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Impaired olfaction (a functional decrement in the sense of smell) is not uncommon. It is estimated that at least 2 million Americans suffer from an impaired sense of smell, although the actual number is probably higher. 1 The importance of this primary sense should in no way be minimized, since its absence can result in profound consequences. Both personal protection and quality of life can be compromised by impaired olfaction. Intact olfaction provides an excellent warning system for detection of hazardous conditions including smoke from fires, ingestion of spoiled foods, and hazardous materials encountered on the job. An employee lacking intact olfaction could be seriously impaired in certain settings, and indeed might be precluded from selected duties as a result. Even appropriate respiratory protection (ie, air-purifying respirators) might not offer sufficient assurance against toxic exposures because the impaired person would not be able to detect respirator leaks or cartridge breakthrough.2 The senses of taste and smell are intertwined; loss of smell can adversely affect gustatory pleasure or, more importantly, can lead to anorexia. Despite the frequency of irritant upper airway exposures occupationally,3 published cases of work-related residual olfactory impairment have frequently lacked documentation of sensory testing. Recognition of the link between irritant exposure and upper airway functional loss is thus important to occupational and general health practice. We report a case in which persistent hyposmia (reduction in the sense of smell) occurred following an acute industrial exposure to ammonia.

Acute-Onset Persistent Olfactory Deficit Resulting From Multiple Overexposures to Ammonia Vapor at Work