Water Quality Control Commission

Hearing on New Mexico Department of Game and Fish Petition

to Deploy Piscicides in the Rio Costilla Drainage

February 22, 2006

Technical Testimony

by Ann McCampbell, MD

11 Esquila Rd., Santa Fe, NM 87508

\(505\) 466-3622

\[Note: "Exhibits" listed are references only\]

ANTIMYCIN A

Antimycin A is a highly toxic pesticide and poison. It is not an
antibiotic (Exhibit 1). Although antimycin A is derived from bacteria,
it has more in common with cyanide than penicillin. Like cyanide,
antimycin A blocks electron transport in mitochondria causing cellular
anoxia.

Fintrol concentrate carries the second highest pesticide hazard warning
issued by the U.S. Environmental Protection Agency (EPA), Toxicity
Category II. The hazard warning to humans and domestic animals on the
label is "*May be fatal if swallowed or absorbed through skin*."

According to its Material Safety Data Sheet (Exhibit 2), the oral LD 50
of antimycin A in rats is 30 mg/kg, that is, it takes 30 mg/kg of
ingested antimycin A to kill half the test animals. According to an EPA
Chemical Profile (Exhibit 3), the LD 50 for guinea pigs is even lower at
an extraordinary 1.8 mg/kg. Pesticides with an oral LD 50 less than 50
mg/kg meet the criteria for EPA Toxicity Category I. To put this in
perspective, pesticides in the other three EPA toxicity categories have
much higher oral LD 50 values. The oral LD 50 for Category II pesticides
is 50-500 mg/kg, for Category III pesticides it is 500-5000 mg/kg, and
is greater than 5000 mg/kg for Category IV pesticides (1).

The acute toxicity of antimycin is only slightly less than that of
cyanide. For example, the oral LD50 of antimycin in rabbits is 10mg/kg
and the LD50 of (potassium) cyanide is 5 mg/kg (ChemIDplus Lite,
[http://chem.sis.nlm.nih.gov](http://chem.sis.nlm.nih.gov/); Potassium
Cyanide MSDS,
[www.omegachemistries.com](http://www.omegachemistries.com/)).

The Hazards Information section of the Material Safety Data Sheet
(Exhibit 2) states that routes of entry for antimycin A include the
skin, inhalation, and ingestion. The ingestion hazard rating is "highly
toxic". Antimycin A is also noted to be an eye, skin and respiratory
irritant. Target organs include eyes, skin, respiratory tract,
cardiovascular system, nervous system, kidneys, and possibly fetus.
Inhalation of vapors or aerosol can irritate the eyes, nose, and
respiratory tract. Direct contact with skin or eyes can produce severe
irritation. And systemic intake can produce a decrease in blood
pressure, nausea, light headedness, dizziness, excitement,
incoordination, weakness, loss of coordinated speech and drowsiness.
Medical conditions said to be aggravated by antimycin A exposure are
pre-existing eye, skin, respiratory, kidney, nervous system or
cardiovascular ailments.

A University of California at Santa Cruz Laboratory Standard Operating
Procedure guide on antimycin A (Exhibit 4) states that this material is
considered a Particularly Hazardous Substance by the CAL OSHA Lab
Standard. It also says that antimycin A is "highly toxic" and "may be
fatal if swallowed, absorbed through skin, or inhaled". It notes that
"respiratory distress, impaired reflexes, incoordination, and terminal
symptoms consistent with CNS (central nervous system) depression have
been reported in experimental animals poisoned by the oral or parenteral
route."

ToxNet Hazardous Substance Databank Information on antimycin A, which
includes data from PoisonDex (Exhibit 5), states that respiratory
distress, incoordination, impaired reflexes, and CNS (central nervous
system) depression have occurred in animals. It further notes that *the
minimum lethal human exposure level is unknown*.

Besides its extreme acute toxicity, ToxNet also states that antimycin A
is an experimental mutagen. The NIOSH Registry of Toxic Effects of
Chemical Substances (RTECS) (Exhibit 6) also includes "mutation data" on
antimycin A. And in 2002, there were 36 references regarding antimycin
on the ToxNet Environmental Mutagen Information Center (EMIC) web page
(2). At least one study describes antimycin-induced DNA fragmentation
and strand breaks (Exhibit 7).

Perhaps most importantly, there is a disturbing lack of knowledge about
the full range of toxicity of antimycin A. Fintrol was initially
registered in 1977 (3) before the EPA adopted more stringent
registration requirements. In a 1987 EPA Chemical Profile on Antimycin A
(Exhibit 3) data was "not found" in most categories evaluated \-- from
physical and chemical properties to health hazards \-- despite a search
of 15 data sources.

In addition, the California Department of Pesticide Regulation recently
rejected the registration of Fintrol in that state because of
insufficient data regarding its toxicity and environmental fate (Exhibit
8). There are as well concerns among fish managers that Fintrol may lose
its federal EPA registration (Exhibits 1 & 9).

There are numerous tests on Fintrol and antimycin that have not been
done, let alone passed. In particular, there is little known about
antimycin's breakdown products, including their toxicity and
persistence, nor is there currently a chemical analytical method capable
of measuring antimycin in deployment concentrations (Exhibit 1).

The data gaps that were identified by California include (Exhibit 8):

1\) Acute dermal studies on the technical grade active ingredient

2\) Primary eye studies on the technical grade active ingredient

3\) Dermal irritation studies on the technical grade active ingredient

4\) Acute dermal studies on the formulated product

5\) Primary eye studies on the formulated product

6\) Dermal irritation studies on the formulated product

7\) Acute oral toxicity study on the diluent

8\) Acute dermal toxicity study on the diluent

9\) Primary eye study on the diluent

10\) Dermal irritation study on the diluent

11\) Product chemistry for Antimycin A technical

12\) Description of the manufacturing process

13\) Discussion of formation of impurities

14\) Preliminary analysis and certified limits of antimycin

15\) Enforcement analytical method for antimycin

16\) Data for hydrolysis

17\) Data for aqueous photolysis

18\) Data for anaerobic aquatic metabolism

19\) Data for aerobic aquatic metabolism

20\) Data for leaching and adsorption/desorption

21\) Data for magnitude of residue in fish

22\) Adequate fish and wildlife data

The New Mexico Department of Health also has reservations about the
safety of antimycin use. Its position as of August 13, 2002 is (Exhibit
10):

"*The New Mexico Department of Health has not yet fully evaluated the
possible adverse health effects of human exposure to antimycin used in
native fish restoration projects. We understand that, on our
recommendation, the New Mexico Department of Game and Fish is
contracting with a toxicologist to conduct a study of possible health
risks before the next intended application of Fintrol (active
ingredient: antimycin). The Department of Health awaits the results of
this study in determining its opinion.*"

Barbara Malczewska-Toth, Ph.D., D.A.B.T.

Environmental Health Epidemiologist

Office of Epidemiology

New Mexico Department of Health

\(505\) 476-3028

barbarat@doh.state.nm.us

DIETHYL PHTHALATE

The EPA considers diethyl phthalate to be an endocrine disruptor.
Endocrine disruptors mimic natural hormones and have an adverse effect
on the structure or functioning of the endocrine system, which includes
the pituitary, hypothalamus, thyroid, adrenals, pancreas, thymus,
ovaries, and testes. Compounds which are toxic to the endocrine system
can cause health effects ranging from hypothyroidism and diabetes to
infertility, low sperm count, birth defects, and testicular, breast, and
prostate cancer.

There is growing scientific concern about the health impacts of human
exposure to endocrine disrupting chemicals, in large part because of
their widespread presence in the environment and because their adverse
effects can often be caused by extremely minute quantities, at levels
not previously considered to be in the toxic range.

For example, a recent study found that frogs exposed during larval
development to as little as .1 part per billion (ppb) of the herbicide
atrazine developed male and female sex organs (Exhibits 11 & 12). The
authors concluded that "this widespread compound and other environmental
endocrine disruptors may be a factor in global amphibian declines".

Diethyl phthalate is a priority pollutant under the Clean Water Act. It
is also listed as a hazardous constituent under the Resource
Conservation and Recovery Act and as a hazardous substance under
Superfund (4). The EPA may be considering the removal of diethyl
phthalate from all pesticide products (Exhibit 1). Diethyl phthalate is
on the EPA List 2, "Potentially Toxic Inerts, High Priority for Testing"
([www.epa.gov/opprd001/inerts/inerts_list2.pdf](http://www.epa.gov/opprd001/inerts/inerts_list2.pdf)).

According to a National Toxicology Program fact sheet (5), diethyl
phthalate is toxic by ingestion and inhalation and poisonous by the
intravenous route. It is an irritant of the skin, eyes, mucous membranes
and upper respiratory tract. It is a narcotic in high concentrations. It
is also listed as an experimental teratogen, which means it can cause
birth defects in developing fetuses, and it can cause other experimental
reproductive effects. Studies have shown, for example, abnormal
development of male fetuses in rats exposed to this chemical (6).

The New Jersey Department of Health and Senior Services Hazardous
Substance Fact Sheet (7) notes numerous toxic effects of diethyl
phthalate. Exposure to vapors can irritate the nose and throat. Contact
can irritate the eyes and skin, and repeated exposure may damage the
nervous system. It also notes that chronic (long-term) health effects
can occur at some time after exposure to diethyl phthalate even if the
exposure levels were not high enough to make someone immediately sick.
It also warns that there is evidence that diethyl phthalate is a
teratogen in animals and that until further testing is done, this
chemical should be treated as a possible teratogen in humans. And while
those working directly with diethyl phthalate are at higher risk than
the general public, the fact sheet states that people in the community
may be exposed to diethyl phthalate in contaminated water and air and
that children and people who are already ill would be at the most risk
of developing health problems from it.

Diethyl phthalate is moderately persistent in the environment and has
moderate acute and chronic toxicity to aquatic life. According to one
source, the concentration of diethyl phthalate found in fish tissues is
expected to be somewhat higher than the average concentration found in
the water from which the fish was taken (8).

Finally, one can not be sure that the diethyl phthalate in the Fintrol
product is not contaminated with other phthalates, such as diethyl-hexyl
phthalate (DEHP), which is listed as a chemical known to the state of
California to cause cancer (California's Proposition 65 list, June 22,
2001).

NONOXYL-9

According to Philip Dickey in his publication "Troubling Bubbles" (9),
nonoxyl 9 is an alkylphenol ethoxylate that can disrupt the endocrine
systems of fish, birds, and mammals. For example, nonylphenol, a
breakdown product of nonylphenol ethoxylate, can cause a reduction in
testicular size in rainbow trout and cause male trout to produce an
egg-yolk protein that is normally only produced by females. Rats
administered nonoxynol-9 in one study produced a statistically
significant, dose-related number of fetuses with both extra ribs and
slightly dilated pelvic components.

Nonylphenol ethoxylate is also noted for its slow incomplete
biodegradation. It tends to persist in the environment and
bioconcentrate. Many times the breakdown products are more toxic to
aquatic life than the original chemical. There is evidence for synergism
between nonylphenolic metabolites, indicating that the adverse effects
from a mixture of compounds may be greater than the sum of the effects
from the individual compounds. Nonylphenolic compounds have been
detected in groundwater. Alkylphenol ethoxylates have been banned in
many countries in Europe. And it is the recommendation of the author
that the use of alkylphenol ethoxylates as inert ingredients in
pesticide formulations applied to aquatic environments be discontinued.

ACETONE

Acetone is a volatile neurotoxic solvent, which can cause central
nervous system depression (Exhibit 2). It constitutes more than 50% of
the Fintrol product.

POTASSIUM PERMANGANATE

Potassium permanganate is a hazardous caustic alkali. Targets organs
include the respiratory and central nervous system, blood, and kidneys
(10). If swallowed, it can cause nausea, vomiting, gastrointestinal
irritation and burns to the mouth and throat. It may also cause severe
irritation or burns to the eye and skin. Prolonged inhalation of
potassium permanganate can cause manganism from a toxic build up of
manganese in one's body. According to one Material Safety Data Sheet
(11), potassium permanganate has also been reported to cause
reproductive toxicity in laboratory animals and states that the
ecological effects of this product have not been evaluated.

Potassium permanganate can be directly toxic to fish, even at deployment
concentrations of 1 part per million (Exhibit 13). It can also kill
algae which provides oxygen for fish (12) and kill phytoplankton and
macrophytes that fish use for food (13).

Although potassium permanganate will help neutralize the antimycin A it
comes in contact with, it does have its limitations. According to the
authors of "Limitations on Potassium Permanganate Detoxification of
Antimycin" (Exhibit 14), potassium permanganate rapidly detoxifies
antimycin to a toxicity level equivalent to about 4% of the original
concentration. From there on, the detoxification is quite slow. They
conclude that the use of antimycin-potassium permanganate systems in
fish control would probably entail undue risk in most situations
involving antimycin-sensitive fish, soft water and a need for rapid
detoxification. There will also inevitably be some uneven mixing of
potassium permanganate with antimycin A as well as other factors that
retard their chemically reacting with each other.

It is overly optimistic to think that potassium permanganate will
totally neutralize antimycin A or that deploying another toxic chemical
will return the stream to its former non-polluted condition. It also
ignores the fact that potassium permanganate will have little or no
effect on the levels of acetone and nonoxyl-9 present.

ROTENONE

Rotenone is a highly toxic mitochondrial poison whose mode of action is
similar to antimycin. It is used to induce Parkinson-like illnesses in
lab animals. Rotenone is more persistent in the environment than
antimycin.

*In 1997, rotenone was used in a failed attempt to eradicate non-native
fish in Lake Davis, California. Many nearby residents were made sick
from breathing the piscicide fumes, water supplies were polluted (the
town has still not resumed using the lake for drinking water), and the
community and economy were disrupted for years.*

Rotenone products are often formulated with toxic solvents such as
trichloroethylene, xylene, trimethylbenzene, naphthalene,
1-m-naphthalene, 2-m-naphthalene, toluene and a liver poison piperonyl
butoxide (PBO).

Piperonyl butoxide is a possible human carcinogen according to the EPA,
and naphthalene and trichloroethylene are known to the state of
California to cause cancer. 

*Two rotenone products are proposed for use in Rio Costilla drainage --
CFT Legumine and Prentox Rotenone Fish Toxicant Powder. Both product
labels display a skull and crossbones with the highest toxicity warning
given by the EPA, "DANGER, POISON." Both labels state that the product
is "Fatal if inhaled". Applicators must wear personal protective
equipment to mix and deploy these products. NMDGF does not offer
wildlife the same protective gear.*

*CFT Legumine contains rotenone (active ingredient) 5%, other associated
resins 5%, rotenolone (rotenone breakdown product),
n-methyl-2-pyrrolidone, diethylene glycol ethyl ether, 1,3,5 --
trimethylbenzene, sec-butylbenzene, n-butylbenzene, naphthalene, methyl
naphthalene, p-isopropyl toluene. (Source: LFT Legumine label and
analytical report submitted by California Dept of Fish & Game to the
Lahontan Regional Water Quality Control Board on July 8, 2004).*

*Both n-methyl pyrrolidone and diethylene glycol ethyl ether are
reproductive toxins. N-methyl pyrrolidone is on the Proposition 65 list
of chemicals known to the state of California to cause reproductive
toxicity. The MSDS notes that this chemical is rapidly absorbed by the
skin and may affect pregnancy and fetal development.*

*NIOSH Registry of Toxic Effects of Chemical Substances (RTECS) lists
diethylene glycol ethyl ether as a "mutagen, reproductive effector, and
primary irritant". It is on U.S. EPA List 2, "Potentially Toxic Inerts,
High Priority for Testing,
[www.epa.gov/opprd001/inerts/inerts_list2.pdf](http://www.epa.gov/opprd001/inerts/inerts_list2.pdf)).*

*Naphthalene is classified as a possible human carcinogen by the U.S.
EPA and is known by the State of California to cause cancer.*

*Prentox Rotenone Fish Toxicant Powder contains 7.4% rotenone (active
ingredient) and 11.1% other associated resins. 81% of the product is
comprised of unknown ingredients, but likely include some of those
listed above, with the exception of PBO.*

EPA REGISTRATION AND SAFETY

Those in favor of using antimycin in fish restoration projects argue
that Fintrol is an EPA registered product and therefore safe to use. But
**registration of a pesticide by the EPA does not mean it is safe**.
This cannot be stressed enough. Legal use does not equal "safe" use. EPA
has specifically stated that, "Pesticides are *not* safe. They are
produced specifically because they are toxic to something" (14). In
fact, it is against federal FIFRA law for a manufacturer to claim or
imply that its product is "safe", "harmless," or "nontoxic to humans and
pets" (15) or endorsed by the EPA (16).

*[Federal Insecticide, Fungicide and Rodenticide Act
(FIFRA)]{.underline}*

40 CFR 156.10(a)(5), Labeling Requirements for Pesticides, False or
Misleading Statements.

"... a pesticide is misbranded if its labeling is false or misleading
...Examples of statements or representations in the labeling which
constitute misbranding include:

\(ix\) Claims as to the safety of the pesticide or its ingredients,
including statements such as 'safe,' 'nonpoisonous,' noninjurious,'
'harmless' or 'nontoxic to humans and pets' with or without such a
qualifying phrase as 'when used as directed';

\(v\) Any statement directly or indirectly implying that the pesticide
or device is recommended or endorsed by any agency of the Federal
Government;"

Another shortcoming of pesticide regulation is that chronic toxicity
tests are usually only done on the active ingredient rather than the
whole product and manufacturers are not required to reveal the so-called
"inert" ingredients in their products (other than to the EPA) even
though they can be more toxic than the active ingredient. Neither are
the "inert" ingredients required to be listed on pesticide product
labels. The Fintrol label names several "inert" ingredients, but not all
of them are listed (17).

Another argument by proponents for antimycin use is that it will be used
in such low concentrations that no harmful effects will occur. But this
ignores the possibility of misapplications and spills, especially of the
concentrated product (which are not uncommon with pesticides),
endocrine-disrupting effects that can occur at extremely low levels, and
the fact that the full toxicity of the individual or combination of
chemicals in Fintrol is unknown.

CHEMICAL SENSITIVITY

Some individuals are much more sensitive to toxic exposures than others.
Just as different species of fish and different fish of one species have
varying sensitivities to antimycin A, so are there likely to be huge
differences in human susceptibility to it (as well as the other
chemicals in Fintrol). A survey by the New Mexico Department of Health
found that 16% of the respondents to a statewide random population-based
survey reported that they were unusually sensitive to common chemicals,
including pesticides (Exhibit 15). The percentage of respondents who
reported being chemically sensitive were the same for those living in
rural and urban areas in all parts of the state.

The governor and several state agencies in New Mexico acknowledge that
there are New Mexicans who are chemically sensitive. The brochure on
multiple chemical sensitivities which contained the above survey
statistics was written by the Multiple Chemical Sensitivities Task Force
in collaboration with, and endorsed by, the New Mexico Departments of
Health, Environment, and Education and the Governor's Committee on
Concerns of the Handicapped. Governor Gary Johnson also proclaimed
Multiple Chemical Sensitivity Awareness Week in 1998 (Exhibit 16).

Chemically sensitive people can react adversely to even minute exposures
to pesticides at levels that are many orders of magnitudes below levels
that would harm the average person. In addition, at least some
chemically sensitive people already suffer from a defect in oxygen
utilization \-- the exact toxic effect of antimycin A. This is evidenced
by high venous oxygen levels in these individuals indicating that oxygen
is not being taken up and used by body tissues. Thus, these people are
already in cellular respiratory distress. They can ill afford even the
smallest additional loss of mitochondrial function which exposure to
antimycin A could cause. Children, the elderly, pregnant women, and
those with other chronic illnesses are also more susceptible to toxic
chemicals.

Since Fintrol is a pesticide that contains several toxic chemicals, it
is likely that chemically sensitive people would react adversely to even
very low levels of exposure to it. This could occur through consumption
of or contact with downstream water. In addition, some applicators and
staff deploying Fintrol may have some degree of chemical sensitivities
and also be at increased risk from exposure to the chemicals in this
product.

LIMITATIONS OF RISK ASSESSMENT & REFERENCE DOSE

William Ruckelshaus (the first administrator of U.S. Environmental
Protection Agency) said in 1984, \"*We should remember that risk
assessment data can be like the captured spy: If you torture it long
enough, it will tell you anything you want to know*.\"

\[William Ruckelshaus, \"Risk in a Free Society,\" Risk Analysis Vol. 4,
No. 3 (1984), pgs. 157-162. Available at
<http://www.rachel.org/library/getfile.cfm?ID=361>\].

Risk assessments do not take into account mutagenic and carcinogenic
effects of chemicals. They, along with Rederence doses (RfD) also fail
to adequately account for the wide range of variability among humans in
their tolerance for chemicals. Risk assessments typically include a fact
or 10, 100, or 1000 to account for intraspecies variation, but based on
the cumulative experience of people with chemical sensitivities and the
growing body of research on variations in the human genome, gene
expression, and vulnerability to toxic exposures, the true range of
human variability is probably closer to 5 to 10 orders of magnitude.

The U.S. EPA also identifies limitations of using the RfD to estimate
toxicity of chemicals (*Reference Dose(RfD): Description and Use in
Health Risk Assessments*,
[www.epa.gov/iris/rfd.htm](http://www.epa.gov/iris/rfd.htm)).

1.2.2. SOME DIFFICULTIES IN UTILIZING THE TRADITIONAL APPROACH

1.2.2.1. Scientific Issues

While the traditional approach has performed well over the years and the
Agency has sought to be consistent in its application, observers have
identified scientific shortcomings of the approach. Examples include the
following:

a\. Too narrow a focus on the NOAEL means that information on the shape
of the dose-response curve is ignored. Such data could be important in
estimating levels of concern for public safety.

b\. As scientific knowledge increases and the correlation of precursor
effects (e.g., enzyme induction) with toxicity becomes known, questions
about the selection of the appropriate \"adverse effect\" arise.

c\. Guidelines have not been developed to take into account the fact
that some studies have used larger (smaller) numbers of animals and,
hence, are generally more (less) reliable than other studies.

These and other \"scientific issues\" are not susceptible to immediate
resolution, since the data base needed is not yet sufficiently developed
or analyzed. U.S. EPA work groups are presently considering these
issues.

1.2.2.2. Management-related Issues

1.2.2.2.1. The use of the term \"safety factor\"

The term \"safety factor\" suggests, perhaps inadvertently, the notion
of absolute safety (i.e., absence of risk). While there is a conceptual
basis for believing in the existence of a threshold and \"absolute
safety\" associated with certain chemicals, in the majority of cases a
firm experimental basis for this notion does not exist.

1.2.2.2.2. The implication that any exposure in excess of the ADI
\[acceptable daily intake\] is \"unacceptable\" and that any exposure
less than the ADI is \"acceptable\" or \"safe\"

In practice, the ADI is viewed by many (including risk managers) as an
\"acceptable\" level of exposure, and, by inference, any exposure
greater than the ADI is seen as \"unacceptable.\" This strict
demarcation between what is \"acceptable\" and what is \"unacceptable\"
is contrary to the views of most toxicologists, who typically interpret
the ADI as a relatively crude estimate of a level of chronic exposure
which is not likely to result in adverse effects to humans. The ADI is
generally viewed by risk assessors as a \"soft\" estimate, whose bounds
of uncertainty can span an order of magnitude. That is, within
reasonable limits, while exposures somewhat higher than the ADI are
associated with increased probability of adverse effects, that
probability is not a certainty. Similarly, while the ADI is seen as a
level at which the probability of adverse effects is low, the absence of
all risk to all people cannot be assured at this level.

1.2.2.2.3. Possible limitations imposed on risk management decisions

**Awareness of the \"softness\" of the ADI estimate, as discussed above,
argues for** **careful case-by-case consideration of the toxicological
implications of individual situation, so that ADIs are not given a
degree of significance that is scientifically unwarranted. In addition,
the ADI is only one factor in a risk management decision and should not
be used to the exclusion of other relevant factors.** (emphasis added)

Risk assessment also asks the wrong question. It asks "How much toxic
substance can we tolerate?". The preferred approach uses the
Precautionary Principle which asks "How can we avoid exposure to this
toxic substance?". It requires seeking least hazardous alternatives.

ENDOCRINE DISRUPTION

While pesticide active ingredients are evaluated for gross reproductive
and development effects, many endocrine-disrupting effects are far more
subtle. Many effects cause behavioral and other functional abnormalities
rather than obvious birth and other anatomic defects. For example,
several studies have shown that 2,4-D exposure during lactation can
alter brain development and subsequent adult behavior (see reference
below). In addition, endocrine-disruption may occur more prominently
with lower rather than higher doses. This means that diluting
endocrine-disrupting substances can increase rather than decrease their
impact(s).

According to Theo Colborn,

> *The U.S. EPA has rarely used the open literature in its risk
> assessments, generally using only data submitted by manufacturers.
> Industry continues to use traditional toxicology protocols that test
> for cancer, reproductive outcome, mutations, and neurotoxicity, all
> crude end points in light of what is known today about functional end
> points. In using manufacturer data, the U.S. EPA misses almost all
> delayed developmental, morphologic, and functional damage of fetal
> origin ... Brucker-Davis (1998) published a comprehensive review of
> the open literature in which she found 63 pesticides that interfere
> with the thyroid system -- a system known for more than a century to
> control brain development, intelligence, and behavior. Yet, to date,
> the U.S. EPA has never taken action on a pesticide because of its
> interference with the thyroid system*. (*A Case for Revisiting the
> Safety of Pesticides: A Closer Look at Neurodevelopment* by Theo
> Colburn, Env. Health Perspectives, Vol. 114, No. 1, January, 2006,

<http://ehp.niehs.nih.gov/members/2005/7940/7940.pdf>)

The EPA has, however, expressed concern that "*Based on currently
available toxicity data, which demonstrates effects on the thyroid and
gonads following exposure to 2,4-D, there is concern regarding its
endocrine disruption potential*" (EPA Reregistration Eligibility
Decision for 2,4-D, June, 2005, p. 21,
[www.epa.gov/oppsrrd1/REDs/24d_red.pdf](http://www.epa.gov/oppsrrd1/REDs/24d_red.pdf)).
The EPA also noted there was a need for further testing of 2,4-D
regarding its endocrine-disrupting potential.

The EPA is only beginning to look at endocrine effects from pesticide
and other chemicals. The lack of a list of endocrine-disrupting
chemicals is an indication that they have yet to be adequately studied
rather than their not being important to study.

MACROINVERTEBRATES

While the petition acknowledges that antimycin will have an initial
adverse impact on stream macroinvertebrates, it assumes that the
macroinvertebrate community will eventually return to its pretreatment
status. But several studies have found that while macroinvertebrate
communities frequently return, they may be altered from their original
composition (18, 19). And many unanswered questions remain regarding the
long-term effect of antimycin on macroinvertebrates.

According to a NM Department of Game and Fish study, *"Macrobenthic
Analysis for S. Ponil Creek" by Steven Sanders, NMDGF Fisheries
Biologist, 2001*, "the use of antimycin for fish eradication is
extensive in the USA, but its affects on benthic populations are not
well known" (19*). This study also demonstrated that 9 months after an
antimycin application, some macroinvertebrate species that were present
before antimycin deployment were no longer present and some species were
detected that had not been present before the application. In addition,
deformed gill filaments were noted in some species after antimycin
exposure.*

In a report prepared by Daniel McGuire entitled "Aquatic
Macroinvertebrate Survey of Animas, Seco and South Palomas Creeks" (20),
the author states that with respect to proposed use of Fintrol in those
creeks, "a few macroinvertebrate taxa that are particularly sensitive to
antimycin and have poor recuperative powers may suffer long-term impacts
from the (antimycin) treatment". This is also likely true for
macroinvertebrates in the Rio Costilla drainage, with the largest impact
expected to occur in organisms with the longest reproductive cycles.
There may also be uniquely adapted macroinvertebrate species that do not
return at all.

*In a federal court ruling last summer that granted a preliminary
injunction to stop the use of rotenone in Silver King Creek in
California, it states with regard to irreparable harm, \"There is no
dispute that poisoning the waters with rotenone, a highly toxic chemical
lethal to aquatic organisms that obtain oxygen from water, will kill
macroinvertebrates and certain species may never return to the impacted
area.\" (Californians for Alternatives to Toxics v. USDA Forest Service,
No. Civ. S-05-1633 FCD KJM).*

AMPHIBIANS

It is well recognized that there has been a disturbing global decline in
amphibian populations in recent years and many scientists suspect that
exposures to toxic chemicals are a significant cause. Several studies
have linked pesticide exposure to adverse effects in frogs. As mentioned
above, one study found that frogs exposed to as little as .1ppb of the
herbicide atrazine developed male and female sex organs (Exhibits 11 &
12). Another study found that frogs exposed to either atrazine or a
pyrethroid insecticide, esfenvalerate, were more susceptible to
infection by a parasitic worm that caused limb deformities. (Exhibits 17
& 18). The pesticides appeared to depress the frogs' immune systems even
at the low concentrations used, which were within EPA drinking water
standards for humans. The authors concluded that "these negative impacts
may help explain pathogen-mediated amphibian declines in many regions."

In another study (Exhibit 19), frogs given trace amounts of DDT
experienced a near total collapse in their immune systems, which was
identical to their exposure to cyclophosphamide. The latter is a drug
given to humans to suppress their immune systems so they do not reject
organ transplants. The researchers found that as little as 75 ppb DDT
caused frogs' immune systems to malfunction.

In a 2002 report by Bruce Christman, "Investigations of the Status and
Distribution of Amphibians on the Ladder Ranch with Special Emphasis on
the Chiricahua Leopard Frog" (21), he expressed concern about the threat
of chytrid fungus to amphibians on the Ranch. He further noted that this
fungus has been implicated as a cause of a recent decline in a
population of Chiricahua leopard frogs in New Mexico. He then suggests
sanitation measures to help reduce the spread of chytrid fungus.

But as important at these measures are, infectious disease does not just
occur because an animal is exposed to an infectious agent. Disease only
results when an animal's immune system is unable to protect it from the
agent. This is especially true of fungal agents, which often cause
opportunistic infections in hosts with weakened immune systems.
Therefore, in order to reduce the incidence and spread of
chytridiomycosis, it is as important to avoid harming amphibian immune
systems as preventing their exposure to the chytrid fungus.

To avoid causing such harm, the environment must be kept as free of
pollutants as possible since, amphibian immune and endocrine systems are
very fragile and can be adversely impacted by even extremely low levels
of toxic chemicals. Thus, even if poisons such as antimycin/Fintrol or
other piscicides do not kill amphibians immediately, they may still harm
them by making them more vulnerable to serious diseases due to immune
suppression, or cause them to have developmental abnormalities or
reduced fertility via endocrine disruption.

The northern Leopard Frog is present in the Rio Costilla project area
and is considered a sensitive species by the Forest Service.

[REFERENCES]{.underline}:

1\) Federal Register / Vol. 66, No. 241 / Friday, December 14, 2001 /
Rules and

Regulations, p. 64765.

2\) Environmental Mutagen Information Center, Antimycin,
[http://toxnet.nlm.nih.gov/cgi-bin/sis/search/d?./temp/\~AAAN4aqFY:0:BODY]{.underline}

3\) <http://www.cdpr.ca.gov/cgi-bin/epa/mkrep3.pl>

4\) Environmental Defense Scorecard,
[http://www.scorecard.org/chemical-profiles/regulation.tcl?eft_substance_id=84%2d66%2d2](http://www.scorecard.org/chemical-profiles/regulation.tcl?eft_substance_id=84-66-2)

5\) National Toxicology Program Chemical Repository, Diethyl Phthalate,
[http://ntp-db.niehs.nih.gov/NTP_Reports/NTP_Chem_H&S/NTP_Chem8?Radian84-66-2.txt]{.underline}

6\) Personal communication with Gary Timm, U.S. Environmental Protection
Agency, Washington, DC, February 13, 2002.

7\) New Jersey Department of Health and Senior Services Hazardous
Substance Fact Sheet on Diethyl Phthalate, July 1996.

8\) Information provided through EcoGopher of the University of Virginia
Office of Recycling and Environmental Information,
<http://www.familyjeweler.com/fortweb/DiethylPhthalateEPA.htm>

9\) Dickey P, Washington Toxics Coalition, "Troubling Bubbles, the Case
for Replacing Alkylphenol Ethoxylate Surfactants," July 1997.

10\) ProSciTech, Material Safety Data Sheet, Potassium Permanganate, Oct
1998, [www.proscitech.com.au/msds/c364.pdf]{.underline}

11\) Bacharach, Inc. MSDS No: 4099-1456 Material Safety Data Sheet,
Potassium Permanaganate, 3-13-97,
[www.bacharac-inc.com/PDF/MSDS/40991456.pdf]{.underline}

12\) Mississippi State University Extension Service, MSU Cares,
"Potassium Permanganate For Fish Ponds",
[http://www.msucares.com/pubs/is1265.htm]{.underline}

13\) Erik L Johnson, DVM, "Potassium Permanganate: The Perfect Salt
Supplement?", <http://www.arborman.com/potperm1.htm>

14\) U.S. Environmental Protection Agency, 1987, "Citizens Guide to
Pesticides," Washington, DC.

15\) 40 CFR 156.10(5) (ix)

16\) 40 CFR 156.10(5) (v)

17\) Personal communication with Jay Shrider, California Department of
Pesticide Regulation, Medical Toxicology Branch, February 4, 2002.

18\) Minckly WL, Mihalick P, J Ariz-Nev Acad Sci 16 (3): 79-82, 1981.

19\) Sanders, SA, "Macrobenthic Analysis for South Ponil Creek in Colfax
County New Mexico," NM Department of Game and Fish, Fisheries Management
Division, December 5, 2001.

20\) DL McGuire, "Aquatic Macroinvertebrate Survey Animas, Seco, and
South Palomas Creeks, Sierra County, NM, March, 1999.

21\) BL Christman, "Investigations of the Status and Distribution of
Amphibians on the Ladder Ranch with Special Emphasis on the Chiricahua
Leopard Frog *(Rana chiricahuensis)*, January 20, 2002.

[EXHIBITS]{.underline}:

1\) BJ Finlayson, et. al, "Assessment of Antimycin A Use in Fisheries
and Its Potential for Reregistration," Fisheries, Vol. 27 No. 6, June
2002, www.fisheries.org

2\) Aquabiotics Corporation, Material Safety Data Sheet on Antimycin A
in Acetone

3\) U.S. Environmental Protection Agency Profile on Antimycin A (1987)

4\) University of California at Santa Cruz "Laboratory Standard
Operating Procedure for Antimycin A"

5\) ToxNet Hazardous Substance Databank information on Antimycin A

6\) NIOSH Registry of Toxic Effects of Chemical Substances (RTECS) Re:
Antimycin A

7\) Abstract of "Role of caspases (ICE/CED 3 proteases) in DNA damage
and cell death in response to a mitochondrial inhibitor, antimycin A,"
GP Kaushal, N Ueda, and SV Shah, 1997

8\) Letter from Steven Rhodes, California Department of Pesticide
Regulation, to Nicholas Romeo, President of Aquabiotics Corporation,
regarding the proposed denial of application for registration of Fintrol
Concentrate, EPA Reg. No. 39096-2, December 3, 2001

9\) TD Hubert and LJ Schmidt, U.S. Geological Survey, La Crosse,
Wisconsin, "Antimycin A Use in Fisheries: Issues Concerning EPA
Reregistration," March 9, 2001

10\) Email from Dr. Barbara Malczewska-Toth of the New Mexico Department
of Health to Ann McCampbell regarding the department's position on the
use of antimycin for fish restoration, 8/13/02

11\) Abstract of "Hermaphroditic, demasculinized frogs after exposure to
the herbicide atrazine at low ecologically relevant doses," Hayes TB,
et. al, Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 8, 5476-5480, April
16, 2002

12\) Randolph Schmid, Associated Press, "Commonly used pesticide blamed
for mutations in frogs," April 16, 2002

13\) Abstract of "Histological and Hematological Evaluation of Potassium
Permanganate Exposure in Channel Catfish," Darwish AM, et. al, Journal
of Aquatic Animal Health (2002): Vol. 14, No. 2, pp. 134-144

14\) Abstract of "Limitations on potassium permanganate detoxification
of antimycin," Engstrom-Heg R, Colesante RT, N Y Fish Game J, 26(2),
1979, 132-141

15\) Multiple Chemical Sensitivities brochure

16\) State of New Mexico, Executive Office, Santa Fe, New Mexico,
Proclamation of "Multiple Chemical Sensitivity Awareness Week," Governor
Gary Johnson, May 5, 1998

17\) Abstract of "Synergism between trematode infection and pesticide
exposure: A link to amphibian limb deformities in nature," Kiesecker JM,
Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 15, 9900-9904, July 12, 2002

18\) Stentor Danielson, National Geographic News, "Pesticides, Parasite
May Cause Frog Deformities," July 9, 2002

19\) Martin Mittelstaedt, Toronto Globe and Mail, "Study finds DDT may
spur disease," April 24, 2002