United States
                      Environmental  Protection
                      Agency
 Health Effects Research
 Laboratory
 Research Triangle Park NC 27711
                      Research and Development
 EPA-600/S1-84-003 Mar. 1984
&EPA           Project  Summary
                     In   Vitro  and  In   Vivo  Mutagenicity
                     Studies  of  Environmental
                     Chemicals
                      David C.L. Jones, Vincent F. Simmon, Kristien E. Mortelmans,
                      Ann D. Mitchell, Elizabeth L. Evans,  Mary M. Jotz
                      Edward S. Riccio, Douglas E. Robinson, and Barbara A.  Kirkhart
                       The objectives of this project were to
                     evaluate the mutagenicity  of various
                     compounds, mostly pesticides, using
                     microbial and mammalian cell in vitro
                     techniques, as well as in vivo techniques
                     in Drosophila and mice, and to further
                     develop and refine these procedures for
                     application as test batteries.
                       Seventy-nine compounds were evalu-
                     ated for mutagenicity in one or more of
                     11 test systems: S. typhimurium plate in-
                     corporation assay; E. coll WP-2 reverse
                     mutation assay; S. cerevisiae D3 mitotic
                     recombination assay; S. cerevisiae D7
                     assays;  E.  coli,  B. subtilis, and S.
                     typhimurium relative toxicity assays;
                     sister-chromatid exchange  in Chinese
                     hamster  ovary  cells  assay;  L5178Y
                     mouse lymphoma cell forward mutation
                     assay; unscheduled  DNA synthesis
                     assay; mouse  micronucleus assay;
                     Drosophila sex-linked recessive lethal
                     assay; and  mouse dominant  lethal
                     assay.
                       The data from the evaluation of 41
                     pesticides and 10 industrial chemicals
                     are presented, and qualitative inter-
                     pretations of these data and of data ob-
                     tained under a previous  contract, in-
                     cluding those for  an additional 28
                     pesticides, are summarized.
                       This Project Summary was developed
                     by  EPA's Health  Effects Research
                     Laboratory, Research Triangle Park, NC,
                     to announce key findings  of the re-
                     search project that is fully documented
                     in a separate report of the same title (see
                     Project Report ordering information at
                     back).
Introduction

  Under contract to the U.S. Environmental
Protection Agency (EPA), SRI International
evaluated the mutagenicity of various com-
pounds using microbial and mammalian cell
in vitro techniques, as well as in vivo techni-
ques  in Drosophila  and  mice. Simulta-
neously, these test procedures were further
developed and refined.
  This report includes a compilation of all the
quantitative data and a description of the test
results for each of the 51  chemicals (41
pesticides and  10 industrial  chemicals)
evaluated under the contract, together with
a summary table listing the qualitative inter-
pretation of the results. In addition, the sum-
mary table includes the qualitative interpreta-
tions of the results of a previous contract in
which 27 of these 51 chemicals and 28 other
chemicals were evaluated.
  The qualitative interpretations for all 79
chemicals are based on a review of all of the
data generated under both contracts, using
the criteria described in the methods section
of this report. In some cases, this process
resulted in qualitative interpretations that dif-
fered from those in previous reports. For ex-
ample, in previous reports,  results for the
relative toxicity studies in £ co//and B.  sub-
tilis were scored as positive when there was
a clear compound effect or as negative when
there was not. In the present evaluation,
positive or negative interpretation was limited
to clear effect or no-effect results, which any
other finding interpreted as inconclusive.
Those cases in which retesting  and/or
reevaluation was done are specified in the
test and in the summary table.

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Materials and Methods
   Battelle  Memorial Laboratories (Colum-
bus, Ohio) obtained the pesticides from the
manufacturers and subsequently provided
samples to SRI International (Menlo Park,
California) or to  WARF  Institute,  Inc.
(Madison, Wisconsin) for the tests reported
here. A few of the chemicals were obtained
from the manufacturers by the EPA Office
of Pesticide  Programs, Washington, D.C.
Each pesticide was a "technical grade" pro-
duct or its equivalent. Monocrotophos was
tested as a formulated  product,  Azodrin 5
(Shell). Mancozeb was tested as two  dif-
ferent products: Dithane M-45 (Rohm and
Haas) and Manzate 200 (Du Pont). Maneb
was also tested as two different products:
Dithane M-22 (Rohm and Haas)  and Man-
zate D (Du Pont).
  Seventy-nine compounds (69  pesticides
and 10 industrial chemicals) were examined
for mutagenicity in one or more of 11 test
systems.  The   pesticides  are  listed
alphabetically in Table 1 by their common
name, action, and chemical class. Nearly a
third  of  the  compounds are organo-
phosphate insecticides; other classes include
carbamates,  chlorinated   hydrocarbons,
halogenated aromatics, arsenic compounds,
urea derivatives and natural plant products,
and  synthetic derivatives. The mode of ac-
tion  of these  compounds ranges  from
general contact and systemic poisons to
specific preemergence and postemergence
herbicides.
   The 11 assay systems employed are listed
in Table 2, along with references to complete
descriptions  of the assay procedures. The
following bioassays were carried out both in
the presence  and absence of an Aroclor-1254
induced rat liver metabolic activation system:
S. typhimurium plate incorporation, £.  coli
WP-2 uvrA reverse mutation, S.  cerevisiae
D7  reverse  mutation,  mouse  lymphoma
L5178Y cell forward mutation, S. cerevisiae
D3  enhanced mitotic  recombination,  S.
cerevisiae D7 gene conversion and mitotic
crossing-over, human lung fibroblast (WI-38)
unscheduled DNA synthesis, and Chinese
hamster  ovary cell  sister-chromatid  ex-
change. All  experiments were performed
with concurrent positive (known mutagen)
and negative (solvent)  control chemicals.

 Results and Discussion
   Table 3 summarizes the test  results for
 each of the  79 chemicals evaluated. Cases
 involving a retest are identified by footnotes,
 as are cases in which the reexamination of
 previous data resulted in a different inter-
 pretation.  The S.  typhimurium plate incor-
 poration  results were scored  as positive
 when the results of any of the individual
Table 1.    Pesticides Assayed for Genotoxic Effects"

      Name (action)                               Chemical class
Acephate (II
Allethrin (I)
Aspon (I)
Azinphos-methyl (I)
Benomyl (Ft
Biphenyl (Fl
Botran (Ff
Bromacil !H)
sec-Butylamine AB (F)
sec-Butylamine AB»H3/W (F)
Cacodylic acid (HI
Captan IF)
Carbofuran (I)
Chlordimeform III
Chlorpyrifos (II
Creosote Pf
Creosote Pf
Crotoxyphos (I)
2,4-D acid (H)
2,4-DB acid (HI
Demeton (II
Diallate (H)
Diazinon (I)
Dicamba (H)
m-Dichlorobenzene (II
o-Dichlorobenzene (I)
p-Dichlorobenzene (I)
Dinoseb (HI
Disulfoton (II
O£-cis/trans chrysanthemic
  acid (I)
DSMA (HI
Endrin (I)
Ethion (PI
Ethyl chrysanthemate II)
Fensulfothion (I)
Fenthion (II
Folpet (F)
Fonofos (I)
Formetanate hydrochloride (I)
Ma lath ion (I)
Mancozeb (Ff
Maneb IFF
Methomyl (II
Methoxychlor (I)
Monocrotophos (if
Monuron (H)
MSMA (H)
Parathion (I)
Parathion-methyl  (I)
PCNB (F)
Pentachlorophenol (H)
Permethrin  (I)
Phorate  (I)
Polyram (F)
Propanil (H)
Ftesmethrin (I)
Rotenone (I)
Siduron  (HI
Simazine (HI
Sumithrin (I)
2,4,5-T(H)
Triallate (H)
Trichlorfon (II
Jrifluralin (HI
Vegadex (Hf
Thio/dithiophosphoramidate
Pyrethroid
Organo thio I dithiophospha te
Organothio/dithiophosphate
Carbamate
Aromatic
Chlorinated nitroaniline
Diazine
Aliphatic amine
Aliphatic amine
Organoarsenical
Phthalimide
Carbamate
Haloaromatic amidate
Organothio/dithiophosphate
Organothio/dithiophosphate
Halophenoxy
Halophenoxy
Organothio/dithiophosphate
Jhiocarbamate
Organo thio /dithiophospha te
Halophenoxy
Haloaromatic
Haloaromatic
Haloaromatic
Dinitrophenol
Organothio/dithiophosphate
Pyrethroid

Organoarsenical
Chlorinated hydrocarbon
Organothio/dithiophosphate
Pyrethroid
Organothio/dithiophosphate
Organo thio /dithiophospha te
Phthalimide
Phosphonate/thiophosphonate
Carbamate
Organothio/dithiophosphate
Ethylenebisdithiocarbamate
Ethylenebisdithiocarbamate
Carbamate
Aromatic
Organophosphate
Urea
Organic  arsenical
Organothio/dithiophosphate
Organothio/dithiophosphate
Haloaromatic
Haloaromatic
Pyrethroid
Organothio/dithiophosphate
Ethylenebisdithiocarbamate
Haloaromatic
Pyrethroid
Hydrocarbon
Urea
Triazine
Pyrethroid
Halophenoxy
Jhio/dithiocarbamate
Phosphonate/thiophosphonate
Nitroaromatic
Thio/dithiocarbamate

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 Table 1.
(Continued)
   Name {action)
                                                  Chemical class
 Zineb IF)
                                  Ethylenebisdithiocarbamate
 ' I = insecticide, F= fungicide, H = herbicide.
 6 Botran is the chemical name used in report; dichloran is the common name.
 c Compound is actually a complex coal tar mixture containing phenol, creosote, and other compounds.
 d Tested as two products, Dithane M-45 and Manzate 200.
 e Tested as two products, Dithane M-22 and Manzate D.
 ' Azodrin 5 is the chemical name  used in this report; su/fa/late is the common  name.
 9 Vegadex  is the chemical name used in this report; sulfallate is the common name.


 Table 2.    Assay Systems Used for Genotoxic Studies
                Assay
                                     Reference to
                                   method employed
S  typhimurium plate incorporation
E.  coli WP-2 uvrA reverse mutation
S. cerevisiae D3 mitotic recombination
S. cerevisiae D7
  Reverse mutation
  Gene conversion
  Mitotic crossing-over
Relative toxicity
  E. coli, strains W3110 and p3478
  B. subtilis, strains HJ7 and M45
  S. typhimurium, strains SL4525 free  I,
  SL4700 free ~ iTA 1978 (uvrB +), and
  TA1538 fuvrB")
Sister-chromatid exchange in CHO cells
L5178Y TK  / ~~ Mouse lymphoma cell
forward mutation
Unscheduled DNA synthesis in W/-38 cells
Mouse micronuc/eus
Drosophila sex-linked recessive
Mouse dominant lethal
                                  Ames et al. (1)
                                  Bridges 12)
                                  Brusick and Mayer 13)

                                  Zimmerman 14)
                                  Zimmerman (5)
                                  Zimmerman (5)

                                  Slater et al. (6)
                                  Kada (7)
                                  Ames et al. (11
                                  Perry and Evans (8)
                                  Stetka and Wolff (91
                                  Cfive et al. (10)
                                  Simmon (11, 12)
                                  Schmid (13)
                                  Wurgler et al.  (14)
                                  Simmon (15)
strains were positive. The totals indicate the
numbers of tests conducted, excluding in-
conclusive tests, and the numbers of tests
with positive results.  For  computing the
totals, tests with and without activation were
scored as  positive  when either result was
positive. For purposes of this analysis, each
of the three parameters in the S. cerevisiae
D7 system and each of the four strain pairs
in the relative toxicity assays was counted
as a separate test.
   The general problem  addressed by this
research was the classification of pesticides
according  to  their  genotoxic effects.
Genotoxicity was assessed by prokaryotic
and eukaryotic test systems that measured
gene mutation, DNA damage, or chromo-
somal effects. The chemicals studied can be
divided into two groups: those that displayed
no genotoxic response and require little fur-
ther testing, and those that  displayed some
positive response and require further evalua-
tion. The  chemicals that elicited positive
responses in  several  kinds  of  genetic
bioassays are of greatest concern, particu-
larly as  regards  their potential  effect  on
humans.
   Attempts to relate the results  of in vitro
and in vivo bioassays to potential human
health hazards lead naturally to a more
specific classification or ranking of individual
chemicals. The  present  assessment falls
short of a definitive ranking of the chemicals
studied for the following reasons:
Table 3. Summary Data for 79 Chemicals
Relative Toxicity
S.lv/,/, F r-.nl! K ™» S- <=ere O7 f rnl, R Sllh, S typh
PESTICIDES PI. Inc WP-2 D3 MCO MGC RM PolA Rec uvrB Rec
Acephate + +" 	 ++++++-+ ?b 7 -
Al/ethnn - + 	 	 ? -
Aspon 	 — 	 7 7
Azinphos-Methyl - c - c 	 + c - rf 	 	 	 7 7 -
Benomyl
Bipheny/ 	 	 	 7 7
Botrarf 	 	 	


sec Butylamme 2AB 	 	 	 + -
sec Butylamme 2AB H3P04 	 	 	
Cacodylic Acid 	 	 +c + ':-t-+-t-+++ ? 7 - -
Captan + c + c + + +c + c + + + +
Carbofuran 	 	 	 7 7
Ch/ordtmeform 	 	 	 7 -
Chlorpyrrfos -c_c 	 	 + + + +
Creosote PI - + 	 	 - -
Creosote P2 - + 	 	 - _
Crotoxyphos 	 — ++ 	 	 	 ? 7 - _
2,4-D Acid ^_____ _rf +c
2,4-DB Acid 	 ____ + _c
Demeton + + + + ++++++++ -d + - -
Dial/ate -c + c — -+ 	 	 	
Diazmon 	 	 	 7 7
Dicamba 	 	 	 + + - _
m-Dichlorobenzene 	 	 ++ + —
• in most cases tecnnicai graae cnemicais
were used. While this level of purity is
SC£ L5178Y UDS Mouse Dros Mouse No. ± No.
CHO Lymph WI-38 Micro SLRL DL Tests Pos.
+ ++++- - 12 8
51
40
7- -+ -c-d - 13 2
++ ++* + 33
40
5 0

	 ++ 	 — — 15 1
5 1
5 0
--++-- + 12 6
+ +-c-d - 10 8
40
50
84
?+ 6 2
'+ 62
--++-- - 12 2
81
81
+ ++-++ - 14 10
+ + + 84
40
82
5 2

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Table 3. (continued) fle/af/ve Tol(Kity
.
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    most relevant to commercial products,
    it is possible that the genotoxic activity
    of the technical grade chemicals may be
    related to the presence of contaminants.
•   The data base is  incomplete; not all
    chemicals  were evaluated in  all  test
    systems.
•   The quantitative dose-response data that
    exist for each chemical in each test have
    been used only to establish whether the
    test was positive or negative.
•   No dosimetry studies have  been  per-
    formed; only the quantity of chemical to
    which the  organism was exposed has
    been recorded.
Despite these  limitations, a great  deal of
preliminary information has been gleaned
from this examination of the qualitative data.
Undoubtedly, much can be gained from a
careful analysis of the  quantitative data.
  Thirty-nine of  the pesticides  examined
were  positive in  one or more the 11  test
systems employed. Of  these 35 pesticides,
21  caused point/gene mutation and 31
caused DNA damage.  Nine pesticides  pro-
duced chromosomal effects; however, they
also caused gene mutation and/or primary
DNA  damage, and relatively few tests for
chromosomal effects-were performed.
  Six pesticides evaluated in this study
displayed genotoxic acitivity in three or more
eukaryotic bioassay systems.  These com-
pounds are  acephate,   cacodylic acid,
demeton,  diallate, monocrotophos,  and
trichlorfon.  Cacodylic  acid  also  caused
chromosomal damage in the in vivo mouse
micronucleus test;  monocrotophos  was
negative in the relatively insensitive mouse
dominant lethal test. With further testing,
other compounds may also show similar ef-
fects; nonetheless, because of their diverse
genotoxic activities, these six compounds
should be assessed carefully.

References
 1.  Ames,  B.N.,  J.  McCann,  and  E.
    Yamaski. Methods for Detecting Car-
    cinogens  and  Mutagens  with  the
    5a//no/?e//a/Mammalian   Microsome
    Mutagenicity Test.  Mutat. Res., 31:347,
    1975.
 2.  Bridges, B.A. Simple Bacterial Systems
    for Detecting Mutagenic Agents. Lab.
    Pract., 21:413, 1976.
 3.  Brusick, D.J., and V.W.  Mayer. New
    Developments in Mutagenicity Screen-
    ing Techniques with  Yeast. Environ.
    Health  Perspect., 6:83, 1973.
 4.  Zimmerman,  F.K. Procedures Used in
    the Induction of Mitotic Recombination
    and  Mutation  in  the  Yeast Sac-
    charomyes  cerevisiae. Mutat.  Res.,
    31:71, 1975.
 5.  Zimmerman, F.K.  A Yeast Strain for
    Simultaneous Detection of  Induced
    Mitotic Crossing Over,  Mitotic Gene
    Conversion,  and  Reverse  Mutation.
    Mutat. Res., 28:381, 1975.
 6.  Slater, E.E., M.D. Anderson, and H.S.
    Rosenkranz. Rapid  Detection  of
    Mutagens and  Carcinogens.  Cancer
    Res., 31:970, 1971.
 7.  Kada,  T.  Mutagenecity Testing  of
    Chemicals in Microbial Systems. In:
    New   Methods  in  Experimental
    Chemistry and Toxicology, F. Coulston,
    F.  Corte, and M.  Coto, eds. Interna-
    tional Academic  Printing, Tokyo, 1973.
 8.  Perry, P., and H.J. Evans. Cytological
    Detection of Mutagen-Carcinogen Ex-
    posure by Sister Chromatid  Exchange.
    Nature, 158:121, 1975.
 9.  Stetka,  D.G., and  S.  Wolff.  Sister
    Chromatid Exchanges as an Assay for
    Genetic   Damage   Induced  by
    Mutagens/Carcinogens. Part II. In Vitro
    Tests  for   Compound   Requiring
    Metabolic Activation.  Mutat.  Res.,
    41:343, 1976.
10.  Clive, D., K.O. Johnson, J.F.S. Spec-
    tor, A.G.  Batson, and M.M.M. Brown.
    Validation and Characterization of the
    L5178Y/TK + /-Mouse  Lymphoma
    Mutagen Assay  System. Mutat. Res.,
    59:61-108, 1979.
11.  Simmon, V.F. In Vitro Microbiological
    Mutagenicity and Unscheduled DNA
    Synthesis  Studies  of  Eighteen
    Pesticides,  Final  Report.  U.S.  En-
    vironmental Protection Agency, 1978.
12.  Simmon, V.F., A.D. Mitchell, and T.A.
    Jorgenson. Evaluation  of  Selected
    Pesticides as Chemical  Mutagens. In
    Vitro and in Vivo Studies. Report no.
    EPA-600/1-77-028, U.S.  Environmental
    Protection Agency, 1977.
13.  Schmid, W. The Micronucleus Test for
    Cytogenetic  Analysis.  In:  Chemical
    Mutagens, Vol.  4, A. Hollaender,  ed.
    Plenum  Press, New York, 1976.
14.  Wurgler, F.E.,  F.H.  Sobels, and E.
    Vogel. Drosophila as Assay System for
    Detecting Genetic Changes. In: Hand-
    book of Mutagenicity Test Procedures,
    B.J.  Kilbey, M.  Legator, W. Nichols,
    and  C.  Ramels, eds. Elsevier/North
    Holland Biomedical Press, Amsterdam,
    1977.
15.  Simmon, V.F. In vivo and In vitro
    Mutagenicity  Assays  of Selected
    Pesticides. In: A Rational Evaluation of
    Pesticidal vs. Mutagenic/Carcinogenic
    Action, R.W. Hart, H.F. Kraybill,  and
    F.J. de Serres, eds. DHEW Publication
    No. (NIH) 78-1306, U.S.  Department of
    Health,   Education,  and Welfare,
    Washington, D.C. 1978.
   David C. L. Jones, Vincent F. Simmon, Kristien E. Mortelmans, Ann D. Mitchell,
     Elizabeth L Evans, Mary M. Jotz, Edward S. Riccio, Douglas E. Robinson, and
     Barbara A. Kirkhart are with SRI International, Menlo Park, CA 94025.
   Michael D. Waters is the EPA Project Officer (see below).
   The complete  report, entitled "In Vitro and In  Vivo Mutagenicity Studies of
     Environmental Chemicals,"(Order No. PB 84-138 973; Cost: $41.50, subject to
     change) will be available only from:
           National Technical Information Service
           5285 Port Royal Road
           Springfield, VA22161
           Telephone:  703-487-4650
   The EPA Project Officer can be contacted at:
           Health Effects Research Laboratory
           U.S. Environmental Protection Agency
           Research Triangle Park, NC 27711

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