it has been used as methylating agents , laboratory reagents , pesticides , and in microscopy .
the human exposure to methyl iodide occurs through routes like dermal , inhalation , and oral ingestion .
predominantly neuropsychiatric symptoms of acute exposure to monohalomethanes consist of headache , nausea , vomiting , drowsiness , dizziness , giddiness , diarrhea , confusion , ataxia , slurred speech , paralysis , convulsions , delirium , coma , and death.[26 ] one case of suicidal parenteral exposure has been reported .
prominent delayed neuropsychiatric manifestations as behavioral disturbances , cognitive deficits , psychoses , and emotional liability have also been noted lasting for months to years .
the primary target organs in cases of severe poisoning are lungs , liver , kidney , and brain .
animal studies have shown methyl iodide to be a potential carcinogen and teratogen . a case presenting with repeated overexposure producing recurrent attacks of multifocal neurological dysfunction mimicking multiple sclerosis has also been reported .
we report two cases who presented to emergency services of tertiary care public hospital , after accidental exposure to methyl iodide for a short duration .
a 23-year - old industrial worker , was accidentally exposed to an unknown quantity methyl iodide vapors for 5 to 10 seconds at his place of work .
this resulted in loss of consciousness for few minutes . after regaining consciousness , he had altered behavior in the form of muttering to self , running around aimlessly , picking at his clothes and saying fearfully that somebody is coming to kill him .
mental status examination further revealed that he was disoriented in time , place , and person ; physical examination showed pulse was 102 per minute and weak and blood pressure was 100/70 mmhg at the time of emergency evaluation .
his pupils were dilated and he had a left seventh nerve palsy of lower motor neuron type and depressed gag reflex .
the patient reported fearfulness , persecutory delusions , and occasional auditory hallucinations after resolution of neurological symptoms .
a 34 year industrial worker , was brought with accidental workplace exposure to methyl iodide for 15 to 30 s. he had been working there for the past 9 years . on his entry to emergency unit ,
his pulse was 90/min and blood pressure was 110/80 mm of hg and respiratory rate was 30/min .
all routine investigations revealed no abnormality except for small pleural effusion on the chest x - ray .
gradually , the patient 's sensorium improved over next 2 days , he complained of extreme anxiety , fear , restlessness , and poor sleep .
over the same time span , the patient showed complete resolution of the neurological signs . in both these cases
no history of any other organic , metabolic , infective , or intoxication causes was found on detailed enquiry .
they were given benzodiazepine drugs for symptomatic relief , i.e. to control anxiety and agitation .
a 23-year - old industrial worker , was accidentally exposed to an unknown quantity methyl iodide vapors for 5 to 10 seconds at his place of work .
this resulted in loss of consciousness for few minutes . after regaining consciousness , he had altered behavior in the form of muttering to self , running around aimlessly , picking at his clothes and saying fearfully that somebody is coming to kill him .
mental status examination further revealed that he was disoriented in time , place , and person ; physical examination showed pulse was 102 per minute and weak and blood pressure was 100/70 mmhg at the time of emergency evaluation .
his pupils were dilated and he had a left seventh nerve palsy of lower motor neuron type and depressed gag reflex .
the patient reported fearfulness , persecutory delusions , and occasional auditory hallucinations after resolution of neurological symptoms .
a 34 year industrial worker , was brought with accidental workplace exposure to methyl iodide for 15 to 30 s. he had been working there for the past 9 years . on his entry to emergency unit ,
his pulse was 90/min and blood pressure was 110/80 mm of hg and respiratory rate was 30/min .
all routine investigations revealed no abnormality except for small pleural effusion on the chest x - ray .
gradually , the patient 's sensorium improved over next 2 days , he complained of extreme anxiety , fear , restlessness , and poor sleep .
over the same time span , the patient showed complete resolution of the neurological signs . in both these cases no history of any other organic , metabolic , infective , or intoxication causes was found on detailed enquiry .
they were given benzodiazepine drugs for symptomatic relief , i.e. to control anxiety and agitation .
these case reports highlight concurrence of frankly psychotic features and acute confusional state in workers vulnerable to industrial exposure to toxic chemicals .
understanding the mechanism of neurotoxicity will perhaps throw some light on co - existence of both psychiatric and neurological symptoms .
these have been shown to bind to cytochrome oxidase in the mitochondria and thus disrupt the oxidative pathway of atp generation leading to cell death and neurotoxicity .
depletion of gsh has also shown to decrease cell 's ability to combat oxidative stresses and thus the cytotoxicity.[1113 ] further , the presence of psychotic features in such patients does not warrant treatment with antipsychotic drugs and caution should be maintained while doing the same in an already compromised nervous system .
no specific antidote or treatment modality has been studied except for efficacy of n - acetylcysteine in a few cases .
awareness of these toxic effects at vulnerable work places will lead to timely and appropriate interventions .
importance of safety precautions and education of both workers and supervisors can not be overemphasized here .
relatively , the indian literature is found to be inadequate regarding safety exposure limits ( sels ) of individual industrial chemicals .
occupational safety and health administration ( osha ) , 1989 , and american conference of governmental industrial hygienists ( acgih ) , 1984 - 85 , recommend permissible exposure limit ( pel ) of methyl iodide as ( for 8 h ) 2 ppm .
however , timely identification of toxic effects and early intervention will go a long way in these unfortunate accidental events .
 methyl iodide is a monohalomethane and with a chemical formula ch3i . 
 acute exposures to methyl iodide have frequently occurred in the workplace . 
 predominantly , neuropsychiatric symptoms of acute exposure to monohalomethanes consist of headache , nausea , vomiting , drowsiness , dizziness , giddiness , diarrhea , confusion , ataxia , slurred speech , paralysis , convulsions , delirium , coma , and death . 
 we report two cases who presented to our emergency services after accidental exposure to methyl iodide for a short duration . 
 these case reports highlighted concurrence of frankly psychotic features and acute confusional state in workers vulnerable to industrial exposure to toxic chemicals . understanding the mechanism of neuro - toxicity 
 will perhaps throw some light on co - existence of both psychiatric and neurological symptoms . 
 awareness of these toxic effects at vulnerable work places will lead to timely and appropriate interventions . 
 importance of safety precautions and education of both workers and supervisors can not be overemphasized here 
INTRODUCTION
CASE REPORTS
Case 1
Case 2
DISCUSSION