Methyl iodide

Hazardous Air Pollutants (HAPs)

Toxic Gases & Vapors -> Other Toxic Gases & Vapors

Pesticide -> EPA IRIS

Volatile Organic Compound (VOC) (Pesticide/Volatile Organic Compound (VOC))

log Kow= 1.51

1.51

2.279 at 68 °F (USCG, 1999) - Denser than water; will sink

2.28 @ 20 °C/4 °C

DENSITY OF SATURATED AIR: 3.04 (AIR= 1)

Relative density (water = 1): 2.3

2.28

2.2789 @ 20°C

0.606 cP at 0 °C, 0.424 cP at 40 °C.

0.18 mm²/s at 40 °C

10 to 50 mg/mL at 64 °F (NTP, 1992)

Miscible with alcohol, ether.

Sol in acetone

SOL IN CARBON TETRACHLORIDE

1.39X10+4 mg/l at 20 °C in water

Solubility in water, g/100ml at 20 °C: 1.4

108.3 °F at 760 mmHg (NTP, 1992)

42.5 °C

42.5 °C

109 °F

42.43 °C @760 [mm Hg]

109 °F

-87.6 °F (NTP, 1992)

-66.5 °C

-66.5 °C

-88 °F

-66.4 °C

-88 °F

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P203, P261, P264, P270, P271, P280, P301+P316, P302+P352, P304+P340, P316, P317, P318, P319, P321, P330, P332+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.4% (1 of 264) of reports.

Danger

H226 (42.8%): Flammable liquid and vapor [Warning Flammable liquids]

Chemical: Methane, iodo-

Hazard Traits - Carcinogenicity; Neurotoxicity; Respiratory Toxicity

Methane, iodo- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Methane, iodo- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 03-08-2021 https://echa.europa.eu/registration-dossier/-/registered-dossier/12834

Iodomethane: HSNO Approval: HSR003006 Approved with controls

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Special Hazards of Combustion Products: Toxic and irritating gases are generated when exposed to fire or heat.

· Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

Inhalation of vapor causes lung congestion and pulmonary edema. Higher concentrations causes rapid narcosis and death. Contact with liquid irritates eyes and burns skin. (USCG, 1999)

· Highly toxic, may be fatal if inhaled, ingested or absorbed through skin.

Methyl iodide is used as an intermediate in the manufacture of some pharmaceuticals and pesticides, in methylation processes, and in the field of microscopy. In humans, acute (short-term) exposure to methyl iodide by inhalation may depress the central nervous system (CNS), irritate the lungs and skin, and affect the kidneys. Massive acute inhalation exposure to methyl iodide has led to pulmonary edema. Acute inhalation exposure of humans to methyl iodide has resulted in nausea, vomiting, vertigo, ataxia, slurred speech, drowsiness, skin blistering, and eye irritation. Chronic (long-term) exposure of humans to methyl iodide by inhalation may affect the CNS and cause skin burns. EPA has not classified methyl iodide for potential carcinogenicity.

Liquid causes second degree burns after contact for a few minutes. [CHRIS] Corrosive to skin; [Quick CPC] In animal feeding studies, methyl iodide is hepatotoxic, ten times as acutely toxic as carbon tetrachloride. After an industrial accident, an exposed chemical plant worker developed symptoms of central nervous system poisoning and died. [ACGIH] Inhalation can cause pulmonary edema, CNS depression, and death; [CAMEO] A lachrymator; [CHEMINFO] It is an acute pulmonary irritant that can cause chronic neurological symptoms after a heavy dermal exposure. [Reference #1]

2644 151

2644 151

Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:

In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep drums, etc., cool by spraying with water.

Fresh air, rest. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Give a slurry of activated charcoal in water to drink. Refer immediately for medical attention.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

General First Aid:

(General first aid procedures)

· Wear positive pressure self-contained breathing apparatus (SCBA).

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

Self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive-pressure mode.

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself dose not burn or burns with difficulty.) Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Keep run-off water out of sewers and water sources.

Keep containers closed and store in a dark place.

... MATERIALS WHICH ARE TOXIC AS STORED OR WHICH CAN DECOMPOSE INTO TOXIC COMPONENTS DUE TO CONTACT WITH HEAT, MOISTURE, ACID, OR ACID FUMES, SHOULD BE STORED IN COOL, WELL-VENTILATED PLACE, OUT OF DIRECT RAYS OF SUN, AWAY FROM AREAS OF HIGH FIRE HAZARD & SHOULD BE PERIODICALLY INSPECTED & MONITORED.

1. VENTILATE AREA OF SPILL OR LEAK. 2. COLLECT FOR RECLAMATION OR ABSORB IN VERMICULITE, DRY SAND, EARTH, OR SIMILAR MATERIAL.

/In laboratory/ absorb the spills with paper towels, or like materials. Place in hood to evaporate. Dispose by burning the towel.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U138, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

A potential candidate for liquid injection incineration at a temperature range of 650 to 1,600 °C and a residence time of 0.1 to 2 seconds. A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 °C and residence times of seconds for liquids and gases, and hours for solids. A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 °C and residence times of seconds for liquids and gases, and longer for solids.

Evacuate danger area! Consult an expert! Personal protection: self-contained breathing apparatus. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

... SYNERGIZES TOXICITY OF FENITROTHION ELEVEN FOLD & DICHLOROVOS TWO FOLD /IN MOUSE LIVER/.

S-Methyl-N-acetylpenicillamine, S-methylthiol, and S-methylcysteine, as well as iodomethane decreased biliary excretion of methylmercury markedly. Excretion of sulfhydryl in bile was not influenced by S-methylcysteine, S-methylthiol, S-methyl-N-acetylpenicillamine or a low dose of iodomethane (0.5 mmol/kg). This indicated that coupling of methylmercury to glutathione in the liver before biliary excretion was glutathione S-transferase-dependent reaction and the methylthiols tested, or metabolites of these compounds were likely to be inhibitors of S-transferase. The effect of S-methylcysteine and low doses of iodomethane (1 mmol/kg) seem to deplete the liver of reduced glutathione through S-methylation as illustrated by decreased biliary excretion of sulfhydryl.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 14(SRC), determined from a structure estimation method(2), indicates that methyl iodide should have very high mobility in soil(SRC). Volatilization of methyl iodide from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 0.00526 atm-cu m/mole at 25 °C(3). The potential for volatilization of methyl iodide from dry soil surfaces may exist based upon a vapor pressure of 405 mm Hg(4). Cumulative volatilization losses of methyl iodide, applied at 30 cm, from 60-cm soil columns packed with a sandy loam soil ranged from 94% when the soil was untarped to 75% with a high-barrier tarp(5). Volatilization losses were significantly lower, 38% and 53%, from soils high in organic matter and capable of rapidly degrading the chemical. Ten days after methyl iodide was applied to field plots (30 cm depth) covered with a polyethylene film, methyl iodide was detected at most depths(5). It was concluded that should the water table be shallow and the degradation rate in soil low, methyl iodide may leach into ground water(5). Methyl iodide abiotically degrades in soil by hydrolysis and reaction with chloride ions, HS- and other nucleophiles(6). The half-life of methyl iodide in soils that were rich in organic matter was 9-13 days, while in a sandy loam soil it was 42-63 days. The organic-rich soils were thought to contain more nucleophiles with which methyl iodide could react(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 14(SRC), determined from an estimation method(2), indicates that methyl iodide is not expected to adsorb to suspended solids and sediment in water(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 0.00526 atm-cu m/mole at 25 °C(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 1.3 hours and 4.8 days, respectively(SRC). Methyl iodide hydrolyses slowly in water with a half-life of 110-251 days at 20-25 °C(8,9). It reacts with chloride ions in seawater in which its half-life is 20 and 58 days at 19.2 and 10.8 °C, respectively(8). According to a classification scheme(5), an estimated BCF of 2.9(SRC), from its log Kow of 1.51(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low.

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), methyl iodide, which has a vapor pressure of 405 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase methyl iodide is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 220 days(SRC), from its rate constant of 7.20X10-14 cu cm/molecule-sec at 25 °C(3). However the major loss process for methyl iodide in the atmosphere is direct photolysis. The half-life of this reaction is 2.8-5.5 days(3,4). Physical removal of methyl iodide from air may occur via wet deposition since methyl iodide is relatively soluble in water(SRC).

The substance can be absorbed into the body by inhalation of its vapour and by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

Cough. Sore throat. Nausea. Vomiting. Diarrhoea. Headache. Dizziness. Drowsiness. Weakness. Convulsions. Confusion. Death Symptoms may be delayed.

Redness. Pain.

Redness. Pain.

See Inhalation.

irritation eyes, skin, respiratory system; nausea, vomiting; dizziness, ataxia; slurred speech, drowsiness; dermatitis; [potential occupational carcinogen]

Physical examination of workers for placement in operations involving possible exposure to these alkylating agents should include consideration of increased personal risk due to cigarette smoking, pregnancy, or treatment with steroids or cytotoxic agents. /Alkylating agents/

IN HUMANS EXPOSED TO METHYL IODIDE, SERUM LIPID CONTENT, ESP THE TRIGLYCERIDE CONTENT WAS SHARPLY INCR, WITH NO APPARENT NERVOUS DISORDER. THUS, BLOOD EXAM, ESP SERUM LIPID, & FUNCTIONAL EXAM OF LIVER & KIDNEY, MAY BE USED FOR EARLY DETECTION OF METHYL IODIDE POISONING.

Initial Medical Examination: A complete history and physical examination: The purpose is to detect pre-existing conditions that might place the exposed employee at increased risk, and to establish a baseline for future health monitoring. Examination of the central nervous system should be stressed. The skin should be examined for evidence of chronic disorders. Periodic Medical Examination: The aforementioned medical examinations should be repeated on an annual basis.

Using a structure estimation method based on molecular connectivity indices(1), the Koc for methyl iodide can be estimated to be 14(SRC). According to a classification scheme(2), this estimated Koc value suggests that methyl iodide should have very high mobility in soil. The soil/water distribution coefficient of methyl iodide in various soils were (soil, Kd): Greenfield sandy loam, 0.09; Linne clay loam, 0.15; Carsetas loamy sand, 0.16; and potting mix, 0.55(3).

U138; As stipulated in 40 CFR 261.33, when methyl iodide, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Methyl iodide is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Toxicologic and metabolic similarities among the monohalomethanes (chloride, bromide, iodide substituted) suggest a common mechanism of toxic action, probably methylation and disturbance or inactivation of essential proteins (rather than presence of the parent compound or free halide per se).

ORAL DOSES OF IODOMETHANE TO RATS WERE RAPIDLY CONVERTED INTO S-METHYLGLUTATHIONE IN LIVER & EXCRETED IN BILE. IT WAS DEGRADED TO S-METHYLCYSTEINE BY KIDNEY HOMOGENATES. ONLY A SMALL PROPORTION OF THE DOSE OF IODOMETHANE OR ITS METABOLITE, S-METHYLCYSTEINE, WAS EXCRETED AS A CMPD RELATED TO METHYLMERCAPTURIC ACID.

Urinary metabolites (2 percent of the total dose) detected after subcutaneous injection of rats with 50 mg/kg body weight methyl iodide were S-methylcysteine, N-acetyl-S-methylcysteine, S-methylthio-acetic acid and N-(methylthioacetyl)glycine. ... S-Methylglutathione was isolated from livers of rats treated orally with 90 mg/kg body weight methyl iodide; approximately 25% of an oral dose of 50 mg/kg body weight was excreted into the bile as S-methylglutathione. ... Liver and kidney homogenates catalyzed the disappearance of methyl iodide in the presence of glutathione ... . S-Methylglutathione was converted to S-methylcysteine by kidney homogenate.

Methyl iodide reacted in vitro with 4-(para-nitrobenzyl)pyridine and N-7-deoxy- guanosine.

After inhalation of trace amounts of I-methyl iodide, the disappearance of radioactivity from the plasma, uptake in the thyroid and excretion in the urine resembled that of orally administered inorganic iodide.

1-iodomethane has known human metabolites that include methylglutathione.

RETENTION OF INHALED (132)I-METHYL IODIDE IN 18 VOLUNTEERS RANGED FROM 43-92%, WITH MEAN OF 72% OF AMT INHALED; LEVEL WAS HIGHLY DEPENDENT ON RESP RATE, LOW RATES ... ASSOC WITH HIGH RETENTION & VICE VERSA ... INHALED (132)I-METHYL IODIDE WAS RAPIDLY CLEARED FROM LUNGS OF 4 VOLUNTEERS & BROKEN DOWN TO RELEASE IODIDE ION.

ORALLY ADMIN METHYL IODIDE WAS ... EXCRETED IN BILE OF RAT (22-28% OF 50 MG/KG BODY WT DOSE) ...

IN POISONED RABBITS METHYL IODIDE WAS FOUND IN BRAIN, LIVER & KIDNEYS.

Approximately 1% of an oral dose of 76 mg/kg body weight methyl iodide given to rats was expired unchanged within 30 min of administration.

Methyl iodide is used as an intermediate in the manufacture of some pharmaceuticals and pesticides. It is also used in methylation processes and in the field of microscopy. Proposed uses of methyl iodide are as a fire extinguisher and as an insecticidal fumigant.

Used as a methylating agent; used in microscopy because of its high refractive index; [ACGIH]

Methylating agent; in microscopy because of its high refractive index; as imbedding material for examining diatoms; in testing for pyridine. Light sensitive etching agent for electronic circuits; component in fire extinguishers.

2023: 75,000 - <500,000 lb

(1971) 9,000 lb sold

(1972) 18,000 lb

(1977) Iodinated hydrocarbons: 58,000 lb

(1977) AT LEAST 4.99X10+6 G

For more U.S. Production (Complete) data for METHYL IODIDE (9 total), please visit the HSDB record page.

Prepd from methyl alcohol, iodine and red phosphorus; from potassium iodide and methyl sulfate.

From potassium iodide and methyl p-toluenesulfonate; by reaction of dimethyl sulfate with an aqueous iodine slurry containing a reducing agent such as iron or sodium bisulfite; by reaction of methanol and hydrogen iodide; and by reaction of methanol, iodine, and diborane.

Pharmaceutical and Medicine Manufacturing

Methane, iodo-: ACTIVE

... COMMERCIAL PRODN ... IN USA WAS FIRST REPORTED IN 1943, WHEN ABOUT 1400 KG WERE MANUFACTURED ...

Methyl iodide has been investigated in India for use as a fumigant to control internal fungi of grain sorghum.