CASE REPORT
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Anosmia in association with occupational use
of a waterproof coating chemical
Timo Hannu, Elina Toskala, Timo Tuomi and Markku Sainio
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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.
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Key words
Acrylates; anosmia; carbon disulphide; occupational exposure; olfactory function; volatile organic
compounds.
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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]
.
We present a case of acute onset of anosmia in a worker
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]
.
According to the patient, no symptoms of respiratory
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
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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
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3. Amoore JE. Effects of chemical exposure on olfaction in
humans. In: Barrow CS, ed. Toxicology of the Nasal Passages.
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155 – 190.
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5. Apter AJ, April EM, Frank ME, Clive JM. Allergic rhinitis
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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:
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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
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OCCUPATIONAL MEDICINE
Document Outline - Anosmia in association with occupational use of a waterproof coating chemical
- Introduction
- Case report
- &?tpt=0pt;Exposure
- Symptoms and primary investigations
- Investigations at the Finnish Institute of Occupational Health (FIOH)
- Discussion
- References
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