' 530R86103
AT E R
UALITY
MIREX
Criteria and Standards Division
D^ffice n f Water Reulations and Standard
United States
EIn v i r an rue n t al Protection F^gency
MRRCH 1 9 8 G
-------
' t
-------
WATER QUALITY ADVISORY
Number 8 .
MIREX
Criteria and Standards Division
Office of Water Regulations and Standards
United States Environmental Protection Agency
The advisory concentration for Mirex in ambient water for the
protection of freshwater aquatic organisms is estimated to be 0.001
^: ug/L. No saltwater data were reviewed, and no advisory concentration
v for the protection of saltwater aquatic organisms is estimated. Care
should be taken in the application of this advisory, with considera-
tion of its derivation, as stated in the attached support document.
An advisory concentration for the protection of aquatic life can
\,j be derived from several sources: a no observed effect level (NOEL),
the lowest concentration which has been observed to cause acute or
chronic toxicity, or other experimental data which may be applicable.
When there is no valid experimental data, a value may be derived from
a model which uses structure-activity relationships (SAR) as its
basis. The advisory concentrations should be used with caution, since
they may be derived from very limited experimental evidence, or in the
case of SAR derived values, no data on the specific chemical.
The advisory concentration for Mirex in ambient water for the
protection of human health is estimated to be 0.093 ug/L, based on
data and evidence available to U.S. EPA. Care should be taken in the
application of this advisory, with consideration of its derivation, as
stated in the attached support document.
An advisory concentration for the protection of human health can
be derived from a number of sources: The Office of Drinking Water
Health Effects Advisories; Acceptable Daily Intake(ADI) values from
EPA; Office of Pesticides and Toxic Substances risk assessments;
Carcinogen Assessment Group(CAG) cancer risk estimates; risk estimates
derived from the open literature; or other sources which will be given
in the support document. The advisory concentrations derived from
these sources will vary in confidence and usefulness, based on the
amount and quality of data used as well as the assumptions behind the
original estimates. The user is advised to read the background
information carefully to determine the strengths or deficiencies of
the values given in the advisory.
U.S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, IL 60604-3590
-------
HUMAN HEALTH AND AQUATIC LIFE
LITERATURE SEARCH AND DATA BASE
EVALUATION FOR
MIREX
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF WATER REGULATIONS AND STANDARDS
CRITERIA AND STANDARDS DIVISION
WASHINGTON, D.C. 20460
-------
TABLE OF CONTENTS
INTRODUCTION 1
SCOPE OF SEARCH 3
SUMMARY OF FINDINGS 3
Aquatic Toxicity 3
Health Effects 12
RECOMMENDATIONS 17
Aquatic 17
Health 19
REFERENCES 22
LIST OF TABLES
Table 1. Summary of Aquatic Toxicity Literature
Review of Mirex 4
Table 2. Summary of Health Effects Literature
Review of Mirex 13
Table 3. Data Requirements Calcaulation of Aquatic Life
Interim Criteria—Mirex 18
Table 4. Data Requirements for Calculation of Human Health
Interim Criteria—Mirex 21
LIST OF FIGURES
Figure 1. Summary of Toxicity Data for Mirex 9
-------
HUMAN HEALTH AND AQUATIC LIFE
LITERATURE SEARCH AND DATA BASE
EVALUATION FOR
MIREX
U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF WATER REGULATIONS AND STANDARDS
CRITERIA AND STANDARDS DIVISION
WASHINGTON, D.C. 20460
INTRODUCTION
Mirex was first produced commercially by Allied Chemical Corpora-
tion in 1955 as Dechlorane for use as a fire retardant and registered
as an insecticide in 1959. Hooker Chemical Corporation of Niagra
Falls, New York, was the sole manufacturer until 1967 when other
companies including Hexagon Laboratories of New York and Nease
Chemical Company in State College, Pennsylvania, and Salem, Ohio,
supplied the chemical to Hooker (U.S. EPA, 1981). The use of mirex
was banned in 1976 and its registration cancelled in the United States
in December of 1977 because of its toxicity and very long half life in
the environment as well as in the body (Grabowski, 1983).
Insecticidal use accounted for only 26 percent of the mirex pro-
duced by Hooker before 1977; the other 74 percent was Dechlorane
marketed as a flame retardant (Francis and Metcalf, 1984).
Dechlorane was used as a fire retardant for plastics, rubber,
paint, paper, and electrical goods (Windholz, 1976). Little informa-
tion is available concerning the extent of its entry into the environ-
ment. Because Dechlorane is fairly well immobilized in most end
products, it is likely that any environmental contamination by
Dechlorane was associated with its manufacture, rather than the use or
disposal of items containing the chemical (U.S. EPA, 1981).
Mirex was used to control western harvester ants, yellow jackets,
and primarily the imported fire ant, Solenopsis saevissima richteri,
which infests millions of acres in the southeastern U.S. The U.S.
Department of Agriculture sponsored federal-state cooperative programs
from 1962 to 1975 to help control the pest. Over 130 million acres
were treated with an estimated 226,000 kg of mirex bait (containing
0.3 to 0.6 percent active ingredient) during that period (U.S. EPA,
1981) .
-------
Mirex bait consisted of a combination of ground corncob grits,
soybean oil, and technical grade mirex (0.075 percent) (Spencer,
1973). Application was predominately through aerial spraying at low
level rates of about 4.2 g/ha or 1.7 g/acre (Francis and Metcalf,
1984) .
Mirex is a stomach poison with little contact toxicity. The bait
owes its selective effect both to its delayed toxic action and to the
behavior in ants. In scavenging the bait particles and returning them
to their mounds, the entire ant colony becomes exposed to the
pesticide (U.S. EPA, 1981).
The indirect exposure of mirex to non-target organisms occurs
through absorption or ingestion of mirex in water, by direct ingestion
of mirex bait, or by ingestion of other organisms exposed to mirex.
Model ecosystem studies indicate that both bioconcentration and bio-
magnification occur (Frances and Metcalf, 1984).
Mirex is a fully-chlorinated, cage-structured chemical with mole-
cular formula C10C112. It is a white, crystalline, odorless solid not
naturally found in the environment. Physical and chemical properties
of the pure chemical are given below:
Molecular Weight
Melting Point
Vapor Pressure
Solubility in Water
(at room temperature)
Log Octanol: Water Partition
Coefficient
545.59
485 °C
6 x 106 mm Hg at 50 C
<1.0 ppm
6.89
Mirex is an extremely stable compound, resistent to photodegre-
dation and biodegredation. It is unaffected by sulfuric, nitric, and
hydrochloric acids. Mirex is not believed to be metabolized or
detoxified by biological systems. Due to its extreme environmental
persistence and high lipophilicity, mirex has the potential to bio-
accumulate and has been shown to bioconcentrate several thousandfold
in food chains (Doull et al., 1980).
Decomposition of mirex occurs in the presence of sunlight or UV
with chemical catalysts. Photodegredation products are mono- and
dihydro-derivatives, with the major products being chlordectone and 8-
monohydromirex (photomirex). Photomirex is not a commercial product,
but chlordectone was marketed as an insecticide until 1976 when severe
health and environmental effects were identified at its production
site in Hopewell, Virginia (Francis and Metcalf, 1984). Because of
its high melting point and relatively low vapor pressure, mirex is not
readily transmitted by atmospheric routes. Environmental contamina-
tion has occured directly through aerial deposition of mirex bait
particles and industrial discharge and indirectly through surface
runoff.
-------
Significant discharges of mirex are known to have occurred from
the Hooker Plant at Niagra Falls. The Niagra River, which supplies
more than 84 percent of the tributary input to Lake Ontario, is the
major contributor of mirex found in sediments, fish, and wildlife of
Lake Ontario and the St. Lawrence River (Whittle and Fitzsimons,
1983) .
SCOPE OF SEARCH
Sources were identified through computerized literature searches
of the Toxicology Data Base, TOXBACK, TOXLINE, and NTIS files and
manual review of bibliographies. Literature was focused primarily on
controlled, dose-response studies conducted from 1965 to the present
and dealing with human health effects and aquatic toxicity.
The quality assurance/quality control measures employed in the
studies were evaluated specifically on their use of positive and
negative controls, replication, and chemical analysis of test concen-
trations. Information on bioaccumulation, field observations, food
chain effects, and sublethal effects also was extracted from articles.
Data from each literature source were tabulated by biological
species, medium of test exposure (water, fish, sediment, food),
concentration observed effects, and data quality assurance specifica-
tions. Based on these findings, recommendations for appropriate
interim criteria for mirex for the protection of human health and
aquatic life were formulated when the data permitted.
The available dose-response data were compared to the requirements
specified in the "Guidelines and Methodology Used in Preparation of
Health Assessment Chapters of the Consent Decree Water Quality
Criteria Documents" (FR 45:79347, November 28, 1980) and the "Guide-
lines for Deriving Numerical National Water Quality Criteria for the
Protection of Aquatic Life and Their Uses" (Stephan et al., 1985).
SUMMARY OF FINDINGS
Aquatic Toxicity
Although there have been many studies on the acute effects of
mirex to freshwater fish, few of those studies have produced acute
LC50 values, i.e. concentrations lethal to 50 percent of test
organisms (Table 1, Figure 1). Various species including rainbow
trout, yellow perch, fathead minnow, bluegill and walleye have shown
no adverse effects to mirex at concentrations up to 100 mg/L (96 hr
exposure) (Johnson and Finley, 1980). Fathead minnows treated with
concentrations exceeding the maximum water solubility of mirex (<1
ppm) showed no effects in 96-hour studies (Buckler et al., 1981).
-------
-
X
ce
z
u.
O
-»
LU
i j i
ce
LiJ
ce
5
£
!j
^
^"
~
o
X
g
o
1
o
^H
t/5
^
5>
5
O)
u
c
Ol
fc.
Ol
Ol
ce
VI
3
* * o
F— Ol ij
Sg UJ
V
VI
c
0).°.
>i u T,
~§s
•— u *•
•->
§•
S 52
L. c c u- 4J en «
O O — O 0) O -O
4-> Q U VI C 4-> Ol
UOVI^D fOl/l •*-£+*
•^ OJ 3 4J Ol Olk-lO £EOI
*-CO<0 3U~D w J-1 W-
OEVIOIO) — •<- O 1 1 1 1 1 ifc.ol'O
— O 0) ov > virvj i i i i i u
*-> t. I- O "O O) O •— 1 l«_ 4-> >>
10 U- S. Ol k 4J O> O <—
»— .» x *-*>» £1. *J O)
3 OIO £3. V>3OQ X£OI
u e • vi en 1/1 e L, ex o en >
U « CO -^ «• U3 •»-'^£X U-^'O
«t t (NJ M- n »3- 1— 4J *J O) O £ *O
c
CO *O
en w
^« ^~
^ O 0)
»i/ii i n "G i i i ^4-»u
*» -0 EX c «o 0)
-^o o o u ex
I- £ •— O. Q.4-1
3 4J 10 C £
ex oi u oi «— oi vi
Z -^ »— o u —
X C-0 L. C>»-
-HZ £ <0 *J O
P- 0 4J COO
en i/> o< o> o o
en < H- 3 cj ro m
i, «"en
k ro ^
L. i- us >, .-v.
^ 0) ^™ 0) 4«* ^ i-H Ol
OlfOOIfi •^'fOOX
XX XX o-5Sin J
X >,
£ -D U t S. 1. 1. -S
£ £ £ £ £
^H ^n ^n &* CT^ ^R VH
fQ)
,BK .^
U 4-> O» *J
X -*- -i 3
^ *d ^"g
>-C •— 10)
*j *j o C
•w- I/I »—
<• e t. <-» o ^L^ ^.^~^
x o o) o enen 010101
5L"S 4->EuCi/i — i S X £H S
SSI "SIS S A A A A A _^
* o— o ex u o o o o Q u
c x i. E u in ur> tninun --^
o o « £ ••- 3 u u u u u ce
* u E o— vi _ij _i_i_i Z
^v *^ -~. g
vi in i/i 5
" " ~ ~ 1 i
x! xl "i § 1 »
pexj ^o exl *> c vi t. c
•o £ « £ x -> E
I/I VI
5 1
i*. en
o t-
0
C 40
O> l/l
u
0)
CX t-
o
o
in 4J
c
c oi
s_
u o. •*->
O) C
n_ O qj
i*. in E
Ol 3
L. U
en o o
c i«- -c
u c oi
3 O U
•o — i.
O 4J 3
k. 10 O
ex u in
4J
§c c
0) •»-
•*•
-------
o
UJ
Z
F-
z
o
u
«•— 1
UJ
m
Ol
u
c
^
01
K-
O*
ee
•
VI
2 ^ tn
C * 4->
> 0 £
** C "8
*« 3 £
3 vi 5:
O v> u
< 01
I/I
Ml
ll
o -o
UJ
g
4-> -F-
V) 4J
Ol iO
5
g
a
g
o
g
a
0)
"3
v
*5?*
C iO Ol Ol
01
F- 4-> in m
IO Ol C U
co Zro "^
10 01 i^ o en 10 en
* F* Z U FH l/> .— 1
•O in
c c '
F- -F- F"t . O
in •— i/i in 4J • E >n n
OI-F-CF-U'O B.O C
3 JC Ot O F- "O • CJ. E Oin
•2 ii ..1 3 £ "* "S S "«o m vo c Z*
in X F- o >» en *•- 10 o 10*0
oi 01 >o v • u T- C-F-
4J Ol L JC X OJ Ol •*• 4J IO EOI
C *F" ^~ VI O C ^ F— l£- I4_ t *^ L
"" *« 4J a?"^ "S ° "* H °* O "O 4J r—
Oi4-*cc 011/101 in^ v oivi
i/> i- 01 TJ c m c oiCa. voi uir> u- t. L.
10 O E -F- -F- >>-F- 3-F- 34J CCVJO^-3
o>E4?j^in -a u oo EO
i. 10 in c u — o>i/> — oi o • o» £
o TJ i> T3 a> "O vi 10 ^. Oi
•C JZ 4J t.
•• c «n co c a.
VI O -F- O TJ X
SQ.VI- •- u a> ai i/i
T3 4^ fc. e
4J F- 1 O *J 0) Ol EV) -F-
t) IA v> ^3 ^J ^3 4J
b. •• 0) «3 01 O 3
4J— j: 4J E ^ i- jc F-
C «• 4J in 3 4J o
Oi ••— "F- in m «F- o. Ol VI
u X -a c u- £
C *n CO X ^
U C u 0.4J 8 P 0
O 10 10 ^ en i/l 4-1
1 C 01
*J Ol O 4-1 W
•a c E J3 o E ^- ioja^.o>
4J « OICL-F-F* OIIO
»- o.^— -H z: -^ •«-« cn i- r-i < * E — • tax
in i .. _c m
>» — VI !•» >,
•o F- c >>n 01 in J- ie
T3 Q. O ^ CM -H J3 0 JT -O I.
S-F- ^^ ^ OlfU E 45
VO IOCUO1V0 •* OJ 00
x,§
O) -F-
4J 4J
« u
- 1!
«-. wo.
en *~* oi
* F- ^1
§ ?f_ 5
S F- k. IO
ec ae at o«CX3U
Z 9C Z UJ K ^ vf UJ
3
4->
IO
4-1
J= J= U
I/I I/I C
•F- f S IO «
^— 1. Mk f »^ Ff
*^ *»— B4 ^ ^^ •
4-> 4-> O IO O
10 « in 10 01 10
u u ^ Er* E
f W. 14-
V> F- F- 3 10 IO
•»• Ol 0>F- -F- W -F-
K- e e « c oi e
2 s st; *« *
0 -C J=— « X «
(9 O O *^ OP~^ O
»
r««
O «
?a
lOr-l OJ
C * t/i
O >, !_
m i? S
c F- -a FH
-c c c co
O -F. IO Ol
^ U. CO FH
i i i
i i i
•o "n
•F- e
m
I-5
4J ^_
I. F-
4-> E
i/i >t in
O IO "O 4J -o
c *•" 3 4-»
Ol U O OJ Q. Ol
c x -F- £ E
U O "F- I/) Ol OO
•o c -o < 01 <
1 TJ F-
•F- O> F-
4-> N Ol
in -F- x
§T3 C 1.
oj o ex oi
O 4V -F- O Ol 4->
0) 3 Ol CM ft) 10
OC 4J-OX "Of
i. i- L. •—
Ol § IB
«J >
3 >I-F-
£1.
•O 3
F- F- •*«. ex. o> in
^ 01 4J
E f a ^ E O."
8S Q a. 4J e
O O l/l Ol
F-l F* 0 « 01 Ol
• • FH COS-* L.
o o oj
SO Q O Ol
US IA F- It- Ol
U U <_> < <4- C
UJ UJ UJ X OJ "F-
VI
3
F- VI
3 3
U VI
ii i~
X F- Ol
F- 3 — » >
3 F- IO I/It
Oi IB t. 3 10
^ O U O
•F- O) O CO)
c
-------
Ol
u
c:
Ol
1_
Ol
n-
Ol
o>
in
C CO
10 CTv
. in
o
c oo
§TJ
c
U IO
i_ vi w «9-
•— CO >, Ol I
10 JC 10 J-> I ,—
•»- "O
> I. O Ol
3 o 4J .
CO r- or
I X
I O Ol
4J f- L.
o
U I/I
u c
M -^ O
C 1.
IB O
> i— ro
o- t>»
•o at en
-
01
4-1 <
5'
Ol
.
>> u r
OQ
tfl f
o •o
Ol «
f- 1-
Ol
4J
ie
u
"ex
3
a.
ex
S
en
en
01 I.
»• oi
in r-
£i
O) in
— 01
O a
o: t—
f
>4-> O
X O
01 4->
i ex
, £^
o
I/I
O)
ex o 4-> o
* 0) 10 4J
M O
Of) 4-«
O 01
c o
in •*- IB
L.
f
CO
8
IO
I/I
10
O)
01
m
O)
i1
o
o
to
•— ^ IO
•££»
ag>
A
O
in
o
Z—-en ^H
S":
f»>
in
C9
'1
I"
o
o
in
u
o
in
u
fS
ex
I
L. 10
oi x
ok-
-------
ai
0
c
Ol
L.
ai
)+-.
01
ee
in
•3
lit
C M
" » ^
•— "- -
= 5$
^il
. , ex
0 ^
UJ
rj
^
i««
h-
gg
O
U
T i!
_J in f
"* o-o
^ ,&*
£
g
4-> —
in *J
ai 10
t- t-
3
O
O
ir»
U
LL!
g
O
_J
g
O
_l
in
01
o
S
to
4J
in
^
•o TJ-
c rs,
» * * o\
N fsl r^
•e 3 -03 u
CZ t. C L- Ol *
IO U IO CJ "D 4->
*^* *o "^ 10 10 01
>^-n >^n xE
^ f^. cr r*» 01 C
iooicn looicn *— o
X-Q*-I z-o>-i O
OJ VI ^* 1.
Ol ^H Ol • 4-»
•O 4J (— C
IO •• CX O
L. 01 in 01 u
CD C ^
^^ ^^ o • * ••
ro co •— 4J -^ ^ c
• — • — 10 Ol Ol O
O U 4-> »-~
m in •*- ID vi in *J
•• Ol •• 01 c Ol 0) in-w j: c « *J v. 0 — O) V.
4Jt— 4J-- 11 > »— O *J
CO. CO. M 4- 1. Q. C C
001 ooi in*^iooioc
ui- us- en E •— «- o O 4J
o^c-^e^uaj-^ 10
^••UWXOJ**-" >— ^ t — O ^ *-> *
fa>oioi4->ua £aiaiEieia-<-o4-»o ai 10 « >« c « o cc 10
^CXEiotnm T> c * •-! — in in Z *J
in in
u u. t t. m in in >> >, u
£ ff £ >v >» >, CO 10 £
10 10 10 -a tj
CO 9COCVJ ^^^ Pg
V e cx^s co«r>.inin o.
_ I- O O. O. iq-t-lOOOCX
SE OO OOOOO —II
•~H o O f
M CVJ ^ V ^H I
O v^
o« Kin^ inE m
•co o o o u a. o t
<->*r _j _i_i _io. _i.
V)
—» e inU-~
£ 10
•^i— 10 >
U *J •>• L.
B 01 ai e » S .a i/i 4-> »
r— f- o Ol i
10 Ki- in -a i_ *•> c I
•r- C 01 "- 5^1- 0
f 0 -M C 3 S J
Sen 3-^ m er 01 «
I- re ail. oiin , -o o •— t
IO ^ •** OS Ol Z *O «
zl— • oP 5p. o.j
IO
f—
Ol
•O r—
CO IO
•o f>.
c en 4J
IQ ^ ^)
»- . N .* -*
er 3 v i*.
10 i- 3 en
JE U 1 t— 1
V
IN O O
"O O) m .a co
Ol U >i «
in c»— ^- o •»vo
•O O 41 10 CSJOIf-l
01 o m e x —
i. i. — A n
o •o 01 c c •*-
e c > "O —me
i i- 10 c in o
1 -^ O 4J o> *^
>l 0) *> •»- in «— t. *J
IO ^~ « 4J IO
u o u c u
•^ I. f Ol •*•
f— •M E O •—
Q. c 01 c ex
Ol Of O Ol
U O O O I.
X •
. C5 g
— ^- o o —
u E m 01 *» L.
O CO) Q.-» O
^•WJ<>«O «4->OIJ=0)
U 4-1 O Ol *J o *>
Ol 10 *J C O >« C 10 Ol «
•ocvi-^io «-f^*-oe
i- I- U t. U t.
f £ f £ £ £
1C O 10 V CO "3-
en (M CM in TT
<— i «-•
•5 -°
5- °-
Q. Q.
tn ^
4-* 4-1
If | *
H cR *o A
/)«^ *> «J
gg 1 g
33 »«g2K «8
o
e
t-
•o
•a
^
/>
v 3 •«>.
A U «
: — • 10 w
it n
- L. O IO
Sf O V.
in i. u
-------
-
_
o
UJ
3
Z
1—
O
U
UJ
oo
t—
01
u
c
s
Ol
n-
Ol
cc
•5
0 -a
S* w !_»
S * u
0 g UJ
•fW
§
at .2
44*1 £
^™ t ^
J.« !t
a.
*/7
1|
o -5
g
4J "^
VI 44
01 «0
t- «-
g
ft
I
g
U
_J
VI
Ol
Ol
l5%
44
VI
O)
•
•
> "0 « 1_
FH o r^ N ft
r» c in oi 3 ja
en 3 en 3 L. o
-i aC«-l — I O CC
-o --~
44 O> I/I CM
IO 44 Ol
VI 43 ><
C Ol 3 IO
Si1* **£
I/I VI >,
c "o vi
_>>_O 0 4>
•^•44 i "O 3 C X — • O
•—u •— — 01 *r u
>— 44OI3E44
oivio. ew^ue
jcaioi ce oiocuoo
u 44 L. z <_> a. u z tj
^
44 1_ |
1 -^ 44 Ol I/I C
u jaxoo IE lo-a^oi *io
o.»^ o to u— »«• 5. * -o c u
•o u •— -o xr»x vioo. xoio —
44 Ol JC 01 01 ^^ ^ c 44 <^ ^3 ^ ^ ^j E
4-1 O 44 U • 1. b. ••- O •— 1 CL.^-01 S
CIQOIIO — O ••- O I. • . 5 — O u JC
t. t. 1. JC t.
Q)
r— IS L.
a. ie 3
01 I. 44
i. en •—
.«— (J
i/i ie
§u 01
•F- .—
*• c —
44 £ J-
10 O Ol
I. Ol 44
44 44 VI
a-— S. oi«— -^
Ol — o i s^lo
^ F— ai
44 44 t.
4^=44
VI 1*- 44
JJ-
• * »
?rs
^^
o o
I- 44
44 01
g!o
U 1
V* t
log
(J U
44
C
01 44 Ol
Illxil
0) u"o "^ U
E "O VI O— i *4
-I — *'V_
^~ 1
iS E "Si
X >> E S. 3,
•a
1- f- Sit— B. BL 0
•— »— a. ex CXCM Q
IO a Ol • O
44 44 t-l U f»- — 1 C7I •>
O O. O O— rn in en in
• en . , ^
~. — ^ x UJ
a
VI
2
o
I
e
i ?
JC 01
44 b
fe ,9
UJ JC
^^ ^ ^
e
Ol
01
u
en
t.
-------
CO
CO
C—3
crzi
no
rv: rv-
&
!
CfcT
ft—i
CO
C 5
-------
Chronic studies have been conducted with several species of fish
including goldfish, bluegill, channel catfish, trout, sunfish, salmon,
and fathead minnow. These studies show that high residues of mirex
are accumulated and retained, and that there are indications of
effects on survival, growth, and/or reproduction. (U.S. EPA, 1981;
Buckler, et al, 1981). In a chronic study using two species of warm-
water fishes, bluegills were fed 0, 1, 3 or 5 mg/kg of mirex for 168
days (Van Valen et al., 1968). No mortality or tissue pathology
resulted from the mirex exposure; however, growth of the bluegills in
the highest treatment groups was adversely affected. Goldfish in
ponds treated with 1.0 ppm mirex showed gill edema, kidney lesions,
and distended gall bladders. Studies with channel catfish reported
similar results. A three-acre pond and surrounding drainage area were
treated with 1.7 g mirex bait acre. After 6 months exposure, catfish
showed residues of 0.65 ppm; however, no significant increase in
mortality or adverse effects were noted (Collins et al., 1973). Cat-
fish in ponds treated three times in 8 months with 1.25 Ibs mirex
bait/acre showed no adverse effects (Hyde et al., 1974). A study with
fathead minnows estimated an EC50 of 34 ug/L after 120 days exposure
when possible signs of reproductive impairment were noted (Buckler et
al., 1981).
Mirex is retained for long periods of time in fish with little or
no elimination. Brook trout fed a mirex contaminated diet (0.7 mg/kg)
for 104 days showed no significant reduction in mirex residues after
385 days of uncontaminated feed (Skea et al., 1981). Substantial
bioconcentration of mirex was reported in goldfish and bluegills
exposed in ponds treated with mirex bait (Van Valen et al., 1968).
Whole body residues in goldfish exposed at 0.1 and 1.0 ppm increased
throughout the experiment. On Day 224 of the experiment goldfish
taken from the 1.0 ppm group contained 61.0 ppm mirex in muscle and
150 ppm mirex in whole body. In the 0.1 ppm treatment group, 11.6 ppm
in muscle and 45 ppm mirex in the whole body were found. Bluegills
exposed to mirex in ponds treated with 100.2 kg or 0.13 kg mirex bait
(theoretical concentrations of 1.0 or 0.0013 ppm, respecitvely, in
water) accumulated throughout the first 84 days at the 1.0 ppm treat-
ment level; residues were detected up to Day 56.
Three applications of mirex bait (1.25 Ibs/acre) to ponds contain-
ing channel catfish resulted in residues in fish averaging 0.015 ppm
in filets and 0.255 ppm in fat (Hyde et al., 1974). In a large scale
study, adult fathead minnows (Pimephales promelas) were exposed to
mirex in water for 32 days at an average concentration of 1.2 ug/L
(Veith et al., 1979). The resulting bioconcentration factor, based on
a sample of 5 whole fishes, was determined to be 18,100. Fathead
minnows exposed to 34 ug/L mirex for 120 days have accumulation fac-
tors in a range of 12,000 to 28,000 with tissue residues continuing to
increase through the 120-day exposure period (Buckler et al., 1981).
In general, mirex concentrations increase with individual fish
weight and appear to parallel reported lipid concentrations for
similar tissues (Insalaco et al., 1982). The highest tissue concen-
10
-------
trations have been found in the liver and viscera, followed by the
skin and muscle.
Freshwater invertebrates are sensitive to mirex with acute LD50
values for several species ranging from 40 to 1000 ppb. (Naqvi and de
la Cruz, 1983). Other invertebrates including the water flea (Daphnia
magna, D. pulex), midge larvae (Chironomus plumosus), and amphipod
(Gammaris pseudolimaeus) showed 48-hr ECSOs of >1 ppm (Sanders et al.,
1981; Johnson and Finley, 1980). Mosquito larvae exposed to 1.0 and
0.1 ppm mirex in water showed a 48-hr LC50 of 0.489 ppm (Alexander and
Norment, 1974). Muncy and Oliver (1963) found no effect of mirex on
red crayfish (Procambaris clarki) at 0.1 ppm during a 72-hr static
exposure. Acute studies (48-hr) with juvenile crayfish Procambaris
blandingi exposed to 0.1 and 0.5 ppb mirex for 48 hours showed that
mortality was delayed for up to 4 days following treatment, but that
65% and 71% respectively of the exposed populations died.
Hydra, a freshwater cnidarian, treated with 1.0, 0.1 and 0.01 ppm
mirex in acetone solution for 6 days exhibited behavioral changes such
as retracting their body tubes and tentacles after 2 days exposure
(Lue and de la Cruz, 1978). Peak mortality occurred on Day 4 at 1.0
ppm, with a time lag between behavioral changes and death. The 96-hr
LC50 was predicted to be 4.1 ppm.
Lue and de la Cruz (1977) studied the toxicity of mirex on two
soil macroarthropods: the land isopod Armadil 1 idium vulgare and the
soil millipede Oxidus gracilus. Feeding a diet ranging from 25 to 3000
ppm mirex, KD50 (knockdown dose for 50 percent of the exposed popula-
tion) and LD50 values for A. vulgare at 10 days exposure were 11.6
ppm and 35.2 ppm, respectively; and for 0. gracilus, 5.4 ppm and 198.7
ppm, respectively.
The earthworm Eisenia foetida, exposed to deposits of mirex on
filter paper for 48 hours was relatively resistant to mirex within
LC50 >l,000/pg/cm2 (Roberts and Borough, 1984).
Some chronic effects data for invertebrates were located. Studies
with several species including daphnids, midge larvae, and amphipods
estimated a maximum acceptable toxicant concentration of <2.4 ug/L for
Gammarus after 120 days of exposure (Sanders et al., 1981). Tests
performed on Hyallela azteca, an amphipod, by Naqvi and de la Cruz
(1973) and Jessimen and Quashi (1983) report 25 day (600 hours) and 13
day LCSOs at concentrations of 1 ug/L and 100 ug/L respectively.
Other tests showed effects ranging up to 1000 ug/L (Table 1).
Freshwater invertebrates have been found to bioconcentrate mirex
following exposure at levels used in the fire ant control program.
Laboratory studies utilizing concentrations much higher (1 and 5 ppb)
have confirmed this (Ludke et al., 1971). Invertebrates have been
found to accumulate mirex residues in lipid bodies with varying rates
of elimination depending on the species, p. magna exposed to 34 ug/L
mirex for 21 days accumulated 8,025 times the concentration in the
water (Sanders et al., 1981). Species of crayfish accumulated a
11
-------
residue 16,860 fold greater than that in the exposure water (Ludke et
al., 1971).
Two studies analyzed the effect of mirex on freshwater algae.
Kricher et al. (1975) exposed the unicellular green algae Chlorella
pyrenoidosa to 1.0 ppm mirex dissolved in acetone. The 1 percent
acetone concentration was found to be somewhat toxic to Chlorella.
When comparisons were made between the mirex sample and the acetone
control, the mean mirex-exposed density was found to be 19 percent
lower than the acetone control after 164 hours.
In another study, exposure of another uncellular green alga,
Chiamydomonas to 1.0 ppm mirex for 168 hours reduced photosynthesis 55
percent and reduced the respiration rate 28 percent (de la Cruz and
Naqvi, 1973).
Health Effects
Reported single oral dose LDSO's for rats range from 365 to 740
mg/kg (U.S. EPA, 1981) (Table 2). LDSO's for dogs range from 1,000 to
15,000 mg/kg (Larson et al., 1979) (Figure 1). The toxicity rating
for mirex is 4 (very toxic) with a probable oral lethal dose (human)
of 50-500 mg/kg, between I tsp. and 1 ounce for a 70 kg (150 Ib)
person (U.S. EPA, 1981). No studies of mirex effects or toxicity in
humans were found in this investigation. Animal studies indicate that
mirex is not metabolized or detoxified in mammals. Mirex is stored in
adipose tissue and excreted at low rates in the feces and in only
trace amounts in the urine (Chambers et al., 1982). Studies with
mice, rats, dogs, and monkeys have shown that mirex is rapidly
absorbed from the digestive tract and is quickly and readily stored in
adipose and other tissues. Mirex is readily transmitted to offspring
through both placental and lactogenic routes (Chu et al., 1981b;
Rogers and Grabowski, 1983; Grabowski and Payne, 1983a and 1983b).
Effects of mirex include reduced food and water consumption,
decrease in body weight, induced cytochrome P-450, and increased liver
weight. Male mice fed 10 mg/kg mirex for 15 days showed induced
cytochrome P-450, decreased blood glucose levels, and a significant
decrease in body weight (Fujimori et al., 1983). The chronicity
factor for mirex (i.e., the ratio of the single dose LD50 to the 90
dose LD50) is 60.8, the highest value reported for any pesticide (U.S.
EPA, 1981).
Few truly chronic studies of mirex have been published, but sub-
chronic studies report hepatotoxic, enzymatic, reproductive, carcino-
genic, and teratogenic effects. The teratogenicity of mirex has been
shown in numerous studies (Grabowski and Payne, 1980b; Rogers and
Grabowski, 1983; Chu et al., 1981b). Teratogenic effects include
edema, heart defects, and cataracts. Rats and mice treated with mirex
have produced smaller litters with reduced survival in the offspring.
Carcinogenic effects have also been reported (Innes et al., 1969;
Ulland et al., 1977; U.S. DHEW, 1980). Mirex administered in the diet
12
-------
X
ce
£
£•
o
2
UJ
>
o:
L±J
cc
3
^
a
t—
1/1
u
u
LL.
LL.
^^
—
^~
LU
I
i
U.
o
>-
g
^
1 1 (
i
«t
h-
Ol
U
c
Ol
i.
01
o>
ec.
i/i
3
s-g «.
C > 4->
« ? 0
•— m *>
•5|t
yg"
S
in
C
„, o
Ol .f,
X U jj
. 1 f— *•*
2s.s
*O 3 i.
3 i/i ~
^^ 0
«* Ol
D.
1^1
U =
3 1
in —
o -o
ex u
Xy
2.
LU
4- -2
in 4-1
o> ra
t- i-
3
O
I
^
Ol
••jj
£
3
1
^X
X
LU
in
Ol
a
W
#
4-*
in
*
4-*
01
ro
— CO
e>2
j"!
•••^ •
3 t—
LJ- 10
•o
1 O)
CX Ol 4J
g 4J e 10 in
5 .c 5 •»- oi
in en 10 k. u —
§— Ol f O *-"
QJ .C U I/I T-
u S L. o
k. 4-> 10 —
1- X 10 X 4J
Ol X> "O ••- U T3 U
4J O Q) T3 C IO
•0.0 m -c «
X ra O> Ol O)
«^ » Ol L. O O E
•5 c t. oi 3 us s,
o o o > -D «r M
o— oi oi e i c
U. 4J -D l/> «-i O. Ol
i.
Ol "O
X"O Ol
c u
•o ie 3
Ol » "O
4-* cm
IO I*- O ••••—
— o u x o
3 ra i_
u •O in •w 4->
•— O 4J e
re jr in f o
u 4j oi u u
oi 4J ra
in n ««, o> ••
Oi m m
34." 4J Ol O>
•— — C E 4->
IO Ol C Ol — IO
> O 01 E 4-1 U
_J -0 4J H-
O 1- * Oi —
in O) oi oi E d
>- .c 10 X. ra oi
_i 4-> ^ (- m i_
§~~
c .c
1- U
o
U 4->
IO
C Ol l-
U Ol
OI-»- ^
J< £ •>.
••^ 0) en
Oi> E
2^2
X
IO
T3
in
i— i
01
je
~^
i1
CM
m
t— i
IO
"~o
?
_J
ce
i_>
"* 01
•LTl
oi oi n
3 10 O
O E fn
X —
T en
CO i- CO CO IO
n*. 10 f^. r^ Oi
Ol Ol Oi ^^
-H 4J X. X. 1-
a, oi .
1/1 i*. en S 1/1 6 "o
O •— rv o O 3
i-> O Ol •— •— Ol 4J
Z 3 — • Z Z 3C 01
Ol '
O in ^ o
4-> 4-> 4J JE CO I/I
§U 4-> ^H .» 1 4-1
Ol C — 4J X « U
O3—i^ —x-ce—t- oi
O T3 4-> v»_ X Oi 41 4J O 4-1 l>-
•— 10 oi inoio>3EU4Jc: •*-
J3 •— -O OlinkO4JOlOI Ol
01 -^ O 3lO-»-UIOU.^-O i
C>X-r- •OOlSJTOI— H)C U
— oio c — t-4Ji_-oeo -^ '
»— oi m u <*- 4-> o o c
Ol XJ Ol O) C O T3 VI — O>
moioi o i- — QJ i*. oi 4-1 x oi
IOV1UC 4J 4J O 3 t. 1- O
SO c -r- x 1- C m -o o ti 4J
uie u o> oi 3 oi i/> •— cx4-> c ie
u 3 or k. u>ocnxinoQ;o u
oi •— c 10 •^•^•gciooii.'^'^ oi
00101 (j X'-w — 'Oi. ex^o 4J t-
• •
X
Oi in
1- Ol
f 4->
E 10
^r g I I
10 ex
I. 01
en u
^— ••
10 1/1
u •—
— o
C L.
f 4->
U C
Ol O
t- 0
*J
c «^.4J ie
•^- Ol IO
-X O
E X-^W
_ Q.I— Ol(M • _ _ _
tJ °-"Z EQ^ * T9 4-* *V. .V O
Oi E Ol— Ol «^ 5
^ ex i- •— E en 10
•^ ex u 10 g i
01 3 4-> in O
— ^ E eo o u no O
^5 • O O CM «O «*»
^- csj r- O E
O CM -H O O O
— J CM x>* in _i in
p . 4J 4J fCi Op O
^PJ« — O> _lp- _l
m^-»
3 m
u 3
«n 4J
>l O
E C
S S85
J3 Ol P— 4J 4J 4->
O Q. O <0
•o
4J
C
01
u
L
el
O
in
L.
O
M-
§
4-1
V
U
4J
§
u
4J
_J
01
«U
II
S
^-
^j
Ol
4^
in
i
s
•j
»
o
o
£=
J3
4J
C
I
g
•o
ource
in
c
•r-
•c
o>
4J
L.
0
ex
Ol
L.
•s
Z
n
ce
Jg
u
13
-------
^~^
o
LU
Z
Z
o
,
UJ
<
^.
11
c
01
01
o>
cc
i/i
O-o
c 2! 4-»
re £ o
5J O1^
£
c
Ol °
X U ^
*"* re *°
*— u u
re 3 £
3 VI .^.
°"«
(-t
3 D
Iii
1*^ ^^
c
o
I/I 4-1
ai re
i- i-
S
^
Ol
Exposure I
in
01
S
£
(fl
OJ
^
(/I
u
c o^
•o CT>
C3^
1
1
.^
X C
^ o
J- —
1 re
u
O)-f-
•o »—
re Q.
i. Ol
014.
^— • •>
re tn
u »—
-- 0
C i.
u c
O) O
»- u
in 4J
8J=
W*
•— Ol O^i
— JD I
re 3 4->
s- 4-> re x
0 T>
— j= c o
IJ O) J3
^~ re >
o o 01 o
4-1
c in 01 01
k. VI »•»
O X O —
<_) j= o e
>^
•o
•—4
01
1
n
esri
mo
o^
^
c
re i.
E 4-1
in
is
Ol
re i^>
0£— '
1 1
1 1
.„
X C
E re
•§£
re Q.
u 01
01 l-
^— • •
re in
u f~
— 0
C V-
u c
01 0
t- 0
P x—
"re •— "a?
i- ^" J3
o re 3
^ o
— u
o r- re
3 4->
c cm
re t.
0) OX
CL c ^ o
VI
re
•o
•c-
01
-^ Ol
i1 =:!
in inco
o o «•
41. —
— C
£ i.
V 4->
VI
•— c
IE
V
4J _g-
re wo
cc ^~
0
2
^ *
C JZ
re 01
vji
C JD
O i<:
i i
S
Ol
» x
in o> c
O
O t— C
4J O —
c e 3
re k. "-
Ol O O
in
X
re
•o
IT)
Ol
Ol >«.
t *»*
g *~*s
o in in E ^^
SO^-l — 1
unco >HUJ
o o PO o O
O
t-H
•o •
c j:
re 01
vi
01 1-
C J3
f E
cs i
_§
TJ *
X UO
in o in
• «
r- C •
"o — S o.
4-> — O.
C 3
5SSS
VI -0
in re 4-1
X"D re
re oi
•o o
"i re
u
!£
Ol L.
^~ • »
re in
u «—
C L.
U C
O) O
1- 0
4J 01
C -v
^ V—
O> 4-> E
> m
"o 5-^ j:
«- .. . OJ
•DUO*
• • O) **• X
^ r- O ^
re x o
E X O1J3
o ••- s. o
VI
X
re
•o
9-4
Ol
?
,_,
e
•— "O
ii
in
|S
*> J?
re {?>
ef —
CO
Ol
«
in
01
c
u
1
Ol
o
JD
re
in
re
I
i/i
Ol
•re
I/I
(C
u
l^
VI
X
re
T3
•-H
Ol
$
A
1
01-^
»- C
11
in
— c
3 re
4J JT
re to
tt *— ^
^
CO
J= Ol
3
£ :
o —
i.
>- Ol
01 1
in Ol re L. •-
re E L- 01 •— -a i
O) 4-1 in re o> O
u°£-oi?§3i;
*^* c 4-1 re o c •*•
4J •"• O > — O ""
c o> c OJ m 0)
U BO > Ol L. Ol J3
&"~C/1 c— « * OJ
^_ -o o cna. i- +J
K' S43eiJ?S.-S
x
Ol
E o
t.
°g
XO
k VI
3 m
re
X u
in •«-
sii
A k
in
w
g
in
c
in
O J<
of
in
X
•o
CO
X
F~
in
I
t»-
LU
^j
re
ce
c
in *
Ol*O
re re
JE •—
— •o
^l X
14
-------
CO
u
c
Ol
IB
•O
C
•O
•— 10
xi
•O
c
o
CO 00
f*« h»
s
O
IB
01
O
in
IB 0)
o>-*- 01
o •<- -o 10
3 CD
c -o
10
O) c U
L. IB t ••-
/a o *•>
£ s. I us
*• •»• >T3 T3 CU IB
1- 01 J t I ,
*J in .. . I
.:-
3 0)0 E J- — 01 01
~>f~C Ol (j^^fw*^-
>> U ^
IO
u
o
LU
O
o
CD
a.
to
o
LO
O
t.
C
o
*•
3 3
Wl •^>
o-o
o
4-1
IB
a.
Ol
t.
c u
O IB
U QJ
'o o
O X U
CM CU
t en
o'l-g
en IB
-^ c
o •-.••-
IB
O
IB Q
US C
O t-i-t-
u •—
1- IB
01 t
Q. o
I/I 4->
a> IB
•o
CM
Ol
>
Ol
I/I
o
J £
Ol Ol
-* Ji
o, |i
8
go
in
A
g
eo CM
go
u)
q a
t/l
01
10
t
o>
c •—
-3!
I/I
O)
•B e
II
«- c
ai
t IB
€2 §
Ol IB
O E
IS
15
-------
of 26 rats of each sex for 18 months produced statistically signifi-
cant incidences of liver tumors in test animals (Innes et al., 1977).
Forty percent of the treated mice exhibited hepatomas compared to only
4 percent in the control. In a second study, rats receiving 50 or 100
ppm mirex for 18 months showed an increase in liver tumors and lesions
(Ulland et al., 1977). The incidence of these tumors was shown to be
statistically significant. In an unpublished study by the Frederick
Cancer Research Center under contract with the National Cancer Insti-
tute (U.S. DHEW, 1980), preliminary results showed a high and
apparently dose-related incidence of neoplastic nodules of the liver,
hepatocellular carcinoma, and monocytic leukemia in rats at dietary
doses of 25, 50 and 100 ppm for 2 years.
Studies have been conducted with the major photodegredation
products of mirex: chlordectone, photomirex (8-monohydromirex) and
dihydromirex (2.8-dihydromirex). Photomirex and chlordectone have
been found to be very similar to mirex in that they both exhibit
strong lipophilicity (bioaccumulate in fatty tissue), are not readily
eliminated, and are highly persistent in the environment. Though
studies on mirex have been well documented, there is little informa-
tion available on the toxicity of dihydromirex, photomirex and
chlordectone. Chlordectone and photomirex have been shown to cause
similar effects as mirex: increased liver weights, induction of the
microsomal mixed function oxidases, and dose related histological
abnormalities in the thyroid and liver (Fujimori et al., 1983;
Yarbrough et al., 1981; Chu et al., 1981a; Hallett et al., 1978). In
these studies, the toxicities of mirex, photomirex and chlordectone
were compared. Fujimori et al. (1983) treated male mice with 10, 25
or 50 mg/kg chlordectone, mirex and photomirex. Acute test results
showed that clearly distinguishable differences exist between these
three compounds in terms of biological effects. Both daily food and
water intake were significantly decreased in mice treatment with
mirex. In contrast, treatment with chlordectone or photomirex
increased food and water consumption. Chloraectone caused significant
motor incoordination, where mirex and photomirex did not. Mirex and
photomirex caused a significant increase in liver weight, whereas
chlordectone treatment resulted in only a slight increase. Mirex and
photomirex were similar in inducing hepatic MFO (mixed-function
oxidase system).
In a 28-day study by Yarbrough et al., (1981) there did not appear
to be any consistently significant differences between the qualitative
or quantitative toxic effects of mirex and photomirex in rats. These
results suggest that mirex and its degredation products may differ
substantially in their short-term effects, but not in long-term
toxicity.
Tolerances for residues of mirex in food products were set by the
U.S. EPA as follows: 0.1 ppm in fat or meat from cattle, goats, hogs,
horses, poultry, and sheep; 0.1 ppm in eggs; 0.1 ppm in milk fat; 0.01
ppm in or on all other raw agricultural commodities, exclusive of
eggs, milk fat, and animal fat (U.S. EPA, 1981).
16
-------
RECOMMENDATIONS
Aquatic
An Aquatic Life Criterion consists of a Criterion Maximum Concen-
tration (CMC) and a Criterion Continuous Concentration (CCC).
According to EPA guidelines (Stephan et al., 1985), effects data for
eight species including two fish and six invertebrates are required
for establishing criteria (Table 3). Insufficient data on acute
toxicity of mirex precludes the calculation of the FAV and, therefore,
of the CMC.
The Criterion Continuous Concentration (CCC) is equal to the
lowest of three values, the Final Chronic Value, the Final Plant
Value, and the Final Residue Value. Insufficient data on chronic
toxicity of mirex precludes the calculation of a CCC.
A Final Residue Value for freshwater biota was calculated using a
method by EPA (1983) using data discussed above.
The Final Residue Value was calculated as follows:
FinalResidue Value = S. EPA action level for fish
bioconcentration factor
where:
U.S. EPA action level for fish =0.1 ppm
Bioconcentrationfactor (geometric mean) =15,240
therefore:
Final Residue Value = _.__! ppm
15,240
= .007 ug/L
17
-------
TABLE 3. DATA REQUIREMENTS FOR CALCULATION OF AQUATIC LIFE INTERIM
CRITERIA--MIREX
Criterion Requirements
Aquatic Toxicity
Available Data
Acceptability of
Available Data
Acute Test Results from tests on:
A salmonid (class Osteichthyes)
YES
YES
A warm water species commercially
or recreational ly important
important (class Osteichthyes)
Another family in the phylum YES
Chordata(fish,amphibian,etc.)
A planktonic crustacean (cladoceran, YES
copepod, etc.)
Benthic crustacean (ostracod, YES
isopod,scud,crayfish,etc.)
Insect (mayfly, dragonfly, damselfly, YES
stonefly, mosquito, etc.)
Phylum other than Arthropoda/Chordata YES
(Rotifera, Annelida, Mollusca)
Another family of insect YES
NO
(no LC50)
NO
(no LC50)
NO
(no LC50)
YES
(controls; replicates)
NO
(no LC50)
YES
(controls; replicates)
NO
(not aquatic species)
YES
(controls; replicates)
Acute-chronic ratios with species from
three different families:
One fish
One invertebrate
Acutely sensitive freshwater
animal species
NO
NO
NO
Acceptable test results from a test with:
Freshwater algae YES
A vascular plant NO
Bioaccumulation factor with a freshwater YES
species (if a maximum permissible tissue
concentration is available)
NO
(no LC50)
YES
(controls, replicates)
18
-------
This concentration is, lower than 0.1 ppb where delayed mortality
was noted in Procambans blandingi, but higher than the criterion of
0.001 ug/L given in Quality Criteria for Water (1976). The advisory
concentration for mirex will remain 0.001 ug/L, the same as that given
in the 1976 publication, based on the toxicity information above and
incorporating a safety factor at .01.
Health
No epidemiological studies of the effects of mirex on human health
have been found which could contribute data useful to the derivation
of a criterion (Table 4). However, mirex has been determined to be
carcinogenic in three separate studies with mice and rats (Innes, et
al., 1969; Ulland et al., 1977, NIOSH, 1978). Although data generated
by all three studies show statistically significant increases in
heptocellular carcinomas, the U.S. DHEW (1980) study represents the
best candidate for use in calculating a water concentration of mirex
that results in a cancer risk of 10-5. The water quality criterion
for mirex is based on the induction of hepatocellular carcinomas in
male Fischer (F344/N) rats. The results of the unpublished 2-yr
feeding study by the Frederick Cancer Institute show dose-related
incidence with the unadjusted incidence of the low dose group
significantly different from the control group. Because this study
was not available for our review, the criterion estimate for mirex was
determined from data reported by the U.S. EPA (1983). Using the data
from U.S. DHEW (1980), the slope estimate from the multi stage model
is adjusted to give a human carcinogenic potency estimate of 7.15
(mg/kg/day)-l (U.S. EPA, 1983).
The intake of the mirex from ambient water is assumed from two
sources: (1) drinking an average volume of 2 liters of water per day;
(2) ingesting an average of 6.5 grams of fish per day. Because of
accumulation of residues in fish, the amount of mirex in fish is equal
to a factor R times the water concentration (mg/kg/water). Using
methodology reported by EPA (1983), the water concentration in mg/L
corresponding to a life time cancer risk of 10~5 for a 70 kg person is
calculated by the formula:
C = 7_0 kg x 10—
qI (2 + 0.0065R)
where:
q±= 7.15 (mg/kg/day)-1
R = 15,240
For a lifetime cancer risk below 10-6 the criteria for mirex in water
are: 4.9 ng/L if exposure is through water only without consumption
of contaminated aquatic organisms; 0.097 ng/L if exposure is through
aquatic organisms only without ingestion of contaminated water; 0.093
ng/L if exposure is through consumption of both contaminated water and
aquatic organisms.
19
-------
Sufficient data were not provided in the EPA (1983) report of the
DHEW (1980) study, to derive a threshold effect water quality
criterion. A threshold effect criterion is derived from a no-
observed-adverse-effect level (NOAEL), lowest-observed-adverse-effect
level (LOAEL), or lowest-observed-effect level (LOEL) from a chronic
toxicity assay of at least 90 days duration. None of these values
were reported in the EPA (1983) document, nor were they found in
studies reviewed as part of this investigation.
20
-------
TABLE 4. DATA REQUIREMENTS FOR CALCULATIONOF HUMAN HEALTH INTERIM
CRITERIA--MIREX
Criterion Requirements
Human Health Effects
Available Data
Acceptability of
Available Data
Non-Threshold:
Carcinogen YES
Tumor incidence tests (Incidence of YES
tumor formation significantly more
than the control for at least one
dose level), or
Data set which gives estimate of YES
carcinogenetic risk, or
Lifetime average exposure tests, or YES
Human epidemiology studies NO
(if available, not required)
Threshold:
Non-carcinogens NO
No observed adverse effect level NO
(at least 90-day), or
Lowest observed effect level NO
Acceptable Daily Intake: NO
Daily water consumption YES
Daily fish consumption YES
Bioconcentration factor NO
Non-fish dietary intake YES
Daily intake by inhalation NO
Threshold Limit Value:
(Based on 8-hour time-weighted NO
average concentrations in air)
Inhalation Studies:
Available pharmacokinetic data NO
Measurements of absorption efficiency NO
Comparative excretion data NO
YES
(EPA approved)
YES
(3 studies with
valid data., EPA
approved)
YES
(EPA approved)
YES
(EPA approved)
YES
(EPA assumptions)
YES
(EPA assumptions)
YES
(EPA assumptions)
21
-------
REFERENCES
Abraham, R., K. F. Benitz, and R. Mankes. 1983. Ploidy patterns in
hepatic tumors induced by mirex. Experimental and Molecular Patho-
logy. 38:271-282.
Alexander, S. D. and B. R. Norment. 1974. Effects of mirex on popu-
lations of Aedes triseriatus say. Mosquito News. Vol 34, No. 1, p.
112.
Buckler, D. R., W. Arthur, Jr., F. L. Mayer, and J. Huckins. 1981.
Acute and chronic effects of kepone and mirex on the fathead minnow.
Trans. Am. Fish. Soc. 110:270-280.
Buelke, S. J., R. A. Byrd, and C. J. Nelson. 1983. Blood flow during
pregnancy in the rat: III Alterations following mirex treatment.
Teratology. 27:401-410.
Byrd, R. A., J. F. Holson, C. A. Kimmel, M. D. Morris, and J. F.
Young. 1981. Altered pattern of prenatal toxicity in rats due to
different treatment schedules with mirex. Toxic. Appl. Pharmac.
60:213-219.
Cabral, J.R.P., F. Raitano, T. Mollner, S. Bronczyk and P. Shubik.
1979. Acute toxicity of pesticides in hamsters. Toxicol. App.
Pharmacol. Vol 48(1): A 192 (Abstract).
Chambers, J. E., R. S. Case, E. G. Alley, and J. D. Yarbrough. 1982.
Short term fate of mirex and 2,8-dihydromirex in Rats. J. Agric. Food
Chem. 30:878-882.
Chernoff, N. and R. J. Kavlock. 1982. An in vivo teratology screen
utilizing pregnant mice. J. Toxic. Environ. Health. 10:541-550.
Chu, I., D. C. Villeneure, B. L. Macdonald, V. E. Secours, and V. E.
Valli. 1981a. Reversibility of the toxicological changes induced by
photomirex and mirex. Toxicology. 21(3) :235-250.
Chu, I., D. C. Villeneuve, V. E. Secours, V. E. Valli, and G. C.
Becking. 198Ib. Effects of photomirex and mirex on reproduction in
the rat. Toxicol. Appl. Pharmacol. 60:549-556.
Collins, H. L., J. R. Davis, and G. P. Markin. 1973. Residues of
mirex in channel catfish and other aquatic organisms. Bull. Environ.
Contam. and Toxicol. lO(2):73-77.
de la Cruz, A. A. and S. M. Naqvi, 1973. Mirex incorporation in the
environment: Uptake in aquatic organisms and the effects on the rate
of photosynthesis and respiration. Arch. Environ. Contam. Toxicol.
1:255.
22
-------
Doull J., C. D. Klaassen, M. 0. Amdur (eds). 1980. Casarett and
Doull's Toxicology. The Basic Science of Poisons, 2nd ed. Macmillan
Publishing Co., Inc., New York, p. 638.
Federal Register. 1980. Guidelines and methodology used in prepara-
tion at health effect assessment chapters of the consent decree water
quality criteria documents. 45:79347-79356.
Francis, B. M. and R. L. Metcalf. 1984. Evaluation of mirex, photo-
mirex and chlordectone in the terrestrial aquatic laboratory model
ecosystem. Environ. Health Perspectives. 54:341-346.
Fujimori, K., I. K. Ho, H. M. Mehendale, and D. C. Villeneuve. 1983,
Comparative toxicology of mirex, photomirex, and chlordecone after
oral administration to the mouse. 2:49-60.
Gaines, T. D. and R. D. Kimbrough. 1970. Oral toxicity of mirex in
adultsuckling rats. Arch. Environ. Health. Vol 21, 7-14.
Gaines, T. D. 1960. The acute toxicity of pesticides to rats.
Toxicol. and Appl. Pharmacol. 2, 88-99.
Gaines, T. D.. 1969. Acute toxicity of pesticides. Toxicol. Appl.
Pharmacol. 14,515-534.
Grabowski, C. T. 1983. The electrocardiogram of fatal and newborn
rats and dysrhythmias induced by toxic exposure. Dept. of Biology,
University of Miami, Coral Gables, Florida.
Grabowski, C. T. and D. B. Payne. 1983a. The causes of perinatal
death induced by prenatal exposure of rats to the pesticide mirex.
Part 1: Prepaturition observations of the cardiovascular system.
Teratology. 27:7-11.
Grabowski, C. T. and D. B. Payne. 1983b. The causes of perinatal
death induced by prenatal exposure of rats to the pesticide mirex.
Part II: Postnatal observations. J. Toxicol. Environ. Health.
11:301-315.
Hallett, D. J., K. S. Khera, D. R. Stoltz, I. Chu, D. Villeneuve, and
G. Trivett. 1978. Photomirex: Synthesis and assessment of acute
toxicity, tissue distribution and mutagenicity. J. Agric. Food Chem.
26:388.
Hewitt, L. A., W. R. Hewitt, and L. Gabriel. 1983. Fractional
hepatic localization of CHC13 in mice and rats treated with chlorde-
cone or mirex. Fund. Appl. Toxicol. 3:489-495.
Hilton, J. W.. P. V. Hodson, H. E. Braun, J. L. Leatherland, and S. J.
Slinger. 1983. Contaminant accumulation and physiological response
in rainbow trout (Salmo gairdneri) reared on naturally contaminated
diets. Can. J. Fish. Aquat. Sci. 40:1987-1994.
23
-------
Hyde, K. M., S. Stokes, J. F. Fowler, J. Graves, and F. Bonner. 1974.
The effect of mirex on channel catfish production. Trans. Amer. Fish.
Soc., No. 2:366.
Innes, J. R. M., B. M. Ulland, and M. G. Valerio. 1969. Bioassay. of
pesticides and industrial chemicals for tumorigenicity in mice: A
preliminary note. J. Nat'l. Cancer Inst. 422(6):1101.
Insalaco, S. E., J. C. Makarewicz, and J. N. McNamara. 1982. The
influence of sex, size and season on mirex levels within selected
tissues of Lake Ontario salmon. J. Great Lakes Res. 8(4):660-665.
Jessiman, B. J. and S. U. Quadri. 1983. Bioaccumulation kinetics of
the organochlorine pesticide mirex in amphipods. Ecotox. and Environ.
Sat. 7:295-305.
Johnson, W. W. and M. T. Finley. 1980. Handbook of acute toxicity of
chemicals to fish and aquatic intertebrates. Summaries of toxicity
tests conducted at Columbia National Fisheries Research Laboratory,
1965-1978.
Karl, P. I. and J. D. Yarbrough. 1984. A comparison of mirex-induced
liver growth to liver regeneration. Toxicol. Ltrs. 23:127-133.
Kendall, M. W. 1974. Acute hepatotoxic effects of mirex in the rat.
Bull. Environ. Contam. and Toxicol. Vol 12(5):617.
Kricher, J. C., J. C. Urey, and M. L. Hawes. 1975. The effects of
mirex and methoxychlor on the growth and productivity of Chlorella
pyrenoidosa. Bull. Environm. Contam. Toxicol. Vol 14(5) 617-703.
Lai, R. and D. M. Saxera. 1982. Accumulation, metabolism, and
effects of organochlorine insecticides on microorganisms. Microbiolo-
gical Rev. 46(1).95-127.
Larson, P. S., J. L. Egle Jr., G. Hennigar, and J. F. Borzelleca.
1979. Acute and subchronic toxicity of mirex in the rat, dog, and
rabbit. Toxicol. Appl. Pharmacol. 49:271-277.
Lee, J. H., J. R. Sylvester, and C. E. Nash. 1975. Effects of mirex
and methoxychlor on juvenile and adult striped mullet, Mugil cephalus,
L. Bull. Environ. Contam. and Toxicol. Vol. 14(2): 180-
Lue, K. Y., and A. de la Cruz. 1977. Mirex incorporation in the
environment: toxicity in two soil macroarthropods and effects on soil
community respiration. Water, Air and Soil Pollution. 9, 177-191.
Lue, K. Y., and A. de la Cruz. 1978. Mirex incorporation in the
environment: toxicity in hydra. Bull. Environm. Contam. Toxicol.
19:412.
24
-------
Ludke, J. L., M. T. Finley, and C. Lusk. 1971. Toxicity of mirex to
crayfish, Procambarus blandingi. Bull, of Environ. Contain, and
Toxicol. 6:89-96.
Mehrle, P. M., F. L. Mayer, and D. R. Buckler. 1981. Kepone and
mirex: Effects on bone development and swim bladder composition in
fathead minnows. Trans. Am. Fish. Soc. 110:638-643.
Muncy, R. J., and A. D. Oliver, Jr. 1963. Toxicity of ten insecti-
cides to the red crawfish Procambarus clarki (Girard). Trans. Am.
Fish. Soc. 92:428.
Neumeyer, J., D. Gibbons, and H. Trask. 1969. Pesticides. Parts 1
and 2, Chemical Week 104 (April 12 and 26): 37-68 (as cited in
Pimental, 1971).
NIOSH. 1978 Registry of Toxic Effects of Chemical Substances.
National Institutes of Science and Health, p. 751.
Naqvi, S. M. and A. A. de la Cruz. 1973. Mirex incorporation in the
environment: Toxicity in selected freshwater organisms. Bull.
Environ. Contam. and Toxicol. 10(5) :305-308.
Pimenthal, D. 1971. Ecological effects of pesticides on non-target
species. Government Printing Office, Washington, D.C. 858.
Roberts, B. L. and H. W. Dorough. 1984. Relative toxicities of
chemicals to the earthworm Eisenia foetida. Environ. Toxicol and
Chemistry, Vol 3, p. 67-78.
Rogers, J. M., L. Morelli, and C. T. Grabowski. 1984. Plasma glucose
and protein concentrations in rat fetuses and neonates exposed to
cataractogenic doses of mirex. Environ. Res. 34:155-161.
Rogers, J. M. and C. T. Grabowski. 1983. Mirex-induced fetal
cataracts: Lens growth, histology, and cation balance, and relation-
ship to edema. Teratology. 27:343-349.
Sanders, H. 0., J. Huckins, B. T. Johnson, and D. Skaar. 1981.
Biological effects of kepone and mirex on freshwater invertebrates.
Arch. Environ. Contam. Toxicol. 10:531-539.
Skea, J. C., H. J. Simonin, S. Jackling, and J. Symula. 1981.
Accumulation and retention of mirex by brook trout fed a contaminated
diet. Bull. Environ. Contam. Toxicol. 27:79-83.
Smith, M. K., G. L. Kimmel, D. M. Kochar, T. H. Shepard, S. P.
Spielberg and J. G. Wilson. 1983. A selection of candidate compounds
for in vitro teratogenesis test validation. Teratog. Carcinog.
Mutagen. 3:461-480.
Spencer, E. 1973. Guide to the chemicals used in crop protection.
Agriculture Canada, Research Branch, Ottawa, p. 359.
25
-------
Stephan, C. E., D. I. Mount, D. J. Hansen, J. H. Gentile, G. A.
Chapman, W. A. Brungs, 1985. Draft Guidelines for deriving numerical
national water-quality criteria for the protection of aquatic orga-
nisms and their uses U.S. Environmental Protection Agency, Office of
Research and Development, Environmental Research Laboratories, Duluth,
MN.
Ulland, B., E. K. Weisburger and J. H. Weisburger. 1973. Chronic
toxicity and carcinogenicity of industrial chemicals and pesticides.
Abstract. Toxicol. Appl. Pharmacol. 25:446.
Ulland, B., N. P. Page, R. A. Squire, E. K. Weisburger, and R. L.
Cypher. 1977. Carcinogenicity assay of mirex in Charles River CD
rats. J. Nat'l. Cancer Inst. 58(1):133.
U.S. DHEW (U.S. Department of Health, Education and Welfare). 1980.
Experimental design status report and individual animal pathology
table for mirex bioassay. Unpublished data received from Sharon
Leeney, Technical Information Resources Branch, National Cancer
Institute. Computer printout (approx.) 100 p. (as cited in U.S. EPA
1983) .
U.S. Environmental Protection Agency, 1976. Quality Criteria for
Water, EPA document No. 440/9-76-023. Available from NTIS order No.
PB 263-943.
U.S. Environmental Protection Agency. 1981. Ambient water quality
criteria for mirex. Final Report (Contract No. 68-03-2902.1 by
Battelle Columbus Laboratories). U.S. EPA Environmental Criteria and
Assessment Office, Cincinnati, Ohio.
U.S. Environmental Protection Agency. 1983. Multimedia risk
assessment for: Mirex — Final Draft. Environmental Criteria and
Assessment Office.
Van Valen, C. C., A. K. Andrews, and L. L. Eller. 1968. Some effects
of mirex on two warmwater fishes. Trans. Am. Fish. Soc. 97:185.
Veith, G. D., D. L. DeFoe, and B. V. Bergsteat. 1979. Measuring and
estimating the bioconcentration factor of mirex in fish. J. Fish.
Res. Board. Can. 36:1040 (as cited in U.S. EPA, 1983).
Warner, R. W. 1974. Water pollution, freshwater macroinvertebrates.
J. Water Poll. Control Fed. Vol 46(6):1341.
Waters, E. M., J. E. Huff, and H. B. Gerstner. 1977. Mirex, an
overview. Environmental Research 13, 212-222.
Whittle, D. M. and J. D. Fitzsimons. 1983. The influence of the
Niagra River on contaminated burdens of Lake Ontario biota. Great
Lakes Res. 9(2):295-302.
26
-------
U.S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, iL 60604-3590
-------
Windholz, M. (ed). 1976. Merck Index, 9th ed. Merck and Co., Inc.,
Rahway, NJ. p. 807.
Wolfe, J. L., R. J. Esher, K. M. Robinson, and J. D. Yarbrough. 1979,
Lethal and reproductive effects of dietary mirex and DDT on old field
mice, Peromyscus polionotus. Bull. Environm. Contain. Toxicol. 21,
397-402.
Yarbrough, J. D., J. E. Chambers, J. Grimley, E. Alley, M. Fang, J.
Morrow, B. Ward, and J. Conroy. 1981. Comparative study of 8-monohy-
dromirex and mirex toxicity in male rats. Toxic. Appl. Pharmac.
58:105-117.
27
------- |