) is characterized by febrile illness, diffuse pulmonary infiltrates, and pulmonary eosinophilia. The final pathophysiological mechanism underlying this disease remains unknown. Several studies have proposed a causal relationship between cigarette smoking and AEP; however, no studies have provided direct evidence to support this hypothesis.

METHODS: Herein is reported the first case showing the direct evidence of a short-term period of passive smoking caused AEP. The effects of passive smoking were assessed by the measurement of urinary cotinine and nicotine concentrations.

RESULTS: we describe the case of a 22-year-old male graduate student who presented with AEP 2 days after acute passive smoke exposure. He developed acute respiratory failure despite having no history of the disease. He was admitted to our hospital because of dyspnea, cough, and acute respiratory distress syndrome (ARDS). High-flow oxygen of 15 L/min was administered via a reservoir mask to maintain the SpO2 at >90%. No wheezing was detected upon chest auscultation. Computed tomography of the lung revealed diffuse bilateral pulmonary infiltrates. Transbronchial lung biopsy specimens revealed marked eosinophil infiltration in the alveolar septa. Peripheral white blood cells (WBCs) showed progressive eosinophilia with 24% of total WBCs (3264/mm3) on day 5 to 40% of total WBCs on day 9, after which eosinophilia was gradually resolved by treatment with methyl prednisolone (1000 mg). We diagnosed acute eosinophilic pneumonia. In the absence of other causes, we suspected that acute cigarette smoke exposure in a closed area may have caused the acute inflammatory response in the lungs.We measured his urinary cotinine and nicotine levels, which are the biomarkers of tobacco smoke exposure, to assess the effects of passive smoke exposure. The level of cotinine, 0.198 μg/ml (201 ng/mg Cre), was higher than that in nonsmokers.

CONCLUSION: This is the first evidence of a significant association between acute cigarette smoke and the onset of AEP.

CLINICAL IMPLICATIONS: Passive smoking may be harmful for the cigarette smoke-naive young subjects even a short-period time of exposure.

DISCLOSURE: Shunsuke Akashi, No Financial Disclosure Information; No Product/Research Disclosure Information

12:45 PM - 2:00 PM


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