United States
Environmental Protection
1=1 m m Agency
EPA/690/R-09/028F
Final
9-30-2009
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

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COMMONLY USED ABBREVIATIONS
BMD
Benchmark Dose
IRIS
Integrated Risk Information System
IUR
inhalation unit risk
LOAEL
lowest-observed-adverse-effect level
LOAELadj
LOAEL adjusted to continuous exposure duration
LOAELhec
LOAEL adjusted for dosimetric differences across species to a human
NOAEL
no-ob served-adverse-effect level
NOAELadj
NOAEL adjusted to continuous exposure duration
NOAELhec
NOAEL adjusted for dosimetric differences across species to a human
NOEL
no-ob served-effect level
OSF
oral slope factor
p-IUR
provisional inhalation unit risk
p-OSF
provisional oral slope factor
p-RfC
provisional inhalation reference concentration
p-RfD
provisional oral reference dose
RfC
inhalation reference concentration
RfD
oral reference dose
UF
uncertainty factor
UFa
animal to human uncertainty factor
UFC
composite uncertainty factor
UFd
incomplete to complete database uncertainty factor
UFh
interhuman uncertainty factor
UFl
LOAEL to NOAEL uncertainty factor
UFS
subchronic to chronic uncertainty factor
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PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR
IODOMETHANE (CASRN 74-88-4)
Background
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
Program.
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.
Disclaimers
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
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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.
INTRODUCTION
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.
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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,
MEDLINE, TSCATS, GENETOX, HSDB, CANCERLIT, CCRIS, EMIC/EMICBACK,
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.
REVIEW OF THE PERTINENT LITERATURE
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.,
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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
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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.
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC ORAL
RfD VALUES FOR IODOMETHANE
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.
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC ORAL
RfC VALUES FOR IODOMETHANE
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.
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PROVISIONAL CARCINOGENICITY ASSESSMENT
FOR IODOME THANE
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.
REFERENCES
ACGIH (American Conference of Government Industrial Hygienists). 2001. Documentation of
the Threshold Limit Values and Biological Exposure Indices, 7th ed. Cincinnati, OH.
Amacher, D.E. and E.M. Dunn. 1985. Mutagenesis at the ouabain-resistance locus of 3.7.2C
L5178Y cells by chromosomal mutagens. Environ. Mutagen. 7: 523-533.
Amacher, D.E. and I. Zelljadt. 1984. Mutagenic activity of some clastogenic chemicals at the
hypoxanthine guanine phosphoribosyl transferase locus of Chinese hamster ovary cells. Mutat.
Res. 136: 137-145.
ATSDR (Agency for Toxic Substances and Disease Registry). 2008. Internet HazDat-
Toxicological Profile Query. Examined September, 2009. Online, http://www.atsdr.cdc.gov/
toxpro2.html.
Blank, T.L., M.V. Roloff and R.M. Polk. 1983. Report for study No. 810006: One-month
inhalation toxicity of methyl iodide to male and female Sprague-Dawley rats. Monsanto
Company, St. Louis, MO.
Blank, T.L., R.S. Nair, M.V. Roloff et al. 1984. Inhalation toxicity of methyl iodide in rats.
Fed. Am. Soc. Exp. Biol. 68th Annual Meeting, St. Louis, MO. (Cited in U.S.EPA, 1988).
6

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9-30-2009
Blank, T.L., W.E. Ribelin, and M.V. Roloff. 1985. Report for the study no. 810133: Three
month inhalation toxicity of methyl iodide to male and female Sprague-Dawley rats. Monsanto
Company, Environmental Health Laboratory. St. Louis, MO. (Cited in U. S. EPA, 1992a;
ACGM, 2001).
Bolt, H.M. and B. Gansewendt. 1993. Mechanisms of carcinogenicity of methyl halides. Crit.
Rev. Toxicol. 23: 237-253.
Buckell, M. 1950. The toxicity of methyl iodide: Preliminary survey. Brit. J. Ind. Med. 7:
122-124. (Cited in U.S. EPA, 1988).
CalEPA (California Environmental Protection Agency). 2009. Office of Environmental Health
Hazard Assessment: Proposition 65 List of Chemicals. Last updated November 15, 2001.
Online, http://www.oehha.ca.gov/prop65/prop65 list/files/P65single091009.pdf.
Clive, D., K.O. Johnson, J.F.S. Spector et al. 1979. Validation and characterization of the
L5178Y/TK+/" mouse lymphoma mutagen assay system. Mutat. Res. 59: 61-108.
Druckrey, H., H. Kruse, R. Preussmann et al. 1970. Carcinogenic alkylating substances. III.
Alkyl-halogenides, -sulphates, sulphonates, and strained heterocyclic compounds. Z.
Krebforsch. 74: 241-273. (German; Cited in IARC, 1977, 1986; U.S. EPA, 1988).
Gansewendt, B., D. Xu, U. Foest et al. 1991. DNA binding of methyl iodide in male and female
F344 rats. Carcinogenesis. 12: 463-467.
Hemminki, K., K. Falck and H. Vainio. 1980. Comparison of alkylation rates and mutagenicity
of directly acting industrial and laboratory chemicals: Epoxides, glycidyl ethers, methylating and
ethylating agents, halogenated hydrocarbons, hydrazine derivatives, aldehydes, thiuram and
dithiocarbamate derivatives. Arch. Toxicol. 46:277-285.
IARC (International Agency for Research on Cancer). 1977. IARC Monographs on the
Evaluation of Carcinogenic Risk of Chemicals to Man: Some Fumigants, The Herbicides 2,4-D
and 2,4,5-T, Chlorodibenzodioxins and Miscellaneous Industrial Chemicals. Lyon, France. 15:
245-254. Online. http://monoeraphs.iarc.fr/ENG/Monographs/vol 15/volumel5.pdf.
IARC (International Agency for Research on Cancer). 1986. IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans: Some Halogenated Hydrocarbons
and Pesticide Exposures. Lyon, France. 41:213-227. Online.
http://monographs.iarc.fr/ENG/Monographs/vol41/index.php.
IARC (International Agency for Research on Cancer). 1999. IARC Monograph on the
Evaluation of Carcinogenic Risks to Humans: Re-evaluation of Some Organic Chemicals,
Hydrazine and Hydrogen Peroxide. Lyon, France. 71(3): 1503-1510. Online.
http://monoeraphs.iarc.fr/ENG/Monoeraphs/vol71/index.php.
McCann, J., E. Choi, E. Yamasaki et al. 1975. Detection of carcinogens as mutations in the
Salmonella!microsome test: Assay of 300 chemicals. Proc. Natl. Acad. Sci. USA. 2:
5135-5139.
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9-30-2009
Moore, M.M. and D. Clive. 1982. The quantitation of TK+" and HGPRT" mutants of
L5178Y/TK+/" mouse lymphoma cells at varying times posttreatment. Environ. Mutagen. 4:
499-519.
Moore, M.M., D. Clive, B.E. Howard et al. 1985. In situ analysis of trifluorothymidine-resistant
(TFTr) mutants of L5 178Y/TK " mouse lymphoma cells. Mutat. Res. 151: 147-159.
Moura Duarte, F. A. 1972. Mutagenic effects of some inorganic acid esters in Aspergillus
nidulans (Eidam) winter. Cienc. Cult. 24:42-52. (Spanish; Cited in IARC, 1999).
NTP (National Toxicology Program). 2001. Ninth Report on Carcinogens. Appendix B.
Online, http://ehis.niehs.nih.gov/roc/toc9.html.
NTP (National Toxicology Program). 2002a. Health and Safety Report for Iodomethane.
Examined January 2002.
NTP (National Toxicology Program). 2002b.
January 8, 2002.
Oshiro, Y., P.S. Balwierz and S.V. Molinary.
C3H/10T1/2 CL8 cells by alkylating agents.
Testing Information and Study Results. Examined
1981. Morphological transformation of
Toxicol. Lett. 9: 301-306.
Pienta, R.J., J. A. Poiley and W.B. Lebherz III. 1977. Morphological transformation of early
passage golden Syrian hamster embryo cells derived from cryopreserved primary cultures as a
reliable in vitro bioassay for identifying diverse carcinogens. Int. J. Cancer. 19: 642-655.
Poirier, L.A., G.D. Stoner and M.B. Shimkin. 1975. Bioassay of alkyl halides and nucleotide
base analogs by pulmonary tumor response in strain A mice. Cancer Res. 35: 1411-1415.
(Cited in U.S. EPA, 1988).
Rieger, R., A. Michaelis, I. Schubert et al. 1988. Inductions of chromatid aberrations by TEM
and maleic hydrazide is differently affected by pretreatment of Vicia faba root-tip meristems
with methyl iodide. Mutat. Res. 208: 101-104.
Rosenkranz, H.S. and L.A. Poirier. 1979. Evaluation of the mutagenicity and DNA-modifying
effect of carcinogens and noncarcinogens in microbial systems. J. Natl. Cancer Inst. 61:
873-892.
Simmon, V.F. 1979a. In vitro mutagenicity assays of chemical carcinogens and related
compounds with Salmonella typhimurium. J. Natl. Cancer Inst. 62: 893-899.
Simmon, V.F. 1979b. In vitro assays for recombinogenic activity of chemical carcinogens and
related compounds with Saccharomyces cerevisiae D3. J. Natl. Cancer Inst. 62: 901-909.
Simmon, V.F., K. Kauhanen and R.G. Tardiff 1977. Mutagenic activity of chemicals identified
in drinking water. In: Progress in Genetic Toxicology, Vol. 2, Development in Toxicology and
Environmental Sciences, D. Scott, B.A. Bridges and F.H. Sobels, Ed. Elsevier/North Holland
Biomedical Press, Amsterdam, p. 249-258.
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9-30-2009
Takahashi K. and Y. Kawazoe. 1987. Potent induction of the adaptive response by a weak
mutagen, methyl iodide, in Escherichia coli. Mutat. Res. 180: 163-169.
U.S. EPA. 1986. Guidelines for Carcinogen Risk Assessment. Fed. Reg. 51(185):
33992-34003.
U.S. EPA. 1988. Evaluation of the Potential Carcinogenicity of Methyl Iodide. Office of
Health and Environmental Assessment, Environmental Criteria and Assessment Office,
Washington, DC.
U.S. EPA. 1991. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC. April.
U.S. EPA. 1994. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC. December.
U.S. EPA. 1995. Integrated Risk Information System (IRIS). Office of Research and
Development, National Center for Environmental Assessment, Washington, DC. Examined
August 21, 2009. Online, http://www.epa.gov/iris/.
U.S. EPA. 1997. Health Effects Assessment Summary Tables (HEAST). FY-1997 Update.
Prepared by the Office of Research and Development, National Center for Environmental
Assessment, Cincinnati, OH for the Office of Emergency and Remedial Response, Washington,
DC. July 1997. EPA/540/R-97/036. NTIS PB 97-921199.
U.S. EPA. 2005. Guidelines for Carcinogen Risk. Risk Assessment Forum, Washington, DC.
EPA/630/P-03/001F. Online, http://cfpub.epa.gov/ncea/cfm/record isplay.cfm?deid 116283.
U.S. EPA. 2006. Drinking Water Standards and Health Advisories. Office of Water,
Washington, DC. Summer 2000. EPA 822-B-00-001. Examined on August 21, 2009 Online.
http://www.epa.gov/waterscience/criteria/drinkine/dwstandards.html.
WHO (World Health Organization). 2009. Environmental Health Criteria (EHC) Monographs
International Programme on Chemical Safety, Geneva, Switzerland. Examined September,
2009. Online, http://www.inchem.org/.
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