Carbon monoxide poisoning is one of the rare causes of hearing loss which may cause reversible or irreversible, unilateral or bilateral hearing loss after acute or chronic exposure. In this report, we present a case of bilateral sensorineural hearing loss in a secondary smelting workshop worker after an acute exposure to carbon monoxide. This complication was diagnosed by pure-tone audiometry and confirmed by transient evoked otoacoustic emissions. Hearing loss has not improved after 3 months of followup. 1. Introduction Carbon monoxide (CO) is a colorless, odorless, and nonirritant gas which is a common cause of mortality due to acute poisoning [1]. This gas is a by-product of incomplete combustion of hydrocarbons. The most common source of environmental exposure to CO is smoking followed by inadequate ventilation [2]. Affinity of CO for hemoglobin is 200 times that of oxygen. Bonding of CO with hemoglobin results in the production of carboxyhemoglobin, which reduces blood oxygen-carrying capacity, competes with oxygen at the heme binding sites, and shifts the oxygen hemoglobin dissociation curve to the left [3]. CO exposure also may cause inflammation through mechanisms independent of hypoxia, resulting in neurologic and cardiac injuries [4]. The symptoms of CO poisoning are nonspecific [5]. Acute mild exposure to CO leads to headache, myalgia, dizziness, and neurologic disturbance [1, 6], while heavier exposure may lead to retinal hemorrhage, myocardial infarction [2], loss of consciousness, coma, and death [4]. After CO poisoning, patients may suffer from some neurologic sequelae such as motor disturbances, peripheral neuropathy, and hearing loss [4]. In contrast, chronic exposure may produce different symptoms comprising fatigue, memory loss, sleep disturbance, vertigo, and hearing loss [7, 8]. Sensorineural hearing loss is among the complications that may be caused by either acute or chronic exposure to CO. 2. Case Presentation Our case was a 22-year-old male working in a secondary smelting workshop in a rotating shift schedule. He was healthy without any history of hearing loss in his preplacement evaluations. The night before his admission, he had worked the night shift of the factory. In the morning, his coworkers found him unconscious. Immediately, he was brought unconscious to the hospital. After intubation, fluid therapy was begun, and he was transferred to the intensive care unit. His vital signs at admission were as follows: pulse rate: 115 beats/min; respiratory rate: 14/min; blood pressure: 115/80？mmHg; temperature: 37.3°C. His Glasgow
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