Download McCance Page October 3, 2011 PO Box 1454 Boulder, UT 84716

October 3, 2011
PO Box 1454
Boulder, UT 84716
Appeal Deciding Officer
Intermountain Region USFS
324 25th Street
Ogden, Utah 84401
Subject: Appeal for the East Fork Boulder Creek Native Trout Restoration Project-Decision
Notice and FONSI
To Whom It May Concern:
It is early morning not quite light and I sit in front of my computer. I am surrounded by
numerous studies and documents and wonder, will it be possible to really understand
exposure to pesticides and health effects because of competing priorities like financial
interests, jobs, recreational needs, health necessity, and methods to accurately measure
exposure? Given this complex web of priorities data interpretation needs an unbiased
approach.
In medicine today and because of the many factors impinging on public health, twin studies,
adoption studies, family studies, and international studies have become very important to
understand gene-environment interaction and disease susceptibility and outcome. Key for
many diseases is comparisons between countries and researcher groups that seemingly
have no conflict of interest in outcomes. This may be hard to achieve but it is happening all
around the world with groups of scientists who are grappling with these environmental
and health effect studies. These approaches are critical for public health and now it is being
understood that a long latency period precedes the adult onset of certain diseases, like
cancer and neurodegenerative disorders. Investigators have now turned into blood-hounds
trying to uncover early life events that can have immediate and lifelong consequences. In
fact, what may be new to readers of this appeal is the concept called developmental
plasticity, or the degree to which an organism’s development is contingent on its
environment. It requires stable gene expression that, in part, appears to be modulated by
epigenetic processes. Sensitivity to environmental-lifestyle factors influences the mature
phenotype and is dependent on the interactions of both the genome and epigenome.
Studies of gene-environmental interactions whereby individuals with particular genetic
predispositions may be more susceptible to the biologic effects of environmental exposures
cannot explain the increased cancer risk in studies of exposed groups. More simply, it
appears that the majority of cancers are caused by carcinogen exposure rather than by rare
genetic conditions. For example, women who have mutated cancer susceptibility genes
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BRCA1 or BRCA2, the risk of having breast cancer at age 50 is 24% for those born before
1940 but 67% for those born later. The implication here is related to lifestyle factors that
changed from 1940 (i.e., hormonal therapy, later age at first pregnancy, increased
nulliparity, etc.). Investigations of more complex gene-gene environmental interactions and
proteomics may or may not alter these conclusions. This model of disease origin is a
relevant model for pesticides and disease onset. Therefore, I have summarized studies in
this appeal and overview as a response to the EA that includes both biological and
epidemiological evidence connecting PD to exposure to rotenone.
Important for me and after reviewing many studies is the fact that UDWR is not using
powder for the rotenone treatment because of the known dangers with inhalation but will
use liquid formulations that are more effectively dispersed (see appeal from Matt Cochran
for rotenone formulations). So the choice for Boulder, Utah, is to use liquid. Liquid
formulations of rotenone require dispersing agents, often petroleum chemicals, and herein
is another concern. Numerous chemicals are listed in the EA as dispersing agents but no
data are discussed specifically on the health effects of these combinations of chemicals,
their longevity in water, their persistence in the environment (not just water but also soil
and organic components in the water), and their synergistic effects with rotenone. This is a
big problem for me and from reading other documents it has created public health
concerns. Boulder is no different from the concerns generated in California, Arizona, New
Mexico, and other states. I have read the EA on dosing and the mathematical extrapolations
of what dose is below toxic levels in adults and possibly children but I am not convinced
from these documents that a lingering persistent low-dose of rotenone, petroleum
products, and maybe oxidizing agents should not be a concern for adults, children,
pregnant women, and fetuses. Although rare, as an example of how mixtures increased
toxicity of rotenone is the child who ingested around 10mL of Galicide that contained 6%
rotenone as well as essential oils of clove, cinnamon, fir, rosemary, and thyme and who
developed a gradual loss of consciousness over two hours and died of respiratory arrest six
hours later (De Wilde et al., 1986), The lethal dose was estimated at 40mg/kg, which is
considerably less than the dose amount given as lethal in many documents (i.e., 300500mg/kg). Key here is that the essential oils in Galicide were alleged to have increased
toxicity by promoting absorption of the water insoluble rotenone from the gastrointestinal
tract and causing acute kidney damage and thereby reducing the clearance rate of rotenone.
The 50% lethal dose (LD50) varies greatly in many species. For example, 13 to 130 mg/kg
in guinea pigs, from 25 to 132 mg/kg in rats, and to 1500mg/kg in rabbits. In humans the
minimum LD is not known. Not discussed in the EA document is that LD50 is a crude
measure of toxicity because it does not recognize any toxic effects short of death. Thus, the
morbidity (not mortality) consequences of mixtures of rotenone and dispersing agents and
oxidizers is not addressed. It was not even addressed as a controversial issue of science.
The EA report did not have much to say about the recent research of Rotenone linked to
Parkinson Disease (PD). This was disappointing especially given that the EPA reviewed
rotenone in 2007, which noted that “…using the existing database, EPA cannot
quantitatively assess a potentially critical effect (neurotoxicity) at doses of which rotenone
users could be exposed.” Essentially neurological impacts of rotenone were not considered
in the EPA assessment and not reviewed carefully in the EA despite the fact that
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neurological impacts are the main health issue of concern for rotenone—so far! They did
state, however, that the epidemiological data was problematic and did not review recent
data from biological studies thoroughly. Perhaps the research of the relationship of
rotenone to PD is not a concern for rotenone use as a piscicide because of the dosages used.
The problem with this, however, is that individuals are exposed to pesticides overtime and
it is unknown what the accumulated chronic exposures are to the early onset and
progression of PD. Particularly concerning may be exposure of pregnant women and
fetuses. Included with my appeal is a 9-page overview of recent biological studies and an
attempt to address the EA concern about epidemiological studies.
Sincerely,
Kathryn L. McCance BSN, MS, PhD
Overview