TERR-O-GAS 57, METHYL BROMIDE, BROMOMETHANE, 


 METHYL BROMIDE
Synonym: TERR - O - GAS, BROMOMETHANE
CASRN: 74-83-9
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAAfTaObf:1

Human Toxicity Excerpts:

CHRONIC EXPOSURE CAN CAUSE CNS DEPRESSION OR KIDNEY INJURY ... .
[Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 950]**PEER REVIEWED**

/In handling methyl bromide in drug industry/ ... severe itching, dermatitis was observed. ... Liq ... can cause severe corneal burns but vapors do not appear to be irritating.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994. 4022]**PEER REVIEWED**

Symptomatology (3-12 hr after inhalation of vapor): 1. Dizziness & headache. 2. Anorexia, nausea, vomiting, & abdominal pain. 3. Lassitude, profound weakness, slurring of speech, & staggering gait. 4. Transient blurring of vision, diplopia, sometimes strabismus & even temporary blindness. 5. Mental confusion, mania, tremors, & epileptiform convulsions. ... 6. Rapid respiration, associated with signs of severe pulmonary edema, cyanosis, pallor & collapse. ... 7. Coma, areflexia & death from respiratory or circulatory collapse. 8. Low-level subacute vapor exposures have produced a syndrome of persistent numbness in the hands & legs, impaired superficial sensation, muscle weakness, unsteadiness of gait & absent or hypoactive distal tendon reflexes. 9. Late sequelae incl bronchopneumonia after severe pulmonary lesions, renal failure with anuria due to tubular degeneration, & severe weakness with or without evidence of paralysis. These difficulties ... subside within a few wk or mo, & complete recovery is the rule. ... Jaundice & other evidence of mild hepatic injury are noted occasionally.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-282]**PEER REVIEWED**

SUFFICIENT PERCUTANEOUS ABSORPTION ... CAN OCCUR TO PRODUCE DEATH IN MAN, & IF EVAPORATION IS DELAYED ... IT IS INTENSE VESICANT ON ... SKIN. BLISTERS PRODUCED ... ARE ENORMOUS BUT RARELY DEEP ENOUGH TO DESTROY ENTIRE SKIN LAYER.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-280]**PEER REVIEWED**

AUTOPSY IN CASE IN WHICH THERE HAD BEEN BLURRING OF VISION & APPEARANCE OF FLICKERING LIGHTS, DOUBLE VISION, & PAIN BEHIND EYES SHOWED MANY MINUTE HEMORRHAGES THROUGHOUT BRAIN, HEART, SPLEEN, & KIDNEYS.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 609]**PEER REVIEWED**

IN 35 METHYL BROMIDE FUMIGATORS EXAMINED, SLIGHT EEG CHANGES (IN 10 SUBJECTS) & SMALL INCR IN SERUM TRANSAMINASES WERE FOUND WHICH COULD BE RELATED TO BROMIDE CONCN IN BLOOD.
[VERBERK MM ET AL; BR J IND MED 36 (1): 59-62 (1979)]**PEER REVIEWED**

THREE CASES OF METHYL BROMIDE POISONING ARE DISCUSSED. A 6 YR OLD BOY HAD CONVULSIONS & BECAME COMATOSE FOLLOWING EXPOSURE TO METHYL BROMIDE. HIS INITIAL EEG SHOWED IRREGULAR WAVES BUT AFTER 3 WK RETURNED TO NORMAL. HIS GRANDMOTHER SHOWED SIGNS OF CONFUSION ACCOMPANIED BY NAUSEA, VOMITING, SEIZURES & COMA. HER EEG WAS AFFECTED BUT NORMALIZED 2 YR AFTER THE INCIDENT. GRANDFATHER'S SYMPTOMS CONSISTED OF NAUSEA & CONFUSION. HIS AWAKE EEG WAS INITIALLY IRREGULAR BUT THE SLEEP EEG WAS NORMAL.
[JAMESON HD; ELECTROENCEPHALOGR CLIN NEUROPHYSIOL 46 (1): 2 (1979)]**PEER REVIEWED**

AFTER SPRAYING METHYL BROMIDE IN STOREROOM OF A HOME, SPASMS OCCURRED IN ALL 4 RESIDENTS, A GIRL 11 YR OF AGE HAD FREQUENT APPEARANCE OF GENERAL MYOCLONIA WHICH WAS FOLLOWED BY COMA. AFTER THE DISAPPEARANCE OF MYOCLONIA, A PERIODIC HIGH AMPLITUDE SLOW WAVE DISCHARGE APPEARED ON THE ELECTROENCEPHALOGRAM. CHARACTERISTIC ACTION MYOCLONIA REMAINED ON THE RIGHT UPPER EXTREMITY. SERUM CONCN OF BROMIDE ION DID NOT SHOW ANY CORRELATION WITH CLINICAL PICTURE (SUGGESTING THAT TOXICITY ... IS DUE TO THE METHYL BROMIDE GROUP RATHER THAN THE BROMIDE ION.)
[TAKAYAMA J, NUMAJIRI S; NIPPON SHONIKA GAKKAI ZASSHI (ACTA PEDIATR JPN) 83 (3): 332-3 (1979)]**PEER REVIEWED**

Human experience indicates that acute fatal intoxication can result from exposures to vapor levels as low as 1164 to 1552 mg/cu m, and harmful effects can occur at 388 mg/cu m or more. Systemic poisoning has been reported to occur from a two week exposure (8 hr/day) at about 136 mg/cu m. Symptoms generally increase in severity with increasing levels of exposure and may vary somewhat according to exposure circumstances and individual susceptibility. In sublethal poisoning cases a latency period of 2 to 48 hr (usually about 4 to 6 hr) occurs between exposure and onset of symptoms.
[USEPA; Ambient WaterQuality Criteria Doc: Halomethanes p.C-24 (1980) EPA 440/5-80-051]**PEER REVIEWED**

A case of fatal methyl bromide poisoning in a 68 yr old male scrapdealer was reported. The subject discharged several obsolete fire extinguishers containing methyl bromide into the atmosphere & proceeded to scrap them. Several hrs later he developed twitching of the arms & became ataxic. On physical exam he had painful, epileptiform tonic, clonic spasms of the face, trunk, & limbs but was fully conscious during these episodes. Anticonvulsant treatment with diazepam, phenytoin, iv chlormethiazole & nitrous oxide by inhalation had no effect on convulsions. Muscle paralysis was induced with pancuronium & positive pressure ventilation begun. EEG showed centroencephalic spike discharges. After 7 days the generalized convulsions had ceased & ventilation was discontinued. There was some neurological improvement over the following week. Despite anticoagulant treatment the patient died 16 days after admission from pulmonary emboli. Serum bromide concn ranged from 130-480 mg/100 ml.
[Behrens RH, Dukes DCD; Br J Ind Med 43: 561-62 (1986)]**PEER REVIEWED**

/Early medicinal/ uses did not last long because of the tendency of methyl bromide to cause throat irritation, to induce vomiting, and to release free bromine, in addition, several deaths were attributed to its medicinal use.
[USDA/Forest Service; Pesticide Background Statements Vol II Fungicides and Fumigants p.MB/C-12 (1986)]**PEER REVIEWED**

The case of action myoclonus following acute methyl bromide intoxication was characterized by marked changes in the inferior colliculi & moderate or mild abnormalities of thalamus, griseum centrale mesencephali, nucleus centralis superior, nucleus reticularis tegmenti pontis, nuclei pontis, & dentatus.
[Hauw JJ et al; Adv Neurol 43: 201-14 (1986)]**PEER REVIEWED**

... Exposure of human lymphocyte cultures to 4.3% methyl bromide for 100 sec increased the frequency of sister chromatid exchanges from 10.0 to 16.8%.
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V41 199 (1986)]**PEER REVIEWED**

Chronic methyl bromide toxicity usually is limited to CNS although mild elevation of serum hepatic aminotransferase levels has been reported in industrial workers. A fumigator chronically exposed to methyl bromide developed paresthesia of the extremities, dysesthesias, & visual impairment secondary to optic atrophy. Mild neurologic dysfunction (eg, decreased finger sensitivity, reduced cognitive performance, & behavioral abnormalities) was detected in a study of soil fumigators.
[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988. 981]**PEER REVIEWED**

Bromomethane is a CNS depressant and may involve pyschic, motor and GI disturbances. In light poisoning cases effects may be limited to mild neurological and GI disturbances, with recovery in a few days. Moderate cases involve the CNS further, with more extensive neurological symptoms and usual disturbance. Recovery may be prolonged for weeks or months, with persisting symptoms and/or disturbed function.
[USEPA; Ambient Water Quality Criteria Doc: Halomethanes p.C-34 (1980) EPA 440/5-80-051]**PEER REVIEWED**

Severe poisoning cases also involve a latent period and similar initial symptoms, with development of disturbed speech and gait, incoordination, tremors that may develop to convulsions, psychic disturbances. Recovery can be quite protracted with persisting neurological disorders.
[USEPA; Ambient Water Quality Criteria Doc: Halomethanes p.C-34 (1980) EPA 440/5-80-051]**PEER REVIEWED**

In fatal cases the convulsions may become more intense and frequent, with unconscious periods. Death may occur in a few hours from pulmonary edema or in one to three days from circulatory failure. Pathology often includes hyperemia, edema, and inflammation in lungs and brain. Degenerative changes occur in the kidneys, liver and/or stomach, and perhaps the brain; although brain changes are usually more functional in character.
[USEPA; Ambient Water Quality Criteria Doc: Halomethanes p.C-35 (1980) EPA 440/5-80-051]**PEER REVIEWED**

A case of brief skin exposure (spray) to liquid bromomethane, quickly decontaminated, did not produce a burn, but resulted in severe, delayed neuromuscular disturbances (twitching, fits, convulsions) and permanent brain damage (cerebellum and pyranedal tract).
[USEPA; Ambient Water Quality Criteria Doc: Halomethanes p.C-35 (1980) EPA 440/5-80-051]**PEER REVIEWED**

The signs & symptoms of methyl bromide poisoning vary according to the degree of exposure. In most instances, the onset of the symptoms is delayed & this latent period varies from 1/2 to several hrs & occasionally 12, 24, or 48 hr. The symptoms may be fatigue, headache, dizziness, nausea & vomiting, disturbances of hearing, vision, mental confusion, muscular weakness, collapse, respiratory difficulties & coma. Death is usually due to lung damage, but damage to the CNS may accompany pulmonary damage.
[Braker W, Mossman A; Matheson Gas Data Book 6th ed p.457 (1980)]**PEER REVIEWED**

Exposure to low, but harmful, concns of methyl bromide over a period of time results in a varied picture of signs & symptoms. In order of frequency of occurrence, these symptoms are: visual disturbances, disturbances of speech, numbness of the extremities, mental confusion, hallucinations, tremors, coma & frequent fainting attacks. Most symptoms disappear in a few days /after/ the exposure /is terminated/, but numbness of the extremities & visual disturbances may persist from 2-5 mo.
[Braker W, Mossman A; Matheson Gas Data Book 6th ed p.457 (1980)]**PEER REVIEWED**

NO REASONS HAVE BEEN ADVANCED FOR COMPLETE SPARING OF LUNGS IN SOME CASES WHERE BRAIN DAMAGE HAS BEEN BOTH SEVERE & PERMANENT. SEVERE NEUROLOGICAL SIGNS SEEM TO BE DEPENDENT ON A SUDDEN EXPOSURE TO HIGH CONCN FOLLOWING CONTINUOUS SLIGHT EXPOSURE.
[International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 330]**PEER REVIEWED**

METHYL BROMIDE IS A DANGEROUS CUMULATIVE POISON WITH DELAYED SYMPTOMS OF CENTRAL NERVOUS SYSTEM INTOXICATION THAT MAY APPEAR AS LONG AS SEVERAL MONTHS AFTER EXPOSURE.
[White-Stevens, R. (ed.). Pesticides in the Environment: Volume 1, Part 1, Part 2. New York: Marcel Dekker, Inc., 1971. 130]**PEER REVIEWED**

Fatal poisoning has ... resulted from exposures to relatively high concn of methyl bromide vapors (from 8600 to 60000 ppm).
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996. 2196]**PEER REVIEWED**

When used as a fumigant for various foodstuffs in the past, methyl bromide caused more fatalities among California workmen than any other agricultural chemical.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-280]**PEER REVIEWED**

The toxic effects of aliphatic chlorinated, brominated, fluorinated & iodinated hydrocarbons, alcohols, acids, & thioacids, were reviewed, with emphasis on their action at the level of the CNS in both man & experimental animals as well as their metab & effects on other organs. Methyl iodide, methyl bromide, methyl chloride & ethyl chloride were shown to induce signs, symptoms, or lesions of the cerbellum in both humans & experimental animals.
[O'Donoghue JL; Neurotoxicity of Industrial and Commerical Chemicals 2: 99-126 (1985)]**PEER REVIEWED**

The effects of exposure of the skin to high concentrations of methyl bromide were studied in 6 cases, who had been unintentionally exposed. Exposure to high concentrations of methyl bromide (approximately 40 g/cu m) for 40 min can lead to redness and blistering of the skin. This cannot be prevented by wearing standard protective clothing. Skin lesions show a preference for relatively moist skin areas. Plasma bromide levels were highest immediately following exposure (mean 9.0 + or - 12.4 mg/l) and fell in subsequent hours (mean 6.8 + or - 2.3 mg/l 12 hr after the exposure). No systemic effects were noted in this series.
[Zwaveling JH et al; Hum Toxicol 6 (6): 491-6 (1987)]**PEER REVIEWED**

Neurobehavioral functions affected by methyl bromide exposure were evaluated in California structural and soil fumigators using methyl bromide and sulfuryl fluoride. Sampling data revealed that structural fumigators are exposed for up to 1.5 hr/day to 0-2.2 ppm methyl bromide and/or 10-200 ppm sulfuryl fluoride, and soil fumigators can be exposed to 2.3 ppm methyl bromide over an 8 hr day. Subjects were grouped for statistical analysis on the basis of exposure history: Those exposed primarily (80% or more of the work period with exposure potential) to methyl bromide (n= 32), primarily to sulfuryl fluoride (24), or to a combination of methyl bromide and sulfuryl fluoride (40-60% of each) for a minimum of one year (18), and those not exposed to high concentrations of any chemicals (29 Referents). Fumigators using methyl bromide reported a significantly higher prevalence of 18 symptoms consistent with methyl bromide toxicity than did referents. Methyl bromide fumigators did not perform as well as referents on 23 of 27 behaviorial tests (chosen to reflect methyl bromide effects), and were significantly lower on one test of finger sensitivity and one of cognitive performance.
[Anger WK et al; Neurotoxicology 7(3): 137-56 (1986)]**PEER REVIEWED**

A 32 year old fumigationassistant developed systemic and neuro-ophthalmic manifestation of methyl bromide poisoning, including increased serum bromide level (6.6 mg/100 ml), paresthesias and burning dysesthesia on his hands and feet, and visual impairment. Ocular examination showed mild bilateral decrease in vision, temporal optic nerve head pallor, severely attenuated visual-evoked response amplitudes and normal latencies, a normal electroetinogram, an abnormal electrooculogram, and a severe deuteranomalous (green) defect on Farnsworth-Munsell 100 hue testing. His vision had not improved 12 mo after the initial exposure.
[Chavez CT et al; Am J Ophthalmol 99 (6): 715-9 (1985)]**PEER REVIEWED**

A technique was described which used sister chromatid exchanges in human peripheral blood lymphocyte cultures to assess the genotoxic potential of vapors. Cultures were exposed to 4.3% methylbromide. Methylbromide increased sister chromatid exchange frequency from 9.90 to 16.84 per cell.
[Tucker JD et al; Teratogenesis Carcinog Mutagen 6 (1): 15-21 (1986)]**PEER REVIEWED**

High concns of methyl bromide can produce rapid unconsciousness during exposure, leading to a prompt "anesthetic" death. However, anesthesia plays no part in the great majority of cases, which are characterized by delayed onset, a great variety of symptoms, & delayed recovery, if death does not occur. The delay in onset usually is several hours, but a delay of only a few min & a delay of 48 hr have been observed. In fatal cases with delayed onset, death generally occurs within 4-6 hr but sometimes after 24-48 hr. In rare instances, death may be delayed as much as 18 days. The cause of death in these cases usually is circulatory failure.
[Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991. 670]**PEER REVIEWED**

...Two cases of testicular cancer mortality versus 0.11 expected (SMR= 1.799, p <0.05) among workers exposed to organic bromides /were reported/. ...Based on the recorded work histories, the only known shared potential exposure was methyl bromide.
[Hayes, W.J., Jr., E.R. Laws Jr., (eds.). Handbook of Pesticide Toxicology Volume 1. General Principles. New York, NY: Academic Press, Inc., 1991. 329]**PEER REVIEWED**

Characteristically during exposure to the gas there are no warning sensations, but after a latent period of several hr the victim has headache, nausea, vomiting, vertigo, & staggering. He may then also have lacrimation from irritation of the eyes, & may experience blurring & diplopia. Transient dimming of vision & blindness for twelve hr has been reported associated with severe nausea & vomiting, but with recovery within a few days. In other cases, nystagmus on lateral gaze, diplopia, & blurring of vision, especially when attempting to read, have been associated with the general neurologic disturbances. In severe cases, convulsion, delirium, & sometimes mania ensue, followed by collapse & possible death. Patients who recover may have a protracted period of apathy & depression, incoordination, tremors, & bothersome visual complaints. As a rule those who recover eventually recover completely.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 607]**PEER REVIEWED**

In a carefully studied case in 1937, a man exposed to methyl bromide while filling fire extinguishers did not develop symptoms until 48 hr later; then he began to have vertigo, aphasia, and ataxia. At the end of a week, when speech was improving, he noted that the contour of objects appeared blurred. His amblyopia became worse, approaching almost complete blindness in a few days. At the same time, vertigo became worse, and one arm was paralyzed. Three weeks after exposure he began to discern objects better, and there was general improvement. At a month, vision in both eyes could not be improved beyond 5/10 with glasses, but the pupils and fundi were normal. There appeared to be weakness of accommodation (requiring 3.5 D for near vision), and central scotomas were found for green, but not for white. By two months, vision in each eye improved to 8/10, and only 1.5 D was required for near vision. His other neurologic disturbances had also subsided.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 609]**PEER REVIEWED**

... A man exposed to pure methyl bromide gas for about half an hour became weak and stupified, unable to walk, but able to crawl out of the room. He saw lights doubled, and they appeared to dance in front of this eyes. He could not place his hands on things accurately. He had neither headache nor vomiting, but in the next few days ataxia increased so that he could scarely stand, and he had marked intention tremor of the hands. The eyes appeared normal externally, and he made no complaint of ocular irritation. The optic nerveheads were described as abnormally red. The retinal arteries seemed normal, but the veins were distended and tortuous. In one eye a retinal hemorrhage slightly larger than the disc extended from the nervehead inferiorly along the course of the verve fibers. Visual acuity varied from 3/4 to 1. There seemed to be slight paresis of abduction in each eye, but psychic disturbance made testing difficult, and the patient complained not only of doubled vision, but of seeing things four or five fold. Ataxia and psychic symptoms became more severe, wth hallucinations of hearing and vision, epileptiform attacks and periods of coma. The hemorrhage in the fundus spread, and it was postulated that the patient must have small hemorrhages in various parts of the central nervous system.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 608]**PEER REVIEWED**

Local contact of methyl bromide with the eye either as concentrated vapor or as a splash of liquid has resulted in no more than transient irritation and conjunctivitis in the few cases in which this accident has been observed.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 616]**PEER REVIEWED**

Methyl bromide is reported to be eight times more toxic on inhalation than ethyl bromide. Moreover, because of its volatility, it is a much more frequent cause of poisoning. Death following acute poisoning is usually caused by its irritant effect on the lungs. In chronic poisoning, death is due to injury to the CNS. ... In addn, to injury to the lung & CNS, the kidneys may be damaged, with development of albuminuria &, in fatal cases, cloudy swelling &/or tubular degeneration. The liver may be enlarged. There are no characteristic blood changes.
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996. 2196]**PEER REVIEWED**

Signs & symptoms of chronic exposures include those from acute exposure plus visual & hearing disorders, numbness or tingling in the extremities, incoordination, ataxia, & loss of consciousness. Psychologic symptoms have been associated with chronic exposure, including loss of initiative, depressed libido, personality changes, hallucinations, & an intolerance to alcohol.
[Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992. 1059]**PEER REVIEWED**

The concn immediately dangerous to life & health (IDLH) is 2000 ppm, & at this concn, methyl bromide produces pulmonary edema, seizures, & death.
[Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992. 1059]**PEER REVIEWED**

Both acute & chronic exposure can result in behavioral toxicity manifested by psychosis, delirium, hallucinations, aggression, & mania. Cases of homicidal ideation & acute psychosis have been described following serious exposures.
[Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992. 1059]**PEER REVIEWED**

SUFFICIENT PERCUTANEOUS ABSORPTION ... CAN OCCUR TO PRODUCE DEATH IN MAN, & IF EVAPORATION IS DELAYED ... IT IS INTENSE VESICANT ON ... SKIN. BLISTERS PRODUCED ... ARE ENORMOUS BUT RARELY DEEP ENOUGH TO DESTROY ENTIRE SKIN LAYER. LIKE OTHER VESICANTS ... METHYL BROMIDE INHIBITS SKIN GLYCOLYSIS AT HEXOKINASE LEVEL.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-280]**PEER REVIEWED**

Methyl bromide poisoning is difficult to confirm because routine laboratory testing has not been reliable. Measurable levels of the parent agent are rapidly reduced, probably as a result of direct tissue chemical reaction. Serum bromide levels have been used as an indirect measure of exposure and/or toxicity but are inconsistent. Recently special testing has shown that protein adducts formed after exposure to methyl bromide may be a better measure of significant exposure. The S-methylcysteine adduct was used to confirm acute methyl bromide toxicity 10 weeks after an exposure.
[Buchwald AL, Muller M; Vet Hum Toxicol 43 (4): 208-11 (2001)]**PEER REVIEWED**

CASE REPORT: We describe a case of early peripheral neuropathy and central nervous system toxicity as a result of acute predominantly dermal exposure to methyl bromide. A 32-year-old male was admitted after an accidental predominantly dermal exposure to methyl bromide while fumigating soil for pest control. The patient suffered dermal burns and vesicles on the upper and lower limbs. One week following exposure, he developed progressive weakness of the lower limbs, ataxia, paresthesiae of both legs and the left arm, hyperactive tendon reflexes in the lower limbs, and left Babinski sign. Nerve conduction velocity testing was compatible with axonal neuropathy. The patient recovered gradually from his burns. Three months postexposure he showed no signs of central nervous system toxicity, but the peripheral neuropathy was still present. Neurological effects primarily referable to the central nervous system following severe inhalation of methyl bromide have frequently been reported. The patient described in this study developed an unusual early peripheral neuropathy following dermal exposure. Peripheral neuropathy can be an outcome of methyl bromide intoxication, but is usually a late sequela of acute central nervous system toxicity or an aftereffect of repetitively inhaled chronic exposure. In this case, exposure to methyl bromide through abraded skin caused early peripheral neuropathy and central nervous system toxicity.
[Lifshitz M, Gavrilov V; J Toxicol Clin Toxicol 38 (7): 799-801 (2000)]**PEER REVIEWED**

Skin, Eye and Respiratory Irritations:

Contact of the skin with high concns of vapor or with liquid methyl bromide produces a tingling & burning sensation.
[Braker W, Mossman A; Matheson Gas Data Book 6th ED p.457 (1980)]**PEER REVIEWED**

Corrosive to skin; can produce severe burns.
[Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996. 2196]**PEER REVIEWED**

Liquid can cause eye and skin burns.
[Tomlin, C.D.S. (ed.). The Pesticide Manual - World Compendium. 10th ed. Surrey, UK: The British Crop Protection Council, 1994. 686]**PEER REVIEWED**

http://pmep.cce.cornell.edu/facts...
CHEMICAL FAMILY:   METHYL BROMIDE, ETHYLENE OXIDE AND PROPYLENE OXIDE

http://www.alternatives2toxics.org/tric.htm
Methyl bromide is a soil sterilant injected into soil prior to planting new grapevines. It is extremely toxic and can kill outright if inhaled. Methyl bromide causes a significant amount of destruction to the earth's protective ozone layer. Most methyl bromide evaporates during and after soil fumigation and can drift off site for up to several miles.

http://www.nycwasteless.com/gov-bus/citysense/....
Acute Health Effects:
Can produce central nervous system and respiratory system failure, as well as specific and severe effects on the lungs, eyes, and skin. Common initial symptoms include weakness, despondency, headache, visual disturbances, nausea, and vomiting. Exposure to high concentrations has resulted in a number of human deaths.

Chronic Health Effects:
Central nervous system symptoms including numbness, defective muscular coordination, tremor, muscle spasms, lack of balance, extreme agitation, coma, and convulsions. Exposure of pregnant women may result in fetal defects. Depending on the dose, gross permanent disabilities or death may result.

http://www.eco-usa.net/toxics/brometh.shtml
Fate & Transport

Exposure Pathways Health Effects

If you breathe bromomethane you may develop a headache and begin to feel weak and nauseated several hours later. If you breathe large amounts, fluid may build up in your lungs and it may be hard to breathe. It could cause muscle tremors, seizures, kidney damage, nerve damage, and even death. Exposure levels leading to death vary from 1,600 to 60,000 parts of bromomethane in 1 million parts of air (1,600-60,000 ppm), depending on the length of the exposure. These levels are much, much higher than those to which you would normally be exposed. The respiratory, kidney, and neurologic effects are of the greatest concern to people. No cases of severe effects on the nervous system from long-term exposure to low levels have been noted in people, but studies in rabbits and monkeys have shown moderate to severe injury.

Swallowing bromomethane may cause stomach irritation. If bromomethane gets on your skin, it can cause itching, redness, and blisters. These effects are caused by levels that are higher than levels you might normally encounter. We do not know if it affects our ability to reproduce. Studies in animals suggest that bromomethane does not cause birth defects and does not interfere with reproduction, except at high exposure levels.

http://www.atsdr.cdc.gov/tfacts27.html
Exposure to bromomethane occurs mostly from breathing contaminated air in the workplace or at waste sites. It is usually not found in surface water, soil, or food. Exposure to high levels can affect your lungs and cause breathing difficulty. It can also damage your kidneys and nervous system, and can even cause death. This chemical has been found in at least 74 of 1,416 National Priorities List sites identified by the Environmental Protection Agency.

How might I be exposed to bromomethane?

How can bromomethane affect my health?

If you breathe bromomethane you may develop a headache and begin to feel weak and nauseated several hours later. If you breathe large amounts, fluid may build up in your lungs and it may be hard to breathe. It could cause muscle tremors, seizures, kidney damage, nerve damage, and even death.

Exposure levels leading to death vary from 1,600 to 60,000 parts of bromomethane in 1 million parts of air (1,600-60,000 ppm), depending on the length of the exposure.

The respiratory, kidney, and neurologic effects are of the greatest concern to people. No cases of severe effects on the nervous system from long-term exposure to low levels have been noted in people, but studies in rabbits and monkeys have shown moderate to severe injury.

http://www.nsc.org/library/chemical/Bromomet.htm
Death following acute poisoning by bromomethane is usually caused by its irritating effect on the lungs. In chronic poisoning, death is due to injury to the central nervous system. Breathing bromomethane can cause headaches, weakness, confusion, numbness, visual disturbances, vomiting, lack of coordination, convulsions, and nausea. Breathing large amounts may cause fluid to build up in the lungs, resulting in difficult breathing; it may also cause muscle tremors, ataxia, paralysis, coma, and seizures. Kidneys may be injured, and urine production may slow or stop. In severe cases, these effects can lead to death. The lung may be severely injured by inhalation exposure to bromomethane; edema is a common effect, often accompanied by focal hemorrhagic lesions.

High levels of exposure to bromomethane vapor can result in adverse renal effects, including congestion, anuria or oliguria, and proteinuria. Bromomethane vapor can also cause conjunctivitis, erythema, rashes, or blisters. Skin contact with bromomethane can cause severe burns, itching, redness, and blisters. Because bromomethane has very little odor at potentially toxic levels, and because effects on the body are generally delayed, people may be exposed to hazardous levels without being aware that the exposure is occurring. The general population is not likely to be exposed to high levels of bromomethane except in the immediate vicinity of industrial facilities that release the gas into air, or near locations where it is being used as a soil or a space fumigant.

Bromomethane is classified as a carcinogen, according to the National Institute for Occupational Safety and Health.

http://panna.igc.org/resources/pestis/PESTIS.burst.43.html
A cumulative neurotoxin, methyl brom ide is highly toxic to humans, capable of causing tremors, lack of coordination, staggering, depression of the central nervous syste m, and convulsions.2 Symptoms may be delayed as long as several months after exposure. Chronic symptoms are closely related to acute irritation symptoms: Workers in a methyl bromide factory were found to be more likely to experience dizziness, numbness, weakness o f extremities, nightmares, fatigue, and dry and scaly skin than were age-matched, non-exposed counterparts.3 Like factory workers in methyl bromide manufacturing plants, fumigant applicators are heavily exposed to methyl bromide.

http://www.epa.gov/ttn/uatw/hlthef/methylbr.html
CAUTION: Unless otherwise noted, the quantitative information on these fact sheets are from "EPA Health Effects Notebook for Hazardous Air Pollutants-Draft", EPA-452/D-95-00, PB95-503579, December 1994." Please conduct a current literature search and check the appropriate current online database for the most recent quantitative information.

http://www.ilo.org/public/english/protection/safe...
EXPOSURE:

Inhalation:  Dizziness. Headache. Abdominal pain. Vomiting. Weakness. Hallucinations. Loss of speech. Incoordination. Laboured breathing. Convulsions.

Skin:  MAY BE ABSORBED! Tingling. Itching. Burning sensation. Redness. Blisters. Pain. ON CONTACT WITH LIQUID: FROSTBITE (Further see Inhalation).

Eyes:  Redness. Pain. Blurred vision. Temporary loss of vision.

ROUTES OF EXPOSURE:
The substance can be absorbed into the body by inhalation and through the skin , also as a vapour!

INHALATION RISK:
A harmful concentration of this gas in the air will be reached very quickly on loss of containment.

EFFECTS OF SHORT-TERM EXPOSURE:
The substance irritates the eyes, the skin and the respiratory tract. Inhalation of the substance may cause lung oedema (see Notes). Rapid evaporation of the liquid may cause frostbite. The substance may cause effects on the central nervous system, kidneys and lungs. Exposure to high concentrations may result in death. The effects may be delayed.

EFFECTS OF LONG-TERM OR REPEATED EXPOSURE:
The substance may have effects on the nervous system, kidneys, heart, liver and lungs.

Depending on the degree of exposure, periodic medical examination is indicated. The symptoms of lung oedema often do not become manifest until a few hours have passed and they are aggravated by physical effort. Rest and medical observation are therefore essential. Immediate administration of an appropriate spray, by a doctor or a person authorized by him/her, should be considered. The odour warning when the exposure limit value is exceeded is insufficient. Turn leaking cylinder with the leak up to prevent escape of gas in liquid state. Bromo-O-gas, Dowfume, Embafume, Halon 1001, Haltox, Meth-o-gas, Terabol and Terr-o-Gas 100 are trade names.

http://www.deq.state.la.us/technology/recap/...
Gastrointestinal effects (epithelial hyperplasia of stomach); Nasal cavity effects (degeneration and proliferative lesions of the olfactory epithelium)

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAAfTaObf:
Human Health Effects:

Evidence for Carcinogenicity:

Evaluation: There is inadequate evidence in humans for the carcinogenicity of methyl bromide. There is limited evidence in experimental animals for the carcinogenicity of methyl bromide. Overall evaluation: Methyl bromide is not classifiable as to its carcinogenicity in humans (Group 3).
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V71 721 (1999)]**PEER REVIEWED**

CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS FOR CLASSIFICATION: Inadequate human and animal data: a single mortality study from which direct exposure associations could not be deduced and studies in several animal species with too few animals, too brief exposure or observation time for adequate power. Bromomethane has shown genotoxicity. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Inadequate.
[U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Bromomethane (74-83-9) Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000]**PEER REVIEWED**

A4. Not classifiable as a human carcinogen.
[American Conference of Governmental Industrial Hygienists. TLVs and BEIs. Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati, OH. 2000. 47]**PEER REVIEWED**

Great Lakes Chemical Corporation and the Pathfinders Camp