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Iodomethane (methyl iodide) is a compound with a long history of use as an industrial and pharmaceutical methylating agent and as an intermediate in pharmaceutical and pesticide manufacture. Iodomethane is a volatile and reactive compound and consequently inhalation is the primary route of exposure. Whilst methyl iodide has a long history of use there have been limited case reports regarding poisoning incidents, since the beginning of the 20th century reported cases have only just reached double figures (no doubt due to the limited use of the chemical). The earliest case of iodomethane poisoning can be traced back to 1901 where a gentleman (age 30) developed iodomethane poisoning whilst working in dye industry. Whilst details of duration are non-existent, symptoms reported were vertigo, double vision and ataxia. Tests of the urine confirmed the presence of iodide. Delirium and mania resulted and ensued treatment in a mental hospital was necessary. Mental dullness persisted and the man was unable to resume his work. This poisoning incident occurred due to the production of iodomethane in an open vessel, with exposure resulting from vaporised iodomethane being inhaled. At the time, the risks were not appreciated, with iodomethane now synthesised in a closed system. Recent case reports described below have been taken from the open published literature: 

Additional information

In one reported incident (Hermouet et al., 1996) a previously healthy 59-year old man was admitted for a cerebellar syndrome which had appeared a few hours after iodomethane preparation procedure. He complained of headache and double vision (diplopid). Clinical examination revealed tremor, ataxia, dysmetria and incomplete left third cranial nerve palsy resulting in strabismus without ptosis or mydrioasis. Other cranial nerve functions were normal, as were motor and sensory examination and electroencephalogram (EEG). The neurological symptoms gradually resolved over the following 3 weeks at which time the patient developed depressive ideation. He was discharged in the 5th week after exposure. On re-exposure several months later, developed another episode of dysarthria, hypermetria, ataxia, and tremor. He was not readmitted and was lost to follow up.


In another case, a 42-year old man whose previous medical history was unremarkable, had been preparing methyl iodide for 3 years at the time of his first admission to hospital after heavy exposure to vapours during a decantation procedure. A few hours later symptoms of drowsiness and vertigo resulted. Clinical examination confirmed ataxia. All neurological symptoms resolved within 2 days and the patient discharged. After this episode, the patient felt so depressed that he commenced psychotherapy, but nevertheless returned to work. The subsequent clinical course was characterised by recurrent attacks of focal or multi-focal neurological dysfunction. During the first attack, the ataxic gait recurred and was associated with painful paraesthesia of the feet. These symptoms resolved spontaneously over a few weeks.


Six months later, the patient complained of double vision and slurred speech. This resolved over 1 month. Three months, later, he developed tingling of the lower extremities associated with ataxic gait. Once again, symptoms resolved spontaneously over 1 month. Three months later he developed tingling of the lower extremities associated with ataxic gait. Once again, symptoms resolved spontaneously over 1 month.


Seven months later the patient was admitted with vertigo, ataxic gait, dysarthia, bilateral reduction of visual acuity and dysuria. Clinical examination revealed a pyramidal syndrome, a cerebellar syndrome and incomplete bilateral third nerve palsy. EEG was diffusively abnormal with irregular rhythms and CT scan of the brain revealed a small low-density lesion of the right caudate nucleus.


Multiple sclerosis was diagnosed and treated as such, during which time symptoms resolved over a 3 month period. Following this episode the patient developed a recurrent episode of depression. One year later he developed another episode with tingling of the lower extremities, weakness and fatigability and admitted 2 months later. Clinical examination revealed bilateral pyramidal syndrome with no cerebellar syndrome or visual impairment. Bladder dysfunction with hesitancy were reported by the patient. MRI scan detected lesions of the right internal frontal white matter and pigmented nuclei. Neurobehavioral evaluation revealed impaired performance on memory tests, particularly short term memory. At this point the responsibility of methyl iodide was considered and atmospheric measurement confirmed that high concentrations well above occupational health limits were present. The patient was not re-exposed and changes in working procedures were obtained to limit the risk of poisoning. The patient was then regularly reviewed and did not develop any further episodes. Clinical examination showed gradual improvement of the neurological symptoms and four years post the final attack the clinical signs had completely resolved.


Appel et al., (1975) reported a case involving a 41 year old chemist who three weeks before his admission into hospital had began producing large quantities of methyl iodide in his ‘private laboratory’. The procedure involved prolonged exposure to vapours of this substance each weekend for 3 weeks. The patient remained asymptomatic until 2 days before admission. During his most recent exposure to the vapours he noted the onset of blurred vision and an unsteadiness of gait.


During this episode the patient had lacerated his right thumb, which he bandaged. The symptoms subsided as he left the laboratory, but his wife noted his staggering of gait and slurred speech. The day prior to admission the patient again reported double vision and became progressively lethargic and confused with dysarthric speech and gross dysmetria of the upper extremities.


Upon admission serum chemistry, haematology, cerebrospinal fluid (CSF) blood arterial gas parameters were evaluated and confirmed to be within normal limits. Chest x-ray and electrocardiogram findings were all normal and blood cultures confirmed the absence of tuberculosis or fungi growth.


Further evaluation confirmed the impression of methyl iodide intoxication. A quantitative test for inorganic iodide in urine was strongly positive, although serum thyroxine and T3 uptake were normal, a thyroid scan showed less than 3% uptake. Serum iodine was 0.31 μg/mL and CSF iodine was 0.53 µg/mL. An EEG showed diffuse slowing with delta and theta activity not localised.


The patient was initially treated with large amounts of intravenous saline solution (3 to 4 litres/day) and chlorthalidone (100 mg/day) to facilitate iodide excretion. By the end of the first week of hospitalisation the patient was clearly less lethargic and more responsive. Slurred speech, poor memory and mild dysmetria were still evident although visual blurring had resolved. Facial expression was limited, with lack of emotion and decreased blinking of eyelids. He exhibited little spontaneous movement and at times would assume almost catatonic posturing. During the next two weeks the patient’s neurologic symptoms slowly resolved. He required support for walking and his gait was stooped and low but he displayed good rapid alternating movements of the extremities. At this point symptoms of flagrant paranoia with delusions of persecution and auditory and visual hallucinations appeared. Repeat EEGs were progressively more organised, CSF iodine was within normal limits and serum thyroid tests remained normal. A repeat thyroid scan showed only 4% uptake and serum iodine levels were 0.64 µg/mL 5 weeks after admission. Psychometric testing indicated an overall impression of serious organic impairment in intellectual functioning and personality organisation.


Gradually the patient’s physical activities increased and he became increasingly independent in motor skills with improved gait and facial expression. Mental status also improved with less difficulty in distinguishing fantasy from reality and a decrease in paranoid ideation. The patient was discharged 6 weeks following admission. At follow-up examination 5 months later the patient had a normal neurologic examination, but admitted that he still experienced paranoid feelings on occasion.


Schwartz et al., (2005) reported a case which focused on a 49 year old male, whose job involved carrying and loading tanks of newly manufactured methyl iodide onto trucks. During this time personal protective clothing which included chemical protective suit and full face respirator with air hose were worn. The patient recalled not donning outer boots that day and believed that he may have damaged the soles of this chemical protective suit while walking. At the end of his shift the patient noticed the suit breach on the soles of his suit. The patient went home, showered and noticed an erythematous rash on his genitalia, his inner thighs and groin. He felt tired and had a witnessed syncopal episode in front of his wife who then phoned for an ambulance.


According to the emergency services the patient had a weak and rapid pulse and his blood pressure was not measurable by palpation. He was volume resuscitated with 2 L of crystalloid intravenous fluids. On admission the patient was noted to be in hypovolemic shock, blood pressure was 94/63 mmHg, oxygen saturation was 100% while breathing 15 L of supplemented oxygen by face mask. The patient had another witnessed syncopal episode upon attempting to rise from the stretcher, following which his blood pressure was found to be 78/54 mmHg. At this point the patient began to manifest burns over his torso, back and lower extremities and was transferred to a burns unit. Upon arrival at the burns unit the patient’s hypovolemic state had resolved, blood pressure was 109/86 mmHg and the pulse was 86 bpm.


The patient stayed in the burns unit for 17 days and he was treated for partial thickness burns over 50% of his body surface area which ultimately required several split-thickness skin grafts to his left lower extremity. During the fourth day of the patient’s hospitalisation he had acute delirium, which included confusion, fever (37.8˚C) and increased pulse (100 bpm). Blood pressure during the delirium was 110/50 mmHg and the mean arterial pressure was 70-80 mmHg. The patient required 2L of oxygen (delivered by nasal cannula) to maintain an oxygen saturation of 95%.


After discharge the patient had a follow-up evaluation with a burns surgeon which was remarkable for very satisfactory healing of his skin grafts and satisfactory progress in his rehabilitation despite persistent pain in his left lower extremity. However, the patient began to experience numerous seemingly unrelated constitutional signs and symptoms, as well as self-described problems with memory, concentration and the performance of tasks.


Four months post exposure the patient was refer to a toxicology clinic for the evaluation of possible chronic methyl iodide toxicity. The patient presented for evaluation of cognitive sequelae of methyl iodide exposure. His symptoms were reviewed and were significant for fatigue, hair loss, chronic daily headaches, weight gain and difficulty with memory, concentration and motivation to complete tasks. He stated that his scalp hair loss occurred in the first month; a 40 pound weight gain without change in appetite or activity (except related to his convalescence). Memory problems, lack of recognition for familiar people, places and things as well as loss in activity were also reported.


Serum chemistry was normal (including free thyroixine [0.9 ng/dL]; T3 uptake [43%]; TSH [0.36 mIU/mL]; thyroglobulin [9.7 ng/mL], the exception was a high serum triglyceride level of 221 mg/dL.


The patient denied vertigo, visual or auditory symptoms, respiratory or gastrointestinal symptoms, diaphoresis, weakness, generalised paresthesias or pain (except associated with the skin graft). Depressive or manic symptoms, psychotic symptoms, hallucinations, paranoia or emotional liability were all denied (further corroborated by his wife). The patient noticed small improvements in his ability to concentrate and mental acuity.



Appel, G.B., Galen, R., O’Brien, J. and Schoenfeld, R. (1975). Methyl iodide intoxication. Annals of Internal Medicine,82(4)., 534-536.


Hermouet, C., Garnier, R., Efthymiou, M-L. And Fournier, P-E. (1996). Methyl iodide poisoning: Report of two cases. American Journal of Industrial Medicine,30(6)., 759 -764.


Schwartz, M.D., Obamwonyi, A.O., Thomas, J.D., Moorhead, J.F. and Morgan, B.W. (2005). Acute methyl iodide exposure with delayed neuropsychiatric sequelae: Report of a case. American Journal of Industrial Medicine, 47., 550-556.