Facial nerve palsy after acute exposure to dichloromethane

Case Report
INTRODUCTION
AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 48:389–392 (2005)
Facial Nerve Palsy After Acute Exposure
to Dichloromethane
R.M. Jacubovich, MD, MOccH, D. Landau, MD, Y. Bar Dayan, MD, MHA,
M. Zilberberg, MOccH, and L. Goldstein, MD, MHA
Background Dichloromethane poisoning affects predominantly the central nervous and
the cardiovascular systems, and results from both carboxyhemoglobin formation and
direct solvent-related narcosis. Exposure is frequently occupational and related to paintstripping.
Several reports have described severe adverse effects as well as fatalities.
Conflicting reports regarding peripheral nerve toxicity have been found with no reports of
clinical acute toxicity heretofore.
Methods We present a case report of a patient who developed a facial nerve palsy after
acute occupational exposure to Dichloromethane. The patient was part of a paint removing
crew who have worked without proper protecting measures and were thus exposed to high
levels of Dichoromethane.
Results The patient was involved in paint stripping with Dichloromethane, and developed
facial nerve palsy. Other known causes of facial palsy were excluded, and although
idiopathic palsy cannot be ruled out, there were no corroborating findings. Carboxyhemoglobin
levels taken after a significant delay were normal.
Conclusion This is the first article that describes a case of Facial Nerve Palsy related to
acute dichloromethane exposure, indicating a possible peripheral neurotoxic effect of this
solvent. Am. J. Ind. Med. 48:389–392, 2005. ß 2005 Wiley-Liss, Inc.
KEY WORDS: dichloromethane; methylene chloride; facial nerve palsy; paint
stripping; paint remover; toxicity; ventilation; occupational exposure
Dichloromethane (DCM or Methylene chloride) is a
clear, colorless liquid with a mild sweet odor that can be detected
at concentrations of 100–300 parts per million (ppm)
[ATSDR, 1993; ATSDR, 1998; Mohammad and Stefanos,
1999].
IDF home front command, Neve Savyon, Or Yehuda, Israel
*Correspondence to: Dr.Y. Bar Dayan, Chief medical officer, IDF home front command, 16
Dolev St., Neve Savyon, Or Yehuda, Israel. E-mail: bardayan@netvision.net.il
Accepted 21July 2005
DOI10.1002/ajim.20215. Published online in Wiley InterScience
(www.interscience.wiley.com)
ß2005Wiley-Liss,Inc.
Dichloromethane is lipophilic and is an excellent solvent
for preparation of paint removers, degreasing agents, aerosol
propellants, paint and varnish thinners, fire extinguishers,
adhesives, and in a variety of other industrial settings [Zenz
et al., 1994]. Exposures to high concentrations of Dichloromethane
are generally occupational [ATSDR, 1998].
The principal route of human exposure is inhalation.
Skin absorption is usually minimal because of rapid
evaporation. Following absorption, DCM is distributed
mainly to the liver, brain, and adipose tissue [ATSDR, 1993].
The liver is the primary site of metabolism. Metabolic
conversion to carbon monoxide occurs and the half-life of
carboxyhemoglobin is almost three times that following an
equivalent inhalation of carbon monoxide. This is because
hepatic biotransformation to carbon monoxide is dependent

390 Jacubovich et al.
on the enzymatic metabolic rate, and the rate at which DCM
is released from tissue stores. Consequently, carboxyhemoglobin
production may continue for several hours following
cessation of exposure to DCM [Leikin et al., 1990; Hayes and
Laws, 1991].
Hepatic conversion occurs via two pathways [Hayes and
Laws, 1991]:
Mixed functions oxidase system of cytochrome P450. A
high affinity low capacity pathway, forming carbon monoxide,
carbon dioxide and chloride, via a formylchloride
intermediate. This pathway is associated with detoxification
and is saturable at a few hundred ppm.
Cytosolictransformation (glutathione transferase dependent)
where formaldehyde and formic acid intermediates
are produced. This is a low affinity high capacity system
associated with intoxication, which shows no indication of
saturation up to vapor concentrations of 10,000 ppm.
The extent to which each pathway contributes to total
hepatic metabolism varies in humans, especially with
exposure levels. Thus, toxicity extrapolation between high
and low doses is complex.
Methylene chloride and its metabolites are chiefly
excreted via the lungs with small amounts appearing in the
urine and bile. Low doses of 14 C-labeled methylene chloride
were excreted mainly as 14 C-carbon monoxide (with 14 Ccarbon
dioxide), whereas high concentrations were excreted
in the expirate largely unchanged as 14 C-methylene chloride
[IPCS, 1997].
Toxic effects of DCM have been observed following its
inhalation, due to direct central nervous system depression
[Leikin et al., 1990; Zarrabietia et al., 2001] or from the effect
of carbon monoxide on the central nervous and cardiovascular
systems [Stewart and Hake, 1976; Rioux and Myers,
1989; Savolainen, 1989; Pankow, 1996].
The most serious manifestations of DCM toxicity are
unconsciousness and death, and a number of fatalities
have been reported in the literature [Stewart and Hake,
1976; Winek et al., 1981; Manno et al., 1989; Rioux and
Myers, 1989; Savolainen, 1989; Leikin et al., 1990; Novak
and Hain, 1990; Manno et al., 1992; Goulle et al., 1999].
Most of these cases were associated with furniture paint
stripping.
The objective of this article is to describe a case of facial
nerve palsy in a soldier who was acutely exposed to
Dichloromethane in a paint stripping operation.
CASE REPORT
Eleven Israeli Air Force soldiers used a liquid paint
stripping formulation named TURCO 5873, containing
DCM to remove old paint stains from the floor of a small
building. Four soldiers worked in the entrance to this building,
four soldiers in the hall (2 meter width and 10 meter
length), and three soldiers worked in a closed small room,
25 square meters in size, with one door that opened to the hall,
and one window 10 10 cm in size. There was no ventilation
device in the room.
Shortly after they began working, they experienced
headache, dizziness, and throat irritation. They left the room
every few minutes as they felt insufficient ventilation and
excess solvent vapor in the room-air. They wore no
appropriate protective gloves or masks. After a total of about
3 hr the work was stopped due to excess vapors in the room,
and exacerbation of symptoms.
Two hours later, one of the soldiers, who worked in
the small room, reported to the base clinic. This patient
was 21 years old, non-obese of average height and weight,
who was known to have an atrophic left kidney without
additional co-morbidities or substance abuse (including
tobacco and alcohol). He reported of headache, dizziness,
and nausea. His vital signs were normal as well as the rest
of his physical examination including a thorough neurological
exam. The attending physician ordered a change of
clothes, and he then received IV hydration and a mild
analgesic.
Upon waking up the next morning the patient noticed
weakness and asymmetry of the left side of his face and
immediately went to the base clinic. He was re-interviewed
and reported no preceding viral infection, tinnitus, hearing
diminution, pain behind the ear, hyperacussis, or taste loss.
Additionally, there were no reports of lyme disease in the
areas in which he lives and works nor did he report any
significant travel history. There were no other manifestations
indicating lyme disease (typical rash, arthralgia etc.).
Physical examination revealed features compatible with left
peripheral facial nerve palsy with drooping face and mouth.
The palpebral fissure appeared widened and the forehead
smooth. Upper and lower parts of the face were affected.
There was also a decrease in sensation over the left side of the
face. A possible mild weakness of the muscles of mastication
on the left side was also noted. The rest of the exam was
normal including tympanic membranes and a thorough
neurological examination.
The patient was referred to the emergency department of
a nearby hospital. The diagnosis of peripheral facial nerve
palsy was confirmed. Laboratory tests revealed normal
kidney and liver function tests and oxygen saturation of
98%. Blood carboxyhemoglobin levels were 0.3–0.4% on
serial tests. He was admitted for observation and received a
short course of 1 mg/kg Prendisolone. After his D/C he had a
rapid improvement and an almost complete recovery after
about 3 weeks from the event, although he continued to
complain of left temporal headaches for several weeks. There
is currently no facial asymmetry and only a slight weakness
of the affected side.
The other ten soldiers involved in the incident were
summoned after the patient was diagnosed with facial palsy.
Nine soldiers reported symptoms such as headaches,

dizziness, and nausea for several hours after the event, but
were all symptom free by the next morning. They had no
abnormal findings on physical examination and a laboratory
evaluation that included carboxyhemoglobin levels, liver and
kidney function tests was normal.
DISCUSSION
In the case presented, a worker engaged in paint stripping
with a solvent containing DCM, in an enclosed space
without adequate body protection, developed facial nerve
palsy.
Carboxyhemoglobin levels were found in the normal
range 27 hr after the exposure. The delay was due to the late
development of the facial Nerve palsy and referral to the
hospital. The half-life of carboxyhemoglobin is about 13 hr in
DCM exposure compared with 4 hr in direct carbon
monoxide intoxication [Ratney et al., 1974]. The low levels
found in this case may be due to the delay in the
carboxyhemoglobin sampling. Additionally, carbon monoxide
production varies in different exposure scenarios due to
the complex metabolic breakdown.
Moreover, even after accidental DCM fatality, carboxyhemoglobin
blood levels were low despite lethal levels of
dichloromethane in the blood [Zarrabetia et al., 2001].
Rioux and Myers [1989] reported two workers who were
found unconscious in a semienclosed area with a high level of
DCM fumes, with initial presenting Carboxyhemoglobin
levels of only 5% and 7%.
A compilation of data from case reports in the literature,
show that symptoms like nausea, light-headedness, dizziness,
headaches, correlate with air DCM levels of 1,000–
5,000 ppm, thus, the high probability of a significant
exposure in our case. This level is far greater than the
ambient exposure standard of 50 ppm recommended by the
American Conference of Governmental Industrial Hygienists
as the Threshold limit value (TLV).
The primary target organ of DCM is the central nervous
system [Savolainen, 1989; Hall and Rumack, 1990; ATSDR,
1993]. Both the direct neurologic effects of DCM and carbon
monoxide toxicity appear to contribute to the adverse effects
of DCM exposure. During acute and intense exposures to
DCM, which usually occur in poorly ventilated areas, the
direct solvent-narcotic effect may play a greater initial role in
central nervous system depression [DiVincenzo and Kaplan,
1981; Bakinson and Jones, 1985; Savolainen, 1989; Hall and
Rumack, 1990; Leikin et al., 1990].
Clinical peripheral nervous system toxicity of DCM was
not described heretofore, although one report has linked the
exposure to another chlorinated solvent (trichloroethylene)
with facial anesthesia and pupillary response indicating a
peripheral cranial nerve injury [Feldman and Mayer, 1968].
Regarding the possible effect of DCM on the peripheral
nervous system, there are conflicting reports.
Dichloromethane and Facial Nerve Palsy 391
Workers chronically exposed to DCM reported excess
neurological symptoms compared with a non-exposed
referent group, including numbness and tingling in the hands
and feet. No evidence, however, of slowed motor nerve
conduction velocity in either the ulnar or median nerves was
found [Cherry et al., 1981].
The effects of organic solvents on the myelin sheath of
peripheral nerve tissue, was studied under specified experimental
conditions. This study demonstrated that DCM
produced complete disorganization of the myelin structure
within a few hours after exposure, indicating possible
peripheral nerve toxicity [Rumsby and Finean, 1966].
Experimental neurotoxicologic evaluation of exposure
to high DCM concentrations in rats, revealed no evidence of
peripheral nerve pathology [Mattsson et al., 1990], whereas
another study revealed a decrease in sciatic motor conduction
velocity after intraperitoneal administration of DCM in rats
[Pankow et al., 1979; Winneke, 1981].
Facial nerve palsy following acute DCM exposure has
not been described in the literature. Although known causes
of facial nerve palsy [Cocker and Vrabec, 2003] such as lyme
disease, diabetes mellitus, otitis media or externa, neoplasia,
and ramsy-hunt syndrome are highly unlikely it this case
because of lack of appropriate anamnestic and physical
findings and indolent clinical course, we cannot rule out the
possibility of idiopathic facial palsy. We did not identify any
other medical risk factors for facial nerve palsy and the
occurrence was very close temporally to the exposure, thus
suggesting an association with the exposure, rather than just a
coincidently timed idiopathic occurrence.
CONCLUSION
This is the first report that describes a possible link
between acute dichloromethane exposure and facial nerve
palsy.
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