Methyl bromide, a potent alkylating agent, is an odorless, colorless, extremely toxic gas used as a fumigant in soil, perishable foods, cargo containers, and nonresidential buildings. Commercially known as Halon 1001, methyl bromide was used (until the 1960s) as a refrigerant and fire extinguisher. Fields or buildings to be fumigated are evacuated and covered with a tarp, and the gas is introduced. After 12-24 hours, the tarp is removed, and the area is ventilated and then tested for residual methyl bromide before reoccupation. Methyl bromide is a major source of ozone-destroying bromine in the stratosphere, and most production and use were scheduled to be phased out by 2005 in developed countries and by 2015 in developing countries; however, it is still being used in the United States owing to EPA critical use exemptions.

1. Methyl bromide is a potent, nonspecific alkylating agent with a special affinity for sulfhydryl and amino groups. Limited data indicate that toxicity is the result of direct alkylation of cellular components (eg, glutathione, proteins, or DNA) or formation of toxic metabolites from methylated glutathione. Animal data clearly indicate that its toxicity does not result from the bromide ion.
2. Pharmacokinetics. Inhaled methyl bromide is distributed rapidly to all tissues and metabolized. In sublethal animal studies, approximately 50% is eliminated as exhaled carbon dioxide, 25% is excreted in urine and feces, and 25% is bound to tissues as a methyl group. The elimination half-life of the bromide ion is 9-15 days.

Methyl bromide is threefold heavier than air, may accumulate in low-lying areas, and may seep via piping or conduits from fumigated buildings into adjacent structures. It may condense to a liquid at cold temperatures (3.6°C [38.5°F]), then vaporize when temperatures rise. Methyl bromide gas lacks warning properties, so the lacrimator chloropicrin (2%) usually is added. However, chloropicrin has a different vapor pressure and may dissipate at a different rate, limiting its warning properties.

1. Inhalation is the most important route of exposure. The ACGIH-recommended workplace exposure limit (TLV-TWA) in air is 1 ppm (3.9 mg/m³) as an 8-hour time-weighted average. Toxic effects generally are seen at levels of 200 ppm, and the air level considered immediately dangerous to life or health (IDLH) is 250 ppm. NIOSH considers methyl bromide a potential occupational carcinogen.
2. Skin irritation and absorption may occur, causing burns and systemic toxicity. Methyl bromide may penetrate clothing and some protective gear. Retained gas in clothing and rubber boots can be a source of prolonged dermal exposure.

1. Acute irritant effects on the eyes, mucous membranes, and upper respiratory tract are attributed to the added lacrimator chloropicrin. (Lethal exposures can occur without warning if chloropicrin has not been added.) Moderate skin exposure can result in dermatitis and, in severe cases, chemical burns.
2. Acute systemic effects usually are delayed by 2-24 hours. Initial toxicity may include malaise, visual disturbances, headache, nausea, vomiting, and tremor, which may advance to intractable seizures and coma. Death may be caused by fulminant respiratory failure with noncardiogenic pulmonary edema or complications of status epilepticus. Sublethal exposure may result in flulike symptoms, respiratory complaints, or chronic effects.
3. Chronic neurologic sequelae can result from chronic exposure or a sublethal acute exposure. A wide spectrum of neurologic and psychiatric problems may occur that may be reversible (months to years) or irreversible. They include agitation, delirium, dementia, psychoneurotic symptoms, psychosis, visual disturbances, vertigo, aphasia, ataxia, peripheral neuropathies, myoclonic jerking, tremors, and seizures.

Is based on a history of exposure to the compound and on clinical presentation.

1. Specific levels. Bromide levels in patients with acute methyl bromide exposure are usually well below the toxic range for bromism and may be only mildly elevated compared with levels in unexposed persons (see “Bromides,”). Nontoxic serum bromide levels do not rule out methyl bromide poisoning. Levels of methylated proteins or DNA have been investigated as possible biomarkers of exposure.
2. Other useful laboratory studies include electrolytes, glucose, BUN, and creatinine. If there is respiratory distress, perform blood gases or oximetry and chest radiography.

1. Emergency and supportive measures
   1. Administer supplemental oxygen and treat bronchospasm, pulmonary edema, seizures, and coma if they occur. Intractable seizures usually predict a fatal outcome. Consider induction of barbiturate coma with a short-acting agent such as pentobarbital.
   2. Monitor patients for a minimum of 6-12 hours to detect development of delayed symptoms, including seizures and noncardiogenic pulmonary edema.
2. Specific drugs and antidotes. Theoretically, N-acetylcysteine (NAC) or dimercaprol (BAL) can offer a reactive sulfhydryl group to bind free methyl bromide, although neither agent has been critically tested. There were strikingly different outcomes for two patients with the same exposure but different glutathione transferase activity, suggesting that NAC can possibly exacerbate toxicity. Neither agent can be recommended at this time.
3. Decontamination. Properly trained personnel should use self-contained breathing apparatus and chemical-protective clothing before entering contaminated areas. The absence of irritant effects from chloropicrin does not guarantee that it is safe to enter without protection.
   1. Remove victims from exposure and administer supplemental oxygen if available.
   2. If exposure is to liquid methyl bromide, remove contaminated clothing and wash affected skin with soap and water. Irrigate exposed eyes with copious water or saline.
4. Enhanced elimination. There is no role for these procedures.