Abstract
Mosquito coils, which are commonly used as residential insecticides in Asia, contain different concentrations of octachlorodipropyl ether (S-2) as a synergist or an active ingredient. As bis(chloromethyl) ether (BCME) is an extremely potent lung carcinogen that can be produced by the thermolytic degradation of S-2, contact with mosquito coils is likely to expose individuals to a certain level of BCME, and therefore increase the risk of lung cancer. However, the significance of exposure is uncertain, as clinical and epidemiological studies concerning mosquito coil users and workers are lacking. The present study describes three cases of small cell lung cancer treated at the Shanghai Pulmonary Hospital that were likely to be the result of exposure to mosquito coils. All patients had worked in the mosquito coil manufacturing industry, with an mean occupational duration of 9.1 years, and presented with similar respiratory symptoms, such as cough and dyspnea. Upon diagnosis, no metastasis to other organs was identified in any of the cases. Subsequently, the three patients were treated with chemotherapy as well as radiotherapy in one case, however, all patients succumbed to the disease, with a mean overall survival time of 10.7 months. We conclude that contact with mosquito coils is likely to expose individuals to a level of S-2 that may increase the risk of SCLC.
Highlights
Small cell lung cancer (SCLC) accounts for ~15% of all lung cancers in the USA [1]
Histological analysis may be sufficient for the diagnosis of SCLC, which presents as poorly differentiated tumor that is categorized as a highgrade neuroendocrine carcinoma
The majority of SCLCs are immunoreactive for keratin and thyroid transcription factor-1 (TTF-1)
Summary
BCME is a unique alkylating agent due to the participation of the oxonium ion in addition to the carbonium ion usually encountered with alkylating agent carcinogens The existence of this equilibrium reaction and the resonance stabilization in the ionic species explains the induction of lung cancer in animals and humans by this carcinogen and its potential for resulting in the induction of malignant tumors at distant sites [16]. Following two cycles of chemotherapy with 100 mg/m2 etoposide and 75 mg/m2 cisplatin on days one to three of three‐weekly cycles, the patient exhibited a complete response (CR) (Fig. 1C). Following two cycles of chemotherapy with 100 mg/m2 etoposide and 25 mg/m2 cisplatin on days one to three of three‐weekly cycles, the tumor response was assessed as PD (Fig. 3C).
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