Anosmia in association with occupational use
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CASE REPORT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anosmia in association with occupational use of a waterproof coating chemical Timo Hannu, Elina Toskala, Timo Tuomi and Markku Sainio . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Abstract A case of acute permanent anosmia is described in a renovation worker during exposure to a waterproof coating chemical. The chemical consisted of several substances of which four (acetone, acrylates, butyl acetate and carbon disulfide) has been previously reported to induce hyposmia or anosmia in workers. Other aetiologies were clinically excluded but a large arachnoidea cyst in the frontal part of the left temporobasal fossa with possible compression of the left entorhinal cortex. The toxic aetiology of anosmia is supported by the acute onset and the temporal relationship with occupational exposure. The silent cyst as the cause of anosmia is improbable, but it may have had some contributory role. Our case illustrates both the challenges when clinically examining patients with work-related olfactory impairment and the importance of multi-disciplinary approach to such patients. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Key words Acrylates; anosmia; carbon disulphide; occupational exposure; olfactory function; volatile organic compounds. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Introduction Common causes of disturbances of the olfactory function include nasal or sinus disease, upper respiratory infec- tions and head traumas [1]
. In addition, brain tumours, drugs, or occupational exposure can lead to anosmia (loss of the sense of smell) or to hyposmia (a diminished sense of smell) [2] . Several chemicals, including metals, organic compounds and solvent mixtures can impair olfactory function in humans [3,4] .
during exposure to a waterproof coating chemical. Other aetiologies were excluded but a large arachnoidea cyst with possible compression of the entorhinal cortex. The toxic aetiology of anosmia is evaluated against the facts on onset and the temporal relationship with occupational exposure and its chemical analysis. The role of other aetiologies of the anosmia is also discussed. Case report Exposure The patient was a 31-year-old man who had worked as a renovation worker since 1998 for the same employer. His duties included renovation and repair works of real estates and flats including bathrooms and washrooms. The materials used at work included unplanned con- struction boards, paints, patching materials (fillers or plasters) and waterproof coatings. On September 1999, when the patient renovated bathrooms, he used a waterproof coating chemical. The chemical was a two-component system consisting of a solvent-free, acrylic-based liquid combined with a cement-based powder. Before the use, the two com- ponents are mixed together. The mixing was done outdoors using respiratory mask and protective gloves. The chemical was applied to the floor and wall areas with a paint roller. The duration of the work session was 5 weeks and during this period the patient used the waterproofing chemical once a week, approximately 2 h per work shift. The application of the chemical took 1 – 2 h after which it was allowed to dry up till the next morning. In the rest of the time, the patient installed tiles to the bathrooms. In the bathrooms, neither local exhaust ventilation nor personal respiratory protective device was in use. According to the patient, the temperature was high and the odour of the chemical was very strong under these conditions. Symptoms and primary investigations On September 1999, at 4 weeks from the beginning of the work session, which lasted 5 weeks, the patient experi- enced loss of the sense of smell. He also felt irritation of eyes and mucous membranes and these are the symptoms Occupational Medicine 2005;55:142–144 doi:10.1093/occmed/kqi043 Occupational Medicine, Vol. 55 No. 2 q Society of Occupational Medicine 2005; all rights reserved 142 Correspondence to: Timo Hannu, Finnish Institute of Occupational Health— Department of Occupational Medicine, Topeliuksenkatu 41 a A, FIN-02500 Helsinki, Finland. Tel: +358 03 4742575; fax: +358 03 4742149; e-mail: Timo. Hannu@ttl.fi Finnish Institute of Occupational Health—Department of Occupational Medicine, Topeliuksenkatu 41 a A, FIN-02500, Helsinki, Finland.
that were shared by the other employees. There were no symptoms of respiratory infection. Before this work session, the patient had used the waterproofing chemical for a couple of times experiencing the eye irritation. Since then the patient had not used this chemical. Only after 2 months, he contacted a local health centre, from which he was sent to a local central hospital for an ENT consultation. The ENT examination was normal. A CT scan with gadolinium enhancement was done in November 2000. Apart from normal sinuses, a large arachnoidea cyst was seen in the frontal part of the left temporobasal fossa. In an MRI (1T) with gadolinium enhancement, the 5 £ 5 £ 6 cm cyst, containing cerebrospinal fluid, was non-enhancing and no oedema was present, but it compressed and slightly dislocated the left temporal lobe. The median cerebral artery and its branches were pushed slightly upwards and followed the cranial edge of the cyst. The left lateral ventricle was narrower than the right, the pons was asymmetric and the median line had minutely moved to the right. On the neurological consultation, the anamnesis did not reveal any head trauma or preceding infection and the neurological status was normal. Thus, the cyst was regarded as a coincidental finding without association to the loss of smell. The patient also had almost weekly headache for 2 – 3 years. The ache began usually after a long workday and was felt in the whole cranium area. It was not very intense, not provoked by physical exertion and did not cause discontinuation of work and was relieved by ibuprofen. The patient was sent to a neurosurgeon’s consultation where an operation was recommended but the patient decided not to have it. Patient had atopia and allergic rhinitis for birch pollen in his medical history. He had been examined for dyspnoea in a local central hospital 10 years ago. Then, the PEF monitoring was suggestive of asthma and, in the spirometry, obstruction was noted in the small airways. Skin-prick tests to common allergens showed allergy to birch, alder, hay, dog and cat. Diagnoses of bronchial asthma and allergic rhinitis were established. Since then, he had used antihistamine and nasal corticosteroid spray in the pollen time and inhaled salbutalmol on demand. He had smoked regularly in the past 10 years, approxi- mately 10 cigarettes per day. Investigations at the Finnish Institute of Occupational Health (FIOH) Later, at FIOH in 2002, the patient was still anosmic. Total serum IgE was 172 kU/l. An ENT examination was normal and no nasal polyposis was seen. On smell testing, the patient was unable to smell or identify any of the following odours: aqua, lactose, coffee and coffee 10%, black pepper, cinnamon, oregano, ammonia 0.5 and 3%, white spirit, ethanol, tar, lemon, rose oil and tall oil. On neurological consultation, based on the previous neuro- logical examinations with present normal neurological status, it was concluded that the arachnoidea cyst was not the cause of the anosmia. The chemical constitution of the waterproof coating chemical was analysed at the FIOH. The waterproof coating consisted of the acrylic polymer dispersion and the render including cement, sand calcium sulphate and cellulose. Material samples were incubated in nitrogen in a gas-washing bottle, and the substances were analysed by gas chromatography and by mass selective detector (Table 1) . The total amount of volatile organic com- pounds was determined. The render part included the same compounds as the dispersion but in very small amounts. Furthermore, in a work simulation test at a construction site, we measured the air concentration of organic solvent components and volatile organic com- pounds when the waterproof coating was applied and during the drying period of 1.5 h. The results obtained during the second application round are presented. During the first application, similar or somewhat lower air concentrations were found. At FIOH, on the basis of the medical history and the performed smell tests, a diagnosis of permanent anosmia was established. Avoidance of the waterproof coating chemical was recommended. Since then, the patient has continued to work in the same workplace without using this chemical and has been well. On the control visit 1 year later at FIOH, the patient was still anosmic. On smell testing, the Table 1. Summary of emissions of material sample (dispersion) and air concentrations during work simulation applying the waterproofing compound Emission (mg/m
3 g) Air concentration (mg/m 3 ) 1-Butanolp 145.2
9.0 Acetonep
47.3 5.5
Vinyl acetate 28.0
n.a. Carbon disulfide 23.0 1.24
2-Methyl-2-propanol 16.0
n.a. Butyl ether 10.0 0.74
n-Butyl acetatep 8.0
, 1 Butyl propionate 4.4 n.a.
Bentsaldehyde 1.1
0.05 1.4-Dioxane 1.0 0.25
Butyl butyrate 0.7
0.06 Ethyl benzene 0.6 n.a.
2-Ethylhexylacrylate 0.3
0.08 tert-Butanolp 8.5 Trimethyl amine 0.005 Dimethyl bentsamide 0.007 Acetaldehyde 0.017 Butyl acrylate 0.1 pSampling with active charcoal tubes. n.a., not analysed. T. HANNU ET AL.: ANOSMIA IN ASSOCIATION WITH USE OF WATERPROOF COATING CHEMICAL 143 results were unchanged, and on the ENT consultation, the status was normal. Discussion In our patient, among the subjective complaints of the loss of olfactory function, abnormal objective measures in smell tests were observed. The patient did not have nasal polyposis, but he had a history of perennial rhinitis, which can cause moderate hyposmia but not anosmia [5] .
infection were present when the occupational exposure had taken place. Moreover, our patient had no history of head traumas. The possible olfaction effect of the large arachnoidea cyst could be by direct compression of the ventral surface of the telencephalon, which harbours the olfactory cortex of the left hemisphere. The lesions, e.g. temporal lobectomy, of these higher olfactory centres are known to be associated with dysfunction of odour detection and recognition, but not anosmia [6]
. Also, tumours of the left temporal region compared with the right have been shown to associate only with ipsilateral deficiency in olfactory tasks [7] . Accordingly, in the literature there are no descriptions of anosmia due to benign cysts. The toxic aetiology of anosmia is supported by the acute onset and the temporal relationship with exposure to the occupational use of a waterproof coating chemical. The silent cyst as the cause of anosmia is improbable, but its contributory role cannot be fully excluded. The chemicals are used very often as mixtures, or they emit many different substances. The analysis of the waterproofing chemical revealed nearly 20 different substances. The effects of possible interaction of the emitted substances to the human olfaction are largely unknown. Of the substances of the patients’ water- proofing chemical, however, acetone [3,8] , acrylates [1,9, 10]
, butyl acetate [1]
and carbon disulfide [1,3]
have been reported to induce hyposmia or anosmia in workers. In these studies, the concentrations and durations of occupational exposure are not always measured. In our patient, the occupational exposure was measured in a work simulation test with results pointing out that the observed exposure levels were below the threshold limit values. However, the working conditions were necessarily not the same in the test compared with the real situation, in which the temperature was high and the patients’ sensation of the odour of the chemical was very strong. Also, it has been suggested that the olfactory effects of solvents may occur at levels far below the threshold limit values
[11] . The course and the pathophysiology of the occu- pation-related olfactory impairment are unsettled. In workers exposed to organic compounds, a possible reversibility is reported [9]
, but permanent deficits have been noted in exposure to hydrogen sulphide [12] and to
methyl acrylate [10]
. In our patient, the loss of smell was permanent. Acrylate and methacrylate have caused olfactory neuron loss and changes in the olfactory mucosa in animals [10] , whereas organic solvents may act on the olfactory neuron [11]
. Our case illustrates the difficulties encountered when clinically examining patients with work-related olfactory impairment, and it also demonstrates the importance of multi-disciplinary approach to such patients. Our finding is important, due to the widespread use of waterproof coating chemicals, but epidemiological studies are needed to verify the observed association. Good venti- lation of the work areas and the use of protective masks are recommended when handling such chemicals. References 1. Duncan HJ, Smith DV. Clinical disorders of olfaction. In: Doty RL, ed. Handbook of Olfaction and Gustation. New York: Marcel Dekker, 1995; 345 – 365. 2. Doty RL. A review of olfactory dysfunctions in man. Am J Otolaryngol 1979;1:57 – 79. 3. Amoore JE. Effects of chemical exposure on olfaction in humans. In: Barrow CS, ed. Toxicology of the Nasal Passages. Washington: Hemisphere Publishing Corporation, 1986; 155 – 190. 4. Hastings L, Miller ML. Olfactory loss secondary to toxic exposure. In: Seiden AM, ed. Taste and Smell Disorders. New York: Thieme Medical Publishers, 1997; 88 – 106. 5. Apter AJ, April EM, Frank ME, Clive JM. Allergic rhinitis and olfactory loss. Ann Allergy Asthma Immunol 1995;75: 311 – 316. 6. Eslinger PJ, Damasio AR, Van Hoesen GW. Olfactory dysfunction in man: anatomical and behavioral aspects. Brain Cogn 1982;1:259 – 285. 7. Daniels C, Gottwald B, Pause BM, Sojka B, Mehdorn HM, Ferstl R. Olfactory event-related potentials in patients with brain tumors. Clin Neurophysiol 2001;112:1523 – 1530. 8. Emmett EA. Parosmia and hyposmia induced by solvent exposure. Br J Ind Med 1976;33:196 – 198. 9. Schwartz BS, Doty RL, Monroe C, Frye R, Barker S. Olfactory function in chemical workers exposed to acrylate and methacrylate vapors. Am J Public Health 1989;79: 613 – 618. 10. Braun D, Wagner W, Zenner HP, Schmahl FW. Disabling disturbance of olfaction in a dental technician following exposure to methyl methacrylate. Int Arch Occup Environ Health 2002;75:S73 – S74. 11. Schwartz BS, Ford DP, Bolla KI, Agnew J, Rothman N, Bleecker ML. Solvent-associated decrements in olfactory function in paint manufacturing workers. Am J Ind Med 1990;18:697 – 706. 12. Hirsch AR, Zavala G. Long-term effects on the olfactory system of exposure to hydrogen sulphide. Occup Environ Med 1999;56:284 – 287. 144
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