Acute-Onset Persistent Olfactory Deficit Resulting from Multiple Overexposures to Ammonia Vapor at Work Janice C

J Am Board Fam Pract: first published as 10.3122/15572625-11-1-66 on 1 January 1998. Downloaded from Acute-Onset Persistent Olfactory Deficit Resulting From Multiple Overexposures to Ammonia Vapor at Work janice C. Prudhomme, DO, MPH, DennisJ Shusterman, MD, MPH, and Paul D. Blanc, MD, MSPH

Impaired olfaction (a functional decrement in the Case Report sense of smell) is not uncommon. It is estimated A 41-year-old man was in his usual state of good that at least 2 million Americans suffer from an health until 1993, when he was acutely overex­ impaired sense of smell, although the actual num­ posed to an ammonia leak while employed as the ber is probably higher. 1 The importance of this owner-operator of a fish-processing plant. The primary sense should in no way be minimized, aqueous ammonia involved in the leak was used as since its absence can result in profound conse­ a refrigerant in the fish-processing operation. No quences. Both personal protection and quality of other irritant gases, including sulfur dioxide, were life can be compromised by impaired olfaction. used as refrigerants in the operation. At the time Intact olfaction provides an excellent warning sys­ of the leak, the patient experienced eye and nasal tem for detection of hazardous conditions includ­ irritation and mild facial skin burning. He avoided ing smoke from fires, ingestion of spoiled foods, mouth breathing and denied experiencing any and hazardous materials encountered on the job. other acute respiratory symptoms. He spent an An employee lacking intact olfaction could be se­ entire morning in the vicinity of the leak without riously impaired in certain settings, and indeed wearing respiratory protection. He had previously might be precluded from selected duties as a re­ experienced ammonia leaks with similar but less sult. Even appropriate respiratory protection (ie, severe symptoms. No quantitative industrial hy­ air-purifying respirators) might not offer suffi­ giene measurements of the ammonia concentra­ cient assurance against toxic exposures because tion were made. the impaired person would not be able to detect In contrast to previous ammonia exposures, af­ respirator leaks or cartridge breakthrough.2 The ter this incident the patient's nasal symptoms per­ http://www.jabfm.org/ senses of taste and smell are intertwined; loss of sisted, marked by a sense of nasal stuffiness and in­ smell can adversely affect gustatory pleasure or, termittent epistaxis continuing for 2 weeks. more importantly, can lead to anorexia. Although the nasal congestion later resolved, he Despite the frequency of irritant upper airway also complained of a concomitant, complete loss exposures occupationally,3 published cases of of smell that improved only minimally. \Vhereas work-related residual olfactory impairment have

some sense of smell did return, he noticed diffi­ on 6 October 2021 by guest. Protected copyright. frequently lacked documentation of sensory test­ culty recognizing previously familiar odors, such ing. Recognition of the link between irritant ex­ as his wife's perfume or freshly mowed grass. Foul posure and upper airway functional loss is thus or unpleasant odors did not replace normal smells. important to occupational and general health No other nasal or respiratory tract symptoms, practice. such as rhinorrhea or discharges, persisted. His We report a case in which persistent hyposmia sense of taste returned to baseline after a transient (reduction in the sense of smell) occurred follow­ complaint of a metallic taste. ing an acute industrial exposure to ammonia. His senses of hearing and vision remained in­ tact. He reported no history of atopic disease, in­ cluding allergic rhinitis. He was a lifetime non­ Submitted 2 May 1997. From the Division of Occupational and Environmental smoker and was on no medications at the time of Medicine, University of California, San Francisco. Address exposure. There was no history of nasal trauma reprint requests to Paul Blanc, MD, Division of Occupational and Environmental Medicine, University of California, San related to his symptoms. He was examined by an Francisco, PO Box 0924, San Francisco, CA 94143-0924 otolaryngologist 6 months after the acute expo-

66 JABFP Jan.-Feb.I998 Vol. II No.1 J Am Board Fam Pract: first published as 10.3122/15572625-11-1-66 on 1 January 1998. Downloaded from surej no structural abnormalities were observed. A nasal biopsy or lavage was performed to aid in the brief trial of intranasal flunisolide was prescribed exclusion of inflammatory or infectious cofactors with no effect. known to impact olfaction adversely. When he was examined 30 months after his The occupational importance of olfactory im­ acute exposure, his external nares were patent and pairment has been recognized in two major re­ without apparent abnormality. Bilateral nasal views.4,5 General understanding of this topic can breathing was without deficit, and there was no si­ be hampered by the nomenclature used to describe nus tenderness to palpation. Findings of the the pathology of deficits, which can be confusing. oropharynx and pulmonary examinations were Three conditions with fairly universal definitions unremarkable. Assessment of his olfactory detec­ include anosmia (complete absence of the sense of tion threshold for phenylmethy carbinol using a smell), hyposmia (diminished ability to detect odor­ quantitative Smell Test Kit (Olfactolabj EI Cer­ ants), and dysosmia (distortion of normal smell). Ol­ rito, Calif) was consistent with hyposmia, yielding factory impainnent following specific occupational an olfactory threshold of 40 decismels (dS). * The exposures has been best documented following upper limit of normal (for persons aged 20 to 70 chronic exposure to various metals (chromium, years) on the decismel scale is 25 dSj the absolute nickel, cadmium), solvents, acids, petroleum prod­ cutoff for hyposmia is 35 dS. Using a standardized ucts, and more recently, acrylate and methacrylate diagnostic testing kit - the University of Pennsyl­ vapors.4-9 In contrast, relatively few acute irritant vania Smell Identification Kit (UPSITj Pitts­ exposures have been associated with olfactory burgh) - he was able to identify correctly only 24 deficits (transient or persistent)j these include hy­ out of 40 possible odors. drogen sulfide, hydrogen selenide, sulfuric acid, phosphorus oxychloride, and sulfur dioxide.IO- 14 Discussion Ammonia used in the refrigeration process is This case illustrates acute-onset hyposmia persist­ in a liquid form (ammonium hydroxide or ing more than 2 years after a transient industrial N1-40H). Because of its higher toxicity and flam­ overexposure to ammonia, superimposed upon mability or explosive properties, ammonia is now multiple previous exposures without earlier sub­ often replaced by less-toxic refrigerants.15,16 The jective sequelae. This case is important for several concentration of ammonium hydroxide used in reasons: (1) ammonia is a particularly common in­ refrigeration equipment falls in the range of 9 to dustrial and household chemical, (2) the resultant 38 ppm.17,IS damage became apparent after a single acute ex­ Ammonia can cause immediate irritation and http://www.jabfm.org/ posure, (3) the medical literature documenting inflammation of the mucosal lining of the upper acute olfactory injury following chemical exposure respiratory tract because it is highly soluble in wa­ is scant, and (4) this literature in most cases is ter. 19 Consequently, direct olfactory epithelial cell based upon self-reported olfactory dysfunction damage could result in impaired olfaction. Nasal rather than objective sensory testing. irritation is common to anyone who has used am­

It is important to recognize the limitations of monia during routine household cleaning. It is on 6 October 2021 by guest. Protected copyright. our case report, however. Baseline, objective data important to note that household cleaning prod­ are not available on our patient's olfactory func­ ucts contain approximately 5 to 10 percent ammo­ tion. As is common in the field of occupational nia by weight, whereas industrial strength forms medicine, precise, quantified exposure data are also can be considerably more concentrated.17,IS The lacking. Endoscopic evaluation can detect mucosal nasal mucosa can retain 60 to 80 percent of in­ changes consistent with inflammation or irritation, haled ammonia, regardless of concentration.20 although the otolaryngologist's report did not sug­ In certain occupations, especially agriculture, gest such pathologic changes. Additionally, no exposure to high levels of anhydrous ammonia is not uncommon. Farmers exposed to ammonia lev­ *Decismels (dS) are defined as 20 log (test concentration/refer­ els ranging from 50 to 200 ppm frequently report ence concentration), where the reference concentration is the av­ nasal congestion.21 Similar symptoms have been erage odor threshold in a reference population. Thus, a score of reported following short-term exposures (15 min­ 40 dS indicates that the patient's odor detection threshold was at a test concentration 100 times the population average for the utes) to anhydrous ammonia averaging 90 ppm compound employed. and time-weighted-average concentrations rang-

Persistent Olfactory Deficit 67 J Am Board Fam Pract: first published as 10.3122/15572625-11-1-66 on 1 January 1998. Downloaded from ing from 11.9 ppm to 52.4 ppm.22 Experimental of nasal steroids. This case series provides addi­ data corroborate the irritating effects of ammonia tional support that ammonia can adversely impact on the nasal mucosa. Nasal lavage fluid obtained olfaction. from swine show a dose-response increase in in­ A syndrome known as the reactive upper air­ flammatory cells following exposures of airborne ways dysfunction syndrome, or RUDS, might tan­ ammonia concentrations ranging from 0 to 100 gentially apply to our case. The syndrome helps ppm.23 In humans adaptation to the irritant effect categorize persons who experience persistent of ammonia has been previously described24; how­ nasal symptoms, specifically rhinitis and height­ ever, olfaction was not specifically tested. ened subjective sensitivity to chemical irritants, af­ Interestingly, our patient reported higher ex­ ter a single acute exposure to an upper respiratory posure to ammonia on previous occasions without tract irritant.3o This syndrome is considered anal­ major olfactory effects. It is possible some type of ogous to an asthma-like syndrome known as adaptation had occurred prior to these earlier RADS (reactive airways dysfunction syndrome) events that failed with his final exposure. An alter­ that develops in certain persons following acute native explanation might be that his sense of smell pulmonary tract irritation.31 Symptoms develop was partially compromised from earlier incidents, after a single (generally, intense) exposure and making his olfactory system less accurate in assess­ persist in the absence of additional exposures. Our ing the severity of subsequent exposure levels. patient did develop some pertinent nasal symp­ Although the irritant effects of anhydrous am­ toms following one of multiple acute exposures to monia on both the upper and lower respiratory ammonia. Although an olfactory deficit as such tracts have been extensively reported in the litera­ has not been incorporated into the clinical syn­ ture,19,25,26 documentation of its effects on olfac­ drome definition ofRUDS,3o it is a plausible con­ tion are far less conclusive. Workers at a chemical sequence of any persistent inflammatory process. plant exposed chronically to both sulfur dioxide A major limitation in earlier reports of olfac­ and ammonia were noted to have higher olfactory tory impairment following environmental expo­ thresholds and more self-reported olfactory dys­ sure has been the lack of objective, standardized function than nonexposed workers; however, sim­ measurements of olfactory function. The two tests ilar findings were not observed in workers exposed used in this case, UPSIT (University of Pennsyl­ to ammonia aloneP Similarly, chronic exposure vania Smell Identification Test), a qualitative test (approximately 14 years) to moderate levels of air­ kit, and OLFACTO-LABS (Quantitative Smell borne ammonia (12.5 ppm) had no effect on odor Test Kits) are well-validated32 ,33 and are now http://www.jabfm.org/ sensitivity in a group of workers at a soda ash fac­ widely available. tory.28 Amoore4 cites one incidental report of per­ The upper respiratory tract is inherently sus­ manent hyposmia resulting from "chronic" am­ ceptible to the toxic effects of airborne irritants. monia exposure; however, insufficient detail is The nasal mucosa and olfactory epithelium are available in this report to verify the exposure or primary targets of water-soluble toxicants, of

outcome. which ammonia is prototypic. Such exposures and on 6 October 2021 by guest. Protected copyright. Hyposmia has been previously reported fol­ their resulting impairment are likely far more lowing single, acute exposures to ammonia in one commonly encountered in primary care settings recent case series.29 Of 63 patients seeking care at than is generally appreciated. It has recently been a nasal dysfunction specialty clinic whose primary reported, for example, that family physicians complaint was the loss of the sense of smell, 7 (11 spend 14 percent of their time dealing with occu­ percent) had chemically-induced olfactory dys­ pational health problems overal1.34 Upper airway function. More interestingly, of these 7 patients, 3 disorders, including irritant-related symptoms, (43 percent) had the onset of their hyposmia fol­ are an important occupational problem among lowing exposure to ammonia. Details of the expo­ those likely to be encountered. In the same study, sure are briefly described for only one of the three 29 percent of physicians specified occupational ex­ incidents. In the described case, an acute, over­ posures as a high-priority issue about which more whelming ammonia exposure caused a severe in­ knowledge was needed. Knowledge on olfactory tranasal bum and ultimately irreversible hypos­ impairment is a particularly needed area of better mia. As in our case, there was no response to a trial understanding.

68 JABFP Jan.-Feb.1998 Vol. 11 No.1 J Am Board Fam Pract: first published as 10.3122/15572625-11-1-66 on 1 January 1998. Downloaded from

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