‫ב"ה‬
Facial Nerve Palsy after Acute Exposure to
Dichloromethane
R.M. Jacubovich, MD, MOccH, D. Landau MD, Y. Bar Dayan, MD,
MHA, M. Zilberberg, MOccH, L. Goldstein MD MHA.
Correspondence: Lt. Colonel Dr. Yaron Bar-Dayan, Deputy Surgeon general IAF,
MD, MHA.
Surgeon general headquarters IAF
Adress: 16 Dolev St. Neve Savyon, Or Yehuda, Israel.
Phone: 0097236341039
Fax number: 0097237377468
E-mail: bardayan@netvision.net.il
ABSTRACT
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 paint-stripping, and several reports have described severe adverse affects as
well as fatalities. Conflicting reports regarding peripheral nerve toxicity have been
found with no reports of clinical acute toxicity heretofore.
CASE REPORT: 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 acute 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.
KEYWORDS: Dichloromethane; Methylene chloride; Facial nerve palsy; Paint
stripping; Paint remover; Toxicity; Ventilation; Occupational exposure.
INTRODUCTION
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).
Dichloromethane is lipophilic and is an excellent solvent for preparations 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 small
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 carboxyhaemoglobin is almost three times that following an
equivalent inhalation of carbon monoxide. This is because hepatic biotransformation
to carbon monoxide is dependent on the enzymatic metabolic rate, and the rate at
which DCM is released from tissue stores. Consequently, carboxyhaemoglobin
production may continue for several hours following cessation of exposure to DCM
(Hayes & Laws, 1991; Leiken et al., 1990 ).
Hepatic conversion occurs via two pathways (Hayes & Laws,1991):
1. 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.
2. Cytosolic transformation (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
vapour 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 14C-labelled methylene
chloride were excreted mainly as 14C-carbon monoxide (with 14C-carbon dioxide)
whereas high concentrations were excreted in the expirate largely
unchanged as 14C-methylene chloride (IPCS 1997).
Toxic effects of DCM have been observed following its inhalation, due to direct
central nervous system depression (Zarrabietia et al., 2001, Leiken et al., 1990) or
from the effect of carbon monoxide on the central nervous and cardiovascular systems
(Rioux et al.,1989; Pankow, 1996; Savolainen, 1989; Stewart and Hake, 1976).
The most serious manifestations of DCM toxicity are unconsciousness and death, and
a number of fatalities have been reported in the literature (Rioux and
myers,1989;Savolainen, 1989; Leiken et al.,1990;, Stewart and Hake, 1976; Manno et
al., 1989; Manno et al., 1992; Goulle et al., 1999; Novak and Hain, 1990; Winek et
al., 1981). 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, 4 soldiers in the hall ( 2 meter
width and 10 meter length), and 3 soldiers worked in a closed small room, 25 square
meters in size, with one door that opened to the hall, and one window 10 cm*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 three hours 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-morbities 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 an 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 1mg/kg Prendisolone. After his D/C he had
a rapid improvement and an almost complete recovery after about three 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 hours 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 hours in DCM
exposure compared with 4 hours 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
1000-5000 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 (ATSDR,1993;
Savolainen, 1989; Hall and Rumack,1990). 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 (Savolainen, 1989; Leiken et al.,1990; Hall and
Rumack, 1990; Bakinson and Jones, 1985; DiVincenzo and Kaplan, 1981).
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 (Feldam RG and Mayer RF, 1968). Regarding the
possible effect of DCM on the peripheral nervous system, there are conflicting
reports.
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 (Winneke, 1981; Pankow et al., 1979).
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, otits 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. Nevertheless the temporal correlation with an
acute DCM exposure, and the lack of collaboratory evidence to support the diagnosis
of idiopathic facial palsy, raises the possible causal role of DCM toxicity.
CONCLUSSION
This is the first article, as far as we know, that describes a possible link between acute
dichloromethane exposure and facial nerve palsy.
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