United States
Environmental Protection
1=1 m m Agency
Provisional Peer-Reviewed Toxicity Values for
Iodomethane (Methyl Iodide)
(CASRN 74-88-4)
Superfund Health Risk Technical Support Center
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268

Benchmark Dose
Integrated Risk Information System
inhalation unit risk
lowest-observed-adverse-effect level
LOAEL adjusted to continuous exposure duration
LOAEL adjusted for dosimetric differences across species to a human
no-ob served-adverse-effect level
NOAEL adjusted to continuous exposure duration
NOAEL adjusted for dosimetric differences across species to a human
no-ob served-effect level
oral slope factor
provisional inhalation unit risk
provisional oral slope factor
provisional inhalation reference concentration
provisional oral reference dose
inhalation reference concentration
oral reference dose
uncertainty factor
animal to human uncertainty factor
composite uncertainty factor
incomplete to complete database uncertainty factor
interhuman uncertainty factor
LOAEL to NOAEL uncertainty factor
subchronic to chronic uncertainty factor

On December 5, 2003, the U.S. Environmental Protection Agency's (U.S. EPA) Office of
Superfund Remediation and Technology Innovation (OSRTI) revised its hierarchy of human
health toxicity values for Superfund risk assessments, establishing the following three tiers as the
new hierarchy:
1)	U.S. EPA's Integrated Risk Information System (IRIS).
2)	Provisional Peer-Reviewed Toxicity Values (PPRTVs) used in U.S. EPA's Superfund
3)	Other (peer-reviewed) toxicity values, including
~	Minimal Risk Levels produced by the Agency for Toxic Substances and Disease
Registry (ATSDR),
~	California Environmental Protection Agency (CalEPA) values, and
~	EPA Health Effects Assessment Summary Table (HEAST) values.
A PPRTV is defined as a toxicity value derived for use in the Superfund Program when
such a value is not available in U.S. EPA's IRIS. PPRTVs are developed according to a
Standard Operating Procedure (SOP) and are derived after a review of the relevant scientific
literature using the same methods, sources of data, and Agency guidance for value derivation
generally used by the U.S. EPA IRIS Program. All provisional toxicity values receive internal
review by two U.S. EPA scientists and external peer review by three independently selected
scientific experts. PPRTVs differ from IRIS values in that PPRTVs do not receive the
multiprogram consensus review provided for IRIS values. This is because IRIS values are
generally intended to be used in all U.S. EPA programs, while PPRTVs are developed
specifically for the Superfund Program.
Because new information becomes available and scientific methods improve over time,
PPRTVs are reviewed on a 5-year basis and updated into the active database. Once an IRIS
value for a specific chemical becomes available for Agency review, the analogous PPRTV for
that same chemical is retired. It should also be noted that some PPRTV documents conclude that
a PPRTV cannot be derived based on inadequate data.
Users of this document should first check to see if any IRIS values exist for the chemical
of concern before proceeding to use a PPRTV. If no IRIS value is available, staff in the regional
Superfund and Resource Conservation and Recovery Act (RCRA) program offices are advised to
carefully review the information provided in this document to ensure that the PPRTVs used are
appropriate for the types of exposures and circumstances at the Superfund site or RCRA facility
in question. PPRTVs are periodically updated; therefore, users should ensure that the values
contained in the PPRTV are current at the time of use.
It is important to remember that a provisional value alone tells very little about the
adverse effects of a chemical or the quality of evidence on which the value is based. Therefore,
users are strongly encouraged to read the entire PPRTV document and understand the strengths

and limitations of the derived provisional values. PPRTVs are developed by the U.S. EPA
Office of Research and Development's National Center for Environmental Assessment,
Superfund Health Risk Technical Support Center for OSRTI. Other U.S. EPA programs or
external parties who may choose of their own initiative to use these PPRTVs are advised that
Superfund resources will not generally be used to respond to challenges of PPRTVs used in a
context outside of the Superfund Program.
Questions Regarding PPRTVs
Questions regarding the contents of the PPRTVs and their appropriate use (e.g., on
chemicals not covered, or whether chemicals have pending IRIS toxicity values) may be directed
to the U.S. EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
No RfD, RfC, or carcinogenicity assessments for iodomethane are available on IRIS
(U.S. EPA, 1995), and IRIS does not currently list a weight-of-evidence classification for
carcinogenicity. No information on iodomethane is available in the HEAST (U.S. EPA, 1997) or
in the Drinking Water Standards and Health Advisories List (U.S. EPA, 2006). A cancer
evaluation document (U.S. EPA, 1988) was the only U.S. EPA review located. In that
document, the U.S. EPA (1988) considered the existing data to be inadequate to calculate a slope
factor. Using the criteria outlined in the 1986 Guidelines for Carcinogen Risk Assessment
(U.S. EPA, 1986), U.S. EPA (1988) assigned iodomethane to weight-of evidence Group C,
"Possible human carcinogen," on the basis of no evidence in humans and limited evidence in
animals (production of sarcomas in BD rats administered iodomethane subcutaneously and
equivocal evidence for production of lung tumors in Strain A mice administered iodomethane by
intraperitoneal injection). No other EPA documents relevant to human toxicity or cancer
assessments for iodomethane have been identified in the CARA list (U.S. EPA 1991, 1994).
Other sources of information were consulted for dose-response data on iodomethane.
IARC (1977, 1986, and 1999) has reviewed the toxicity and carcinogenicity of iodomethane
several times. An early evaluation by the IARC (1977) classified iodomethane as carcinogenic
in rats. Two subsequent evaluations (IARC, 1986, 1999) determined that there is limited
evidence for the carcinogenicity of iodomethane in experimental animals and that the compound
is not classifiable as to its carcinogenicity to humans (i.e., weight-of-evidence Group 3).
ACGIH (2001) has also reviewed iodomethane carcinogenicity and classified iodomethane as
category A2, suspected human carcinogen, from 1981 to 1995; however, the A2 classification
was withdrawn in 1996 (ACGIH, 2001). Both the NTP Health and Safety (NTP, 2002a) and the
Testing Information and Study Results (NTP, 2002b) databases for iodomethane were searched.
Iodomethane was delisted as a carcinogen in the NTP 5th Annual Report on Carcinogens on the
basis of the 1986 IARC reevaluation (NTP, 2001). NTP (2002a,b) has not tested iodomethane
for carcinogenicity. The State of California determined under Proposition 65 that methyl iodide
is a carcinogen (CalEPA, 2009), based on the 1977 IARC evaluation. Neither a Toxicological
Profile (ATSDR, 2008) nor an Environmental Health Criteria Monograph (WHO, 2009) has
been published for iodomethane.

Literature searches were conducted for the interval from January 1965 to November 2001
to identify relevant studies. The following databases were examined in the search: TOXLINE,
DART/ETICBACK, CHEMID, BIOSIS, NTIS, and RTECS. A subsequent check of the
published literature was conducted for the interval from June 2002 to July 2009.
Human Studies
No relevant studies on the toxicity or carcinogenicity of iodomethane in humans
following oral or inhalation exposure have been identified.
Animal Studies
Oral Exposure
Subchronic Studies—No chronic oral toxicity or cancer bioassays are available for
iodomethane. Buckell, (1950) determined an LD50 of 0.15 to 0.22 mg/kg, for male white mice
dosed with iodomethane dissolved in arachis oil. In the only available longer-term oral exposure
study, Buckell (1950) gave iodomethane (0; 100; 200; 300; and 500 mg/kg-dose; source and
purity not stated) orally to male mice (six mice per dose) for a total of 43 doses over a 71 day
period. The duration adjusted doses were 0; 61; 121; 182; and 303 mg/kg-day respectively. The
body weight of mice dosed with 303 mg/kg-day was "considerably less than in the controls" but
there was no quantification or significance testing reported. The NOAEL for this effect was
121 mg/kg-day. The test animals were sacrificed at the termination of the study without a
comprehensive histological examination. No additional details of the study were provided in
U.S. EPA (1988). This study does not support assessments of oral toxicity or carcinogenicity
because of its short duration and absence of histopathological examination. No subchronic or
chronic oral exposure studies of iodomethane in experimental animals, having the potential to
support toxicity value derivation, were identified.
Chronic Studies—No oral studies of chronic exposure have been identified in the
published literature.
Inhalation Exposure
Subchronic Studies—Short-term (approximately 1 month) inhalation exposure studies
have been performed in mice (i.e., Buckell, 1950) and rats (i.e., Blank et al., 1983). In a
whole-body inhalation study with male white mice, Buckell (1950) reported renal changes
(degeneration of tubular epithelium and numerous eosinophilous casts) in mice receiving 1 g/m3
of iodomethane (source and purity not stated) in 20 exposures over 30 days. The NOAEL for
renal effects was 500 mg/m3. The total exposure periods ranged from 11 to 43 hours.
Incomplete reporting precludes quantification of the exposures. Blank et al. (1983) reported a
significant (p < 0.01) reduction in body weight gain at the mid-dose and high-dose (421 and
3	3
810 mg/m respectively purity = 86.4%). The low-dose (141 mg/m ) was a NOAEL for all the
observed effects. These studies were not designed to evaluate chronic inhalation toxicity, and no
neoplastic alterations were observed. Subchronic data are available from a 14-week inhalation
study conducted in Sprague-Dawley rats by the Monsanto Company. This study is described in a
published abstract (i.e., Blank et al., 1984) and in an unpublished research report (i.e.,

Blank et al., 1985). The subchronic study did not produce any evidence of neoplastic lesions and
was of much shorter duration than the 50 to 100 week cancer bioassays.
Chronic Studies—No inhalation studies of chronic exposure have been identified in the
published literature.
Other Routes of Administration
Two studies have examined the tumorigenicity of iodomethane administered by
nonstandard routes. Druckrey et al. (1970) gave BD rats (8-16/group; sex unspecified)
subcutaneous injections of iodomethane in vegetable oil. Groups of test animals received weekly
doses of 10 or 20 mg/kg for 1 year, or a single dose of 50 mg/kg, and were observed for life. A
control group (number unspecified) received the vehicle alone. Local subcutaneous sarcomas
occurred 500-700 days after the first injection in 8/16 (50%) rats injected with 10 mg/kg, in
6/8 (75%) rats injected with 20 mg/kg, and in 4/14 (29%) rats injected with the single 50 mg/kg
dose, as reported in U.S. EPA (1988). No tumors were reported in the vehicle control group.
The results of this study have been reported differently in other publications. IARC (1977)
reported incidences of 9/16 and 6/8 for the 10- and 20-mg/kg-day groups, respectively. IARC
(1986) reported incidences of 9/12 and 6/6 for the 10- and 20-mg/kg-day groups, respectively,
after adjustment of the incidence data for premature death of some test animals from pneumonia.
No quantitative assessment of iodomethane carcinogenicity is possible because the animals were
dosed by subcutaneous injection—which is not comparable with either oral or inhalation dosing.
Poirier et al. (1975) administered iodomethane dissolved in tricaprylin to male and
female Strain A mice (10/sex/dose) three times weekly by intraperitoneal injection. The dosing
schedule resulted in total doses of 8.5, 21.3, or 44.0 mg/kg in three treated groups plus one
untreated group and a vehicle control. Surviving mice were sacrificed 24 weeks after the first
injection. The incidence of lung tumors (adenomas) in surviving animals of both sexes
(combined) was 4/19 (21%), 6/20 (30%), and 5/11 (45%) in the three groups, respectively. The
incidence of lung tumors was 34/154 (22%) in vehicle control animals and 6/29 (21%) in
untreated animals. There was a marginally statistically significant (p = 0.048) trend for increased
lung tumor incidence in treated mice compared with vehicle—but not untreated—controls.
Pairwise comparisons showed no significant (p < 0.05) differences between treated and control
mice. This outcome is considered equivocal evidence of carcinogenicity because the observed
results did not meet all of the predetermined criteria for a positive response in Strain A mice,
which include (1) a statistically significant increase in the mean number of lung tumors per
animal, (2) a clear dose-response relationship, and (3) the anticipated number of spontaneous
tumors in untreated control mice. Consequently, no quantitative assessment of iodomethane
carcinogenicity is possible
Other Studies
The mutagenicity of iodomethane has been assessed in multiple test systems in both the
presence and absence of exogenous metabolic activation (Bolt and Gansewendt, 1993;
IARC, 1999). Results of these studies have been mixed. Positive or weakly positive results have
been obtained in bacterial reverse mutation assays conducted without exogenous metabolic
activation in Salmonella typhimurium test strains TA100 (McCann et al., 1975;
Simmon et al., 1977) and TA1535 (Rosenkranz and Poirier, 1979); and in Escherichia coli
strains WP2 uvr (Hemminki et al., 1980) and WP2 (Takahashi and Kawazoe, 1987). The E. coli
spot test was also positive without activation (Rosenkranz and Poirier, 1979). Negative results

for reverse mutation assays were obtained with and without metabolic activation in
S. typhimurium strains TA98, TA100, TA1535, TA1536, TA1537 (Simmon, 1979a), and
TA1538 (Rosenkranz and Poirier, 1979; Simmon, 1979a). Among lower eukaryotes, positive
results were obtained for mitotic conversion in Saccharomyces cerevisiae without metabolic
activation (Simmon, 1979b), while negative results were found for mutation in Aspergillus
nidulans (Moura Duarte, 1972). Iodomethane did not induce chromosomal aberrations in the
plant Vicia faba (Rieger et al., 1988). In mammalian studies, positive or weakly positive results
were obtained for mutagenic potential in Chinese hamster ovary cells at the hprt locus
(Amacher and Zelljadt, 1984); in mouse lymphoma L5178Y cells at the tk locus
(Clive et al., 1979; Moore and Clive, 1982; Moore et al., 1985) and the hprt locus (Moore and
Clive, 1982); and in mouse lymphoma L5178Y cells for ouabain resistance (Amacher and
Dunn, 1985). Negative results were obtained for gene mutation in mouse lymphoma L5178Y
cells with exogenous activation (Clive et al.1979). Cell transformation assays were positive in
Syrian hamster embryo cells (Pienta et al., 1977) but negative in C3H 10T1/2 mouse cells
(Oshiro et al., 1981) without exogenous metabolic activation. Assays for covalent binding to
DNA in F344 rats following oral or inhalation exposure in vivo were positive
(Gansewendt et al., 1991).
Additional information, not summarized in this document, is available from the
U.S. EPA, Office of Pesticide Programs (OPP). Because iodomethane is a currently registered
pesticide, many potentially useful studies have been submitted to the OPP as confidential
business information (CBI). This information is unpublished and is unavailable for use in this
assessment. The OPP maintains its own program for developing health-based values (i.e. RfDs
and RfCs) for pesticides. Consequently, no values will be developed here.
A provisional oral reference dose (p-RfD) are not derived for iodomethane because
iodomethane is a currently registered pesticide. Additional information can be obtained by
contacting the U.S. EPA, Office of Pesticide Programs.
A provisional inhalation reference concentration (p-RfC) are not derived for iodomethane
because iodomethane is a currently registered pesticide. Additional information can be obtained
by contacting the U.S. EPA, Office of Pesticide Programs.

Weight-of-Evidence Descriptor
Under the 2005 Guidelines for Carcinogen Risk Assessment (U.S. EPA, 2005), the lack
of available evidence suggests that there is "inadequate information to assess the carcinogenic
potential" of iodomethane.
Quantitative Estimates of Carcinogenic Risk
Oral Exposure
A provisional oral slope factor (p-OSF) are not derived for iodomethane because
iodomethane is a currently registered pesticide. Further, existing tumor incidence data are not
suitable for derivation of an oral slope factor because they were obtained from studies using
parenteral routes (e.g. i.p injection) of administration. The parenteral route bypasses normal
metabolism of the test agent by the liver and is not representative of oral exposure. Additional
information can be obtained by contacting the U.S. EPA, Office of Pesticide Programs.
Inhalation Exposure
A provisional inhalation unit risk (p-IUR) are not be derived for iodomethane because
iodomethane is a currently registered pesticide. Additional information can be obtained by
contacting the U.S. EPA, Office of Pesticide Programs.
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Amacher, D.E. and I. Zelljadt. 1984. Mutagenic activity of some clastogenic chemicals at the
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