Public
Information and Records Integrity Branch (PIRIB)
Information Resources and Services Division (7502C)
Office of Pesticide Programs (OPP)
Environmental Protection Agency
1200 Pennsylvania Avenue, NW
Washington, DC 20640
Docket
Control Number OPP-34239B – Lindane Revised Risk Assessment
Comments Submitted on Behalf of
the Natural Resources Defense Council
By Gina
M. Solomon, M.D., M.P.H.
Senior
Scientist
April 1, 2002
We are deeply disturbed to observe that EPA has essentially
ignored over a thousand comments from health groups, environmental groups,
public agencies, and members of the public on the Lindane Preliminary Risk
Assessment. Most importantly, EPA failed to adequately address three major
concerns with the lindane risk assessment: (1) the Agency failed to incorporate
pharmaceutical uses of lindane into both the health and ecological risk
assessments; (2) the Agency reduced the 10x child-protective factor to only 3x
despite clear evidence of data gaps and of disproportionate susceptibility of
fetuses and neonates to lindane toxicity; and (3) EPA failed to even respond to
the fact (pointed out in our previous comments on the Lindane Draft Risk
Assessment) that the Agency did not include consideration of the breast milk
pathway in the exposure assessment.
Failure to Include Topical Use of Lindane for Lice and Scabies
The Agency notes that
over a thousand commenters informed EPA that the risk assessment of lindane
would be incomplete without the inclusion of the pharmaceutical use of lindane
as a lice and scabies treatment. The commenters are correct, and EPA should pay
careful attention to these comments and take immediate steps to correct the
problem. EPA should be well aware that the greatest exposure of children to
lindane comes from direct application of the pesticide to their scalp or body
for treatment of head lice or scabies. EPA should be aware that the greatest
current discharges of lindane into the environment come from the 1.41 million
applications per year of lindane shampoo, containing 1,320 pounds of active
ingredient, discharged into the nations sewage systems.
EPA should also be aware that the Food Quality Protection Act (FQPA) was
unanimously passed by Congress in order to prevent exactly this type of
mischaracterization of health risks to children.
The FQPA amended the FFDCA to allow EPA to establish or
leave in effect a tolerance for a pesticide chemical residue in or on a food only
if she determines that the tolerance is safe.
FFDCA §408(b)(2)(A)(i)(emphasis added).
A tolerance can only be considered safe if the Administrator determines
“that there is a reasonable certainty, that no harm will result from the
aggregate exposure to the pesticide chemical residue, including all anticipated
dietary exposures and all other exposures for which there is reliable
information.” FQPA §408(b)(2)(A)(ii).
In making these determinations, special consideration must be given to
the unique effects these pesticide residues may have on infants and children.
FFDCA §408(b)(2)(C). There is no
exception in the FQPA for pesticides that are also used as pharmaceuticals. It
is therefore patently obvious that EPA is ignoring the clear requirements of the
FQPA in failing to consider the major use of lindane, and the major risk of
lindane to children. Any tolerance set without determining that aggregate
exposures to children, including pharmaceutical exposures, are safe, is illegal
under the law. EPA cannot legally proceed to issue any final rules or tolerances
based on a risk assessment that fails to even consider the main exposure pathway
for children to lindane. The agencies response to the public “the Agency is
still exploring this issue.” Is utterly unacceptable. The risk assessment
should not proceed until this issue is addressed.
On November 5, 1979
(44 Federal Register, 63749), when EPA exempted lindane lice and scabies
products from the requirements of the FIFRA, the situation has changed
dramatically, most notably with passage of the Food Quality Protection Act of
1996 (FQPA). In light of the changes in law and science that have occurred in
more than two decades since EPA gave up control of lindane, the Agency must
either reassert its control over lice and scabies treatments under the FIFRA, or
at least consider the human health and environmental impacts of these treatments
in its current risk assessments. As lindane lice and scabies products dominate
the human health and environmental risks of lindane, the risk assessments are
meaningless without them. Under the
FIFRA, EPA has a statutory responsibility to ensure that pesticides are safe and
effective for their intended uses and to prevent unreasonable adverse effects to
man, other animals, and the environment from their usage (7 U.S.C. §136(bb), §136a(a),
§136a(d)(2); §136d(b)). By
ignoring the risks posed by lindane lice and scabies treatments, EPA is not
fulfilling its statutory responsibility.
EPA also fails completely to address public comments and
concerns about the enormous lindane discharges into public sewage systems due to
pharmaceutical uses of this chemical, and the resultant contamination of surface
waters. The Agency responds that it has funded two pollution prevention projects
“to see if the pharmaceutical use of lindane can be altered or replaced
with other treatments that are less persistent and/or less toxic to the
environment. However, the Agency has not evaluated this release scenario to
quantify the risk to human health or the environment.” Obviously EPA is
not au courant with the pollution prevention projects that the Agency funded.
EPA should know that the Region IX project has resulted in the complete ban of
pharmaceutical uses of lindane in California. This ban was possible because
there are ample choices of other treatments that can replace lindane for use
against lice and scabies. In fact, there is no scientific dispute about the
ready availability of alternatives. Most medical organizations no longer
recommend lindane due to the significant risk of childhood poisonings. EPA must
act quickly to evaluate the release scenario of lindane into water and quantify
the risk to human health and the environment. It is insane for EPA’s Office of
Pesticide Programs (OPP) to ignore this exposure pathway, while EPA’s Office
of Water sets a limit of 19 ppt on lindane in water – a level that sanitation
districts will violate unless OPP addresses the enormous problem of lindane
discharges from pharmaceutical uses.
EPA Must Retain the Full 10x Margin of Safety to Protect Children from
Lindane
EPA’s stated rationale for reducing the 10x FQPA margin
of safety to 3x is deeply flawed. EPA gives six reasons for reducing the FQPA
safety factor. Each of these reasons is either incorrect or irrelevant to the
question before the Agency. They are discussed and refuted below:
1)
“The toxicology data base is complete”
EPA repeatedly mentions that lindane has shown endocrine
disrupting effects in numerous studies submitted to EPA and in the open
literature. Rather than regulating lindane as an endocrine disruptor, however,
EPA states the intention to require future studies on the endocrine disrupting
effects of lindane through the Endocrine Disruptor Screening and Testing
Program. This statement of intention amounts to an acknowledgement that there
are significant data gaps in the toxicology database for lindane. If there were
no data gaps, there would be no need for endocrine disruptor testing. In
addition, as detailed below, EPA itself admits that lindane may be transformed
in the environment into the even more toxic isomer, b-HCH,
and the Agency asserts that the issue is still unresolved (discussed in greater
detail below). This is an extremely important data gap that must be addressed or
filled by using the full 10x factor. Thus it is incorrect for EPA to say that
the database is complete.
2)
“Available data provide no indication of increased susceptibility in
rats from in utero exposure to lindane in the prenatal developmental study.”
This statement is misleading and manipulative. EPA uses
three rat studies to assess fetal risk: a prenatal developmental study, a
reproductive toxicity study, and a developmental neurotoxicity study. While it
is true that there was no clear evidence of increased susceptibility in the
first study, the other two both clearly show qualitative, and in one case,
quantitative increased susceptibility in the fetus. If EPA is purporting to use
a weight-of-evidence approach to assessing the scientific literature, the
evidence clearly supports the disproportionate susceptibility of the fetus to
the toxic effects of lindane. Furthermore, biologic plausibility also supports
fetal susceptibility due to the various neurotoxic and endocrine disrupting
modes of action of this chemical in the fetus and neonate. Finally, the one
study that purported to fail to demonstrate increased fetal susceptibility –
the rat developmental study – is the least sensitive of the studies at
detecting functional abnormalities. In addition, there were increased skeletal
malformations compared to controls at all doses tested. The facts that the study
lacked statistical power to detect an effect on skeletal development, and lacked
the sensitivity to address functional endpoints are not be sufficient reason to
reduce the FQPA factor. Reducing the FQPA safety factor based on one study flies
in the face of the weight of scientific evidence and the mode of action of this
pesticide.
3)
“The offspring effects seen in the developmental neurotoxicity study
were the same as those seen in the two-generation reproduction study.”
Even if it were true, this statement would be irrelevant to
the question before the Agency. The more important issue is that both of these
studies clearly showed disproportionate vulnerability in the fetus. In addition,
this statement is incorrect. The developmental neurotoxicity study showed
increased motor activity and decreased motor activity habituation as compared to
controls. These endpoints are important because they are indicative of the same
type of CNS stimulation seen in human children who have been exposed to lindane.
Although full-blown seizures were not observed in this particular study, these
effects are along the continuum of CNS kindling and behavioral alterations that
have been observed in humans. These effects were seen in the offspring in the
absence of maternal toxicity. It should go without saying that CNS
hyperexcitability in the offspring at doses non-toxic to the mother is
indicative of a serious and very disturbing risk to the fetus, infant, and
child.
4)
“Adequate actual data, surrogate data, and/or modeling outputs are
available to satisfactorily assess food exposure and to provide a screening
level drinking water exposure assessment.”
This rationale is rather pathetic in light of the examples
presented in our comments showing that the Agency completely omits numerous
exposure pathways from the risk assessment. The adequacy of the exposure data
should be reconsidered after the agency evaluates and includes the data on
exposure to pharmaceutical lindane, pet products, lindane in breast milk,
lindane in fish, and historical residues of lindane.
5)
“Although the developmental toxicity study in rabbits was classified
unacceptable, the HIARC concluded that a new study is not required.”
This rationale is also irrelevant to the decision about the
10x FQPA factor. Whether or not a new rabbit study is needed, there are obvious
data gaps due to incomplete information about endocrine disrupting effects.
6)
“There are currently no residential uses.”
This is the strangest of the six reasons for abandoning the
FQPA margin of safety. Most members of the public would consider direct
application of lindane to a child’s skin (or to the skin of a household pet)
to be a residential use. Failure to acknowledge this use of lindane has a
Byzantine strangeness that baffles logic. Clearly there are residential uses.
EPA must include them and must use the full 10x FQPA margin of safety because of
these household uses and because none of the six justifications for abandoning
the 10x holds up to logic or scientific scrutiny.
EPA’s Confusion About Human Testing Policies
In Appendix B, page 3, HED responds to comments about the
numerous reports of childhood poisonings related to lindane. The response
asserts “However, current Agency policy is that a regulatory decision
cannot be made based on a human endpoint until a final policy regarding the
ethical aspect of the use of human studies for regulatory purposes is issued.”
Obviously HED is confused about the difference between purposeful dosing of
human subjects with toxic pesticides, and reports of poisonings collected by
Poison Control Centers, FDA, and EPA due to current uses of the chemical in
commerce. The industry practice of paying ‘volunteers’ to drink pesticide
potions is quite rightly under review for ethical and scientific reasons, and
such studies should not be used to support regulatory decisions. The collection
of data on ongoing childhood poisonings from lindane that is sold today in
commerce is an essential function of Poison Control Centers and is required by
law of FDA and EPA. These data can and should form the foundation of regulatory
decisionmaking. It is difficult for this commenter to comprehend how EPA could
be so confused as to conflate these two obviously different types of information
on human health effects.
EPA Fails to Include Exposure to b-HCH
In the response to public comment in Appendix B, page 6,
EPA responds, “HED believes the available data do not support significant
isomerization of lindane (gamma-HCH) to beta-HCH in the environment.”
In the risk assessment itself (p.9), EPA expresses much more uncertainty
than in the response to comments: “lindane can possibly transform to the
alpha and beta isomers of hexachlorocyclohexane by biological and
phototransformation, although this issue remains to be conclusively resolved.”
Furthermore, in the response to public comments in Appendix D, page 3, EFED
asserts that “it appears that there is a high possibility of the formation
of b-HCH
under some circumstances.” The
Agency must address this issue in light of the evidence in the peer-reviewed
scientific literature.
In particular, we suggest that HED and EFED scientists talk with each other
about this specific point. Resolution of this question is of substantial public
health and environmental importance. The beta-isomer of HCH is the most
persistent and bioaccumulative form. As much as 90 percent of HCH detected in
human tissues and breast milk is the b
form of HCH.[i]
EPA must reconsider its position in light of the available evidence and
the major implications of isomerization, and should include a risk assessment
for b-HCH
exposures as a result of lindane use. If the Agency feels that it is unable to
make a decision about whether or not to include b-HCH,
then it must acknowledge this problem as a major source of uncertainty in the
risk assessment and account for the data gap by requiring data collection to
address this important question, and increasing the FQPA safety factor to the
full 10x.
Failure to Include Breast Milk Exposures
EPA completely failed to address a major concern raised in
our previous comments: the fact that the Agency omitted consideration of the
breast milk pathway in the exposure assessment. We would like to know why the
agency failed to even acknowledge this concern in its response to public
comments. We are also deeply concerned that EPA failed to add the breast milk
pathway in the revised risk assessment. It is not acceptable to ignore public
comments, and even less acceptable to fail to include a major exposure pathway
to children as required under the FQPA.
It is bizarre that the EPA document could admit that,
“the milk:plasma concentration ratio for lindane indicates a much more
efficient excretion of the compound in milk…The presence of lindane in
mammalian milk exposes nursing offspring during critical periods of post-natal
development (Dalsenter et al. 1997).” (p. 12 of Lindane RED Chapter:
Environmental Fate and Ecological Risk Assessment) Yet at the same time, EPA
fails to include a nursing infant scenario in the risk assessment. This omission
is particularly egregious because lindane is known to bioaccumulate to higher
levels in breast milk, and because the nursing infant is at higher risk from the
neurotoxic and endocrine disrupting effects of this chemical. Failure to include
the breast milk exposure pathway is a violation of §408(b)(2)(D)(vi) of the
FFDCA.
Worker Risks are High and Underestimated
EPA’s failure to combine risks to workers from dermal
exposures and inhalation exposures to lindane defies logic. It is a slap in the
face of sound science to assume that the same chemical when inhaled has
completely different toxicity than when it penetrates the skin, yet that it
EPA’s current misguided policy. It should be obvious to any scientist or
toxicologist that such an approach makes no sense. It is patently obvious that
an individual exposed to lindane via both skin and lungs is getting an additive
dose of that chemical. It is also obvious that in worker populations such
combined exposures are highly likely, and even inevitable.
Persisting in the policy of considering each of these
exposures separately guarantees that EPA will seriously underestimate real-world
exposures to human beings that are handling this chemical on the job. That
knowledge is particularly sobering in light of the fact that this split risk
assessment still found serious worker risks. NRDC is deeply concerned that
workers (including pregnant and lactating women) may be exposed to dangerous
levels of this chemical. It is not appropriate for EPA to get dermal and
inhalation levels just below dangerous thresholds and claim that the risk
assessment provides adequate protection of worker health and safety. Mitigation
measures must bring levels of exposure low enough that workers who inhale this
chemical and get it on their skin are still protected from health effects. The
Ministry of Agriculture, Fisheries and Food in the United Kingdom ordered that
all uses of lindane for seed treatment be stopped in 1999 after determining that
"the level of exposure of those treating seeds with lindane is considered
to be above acceptable levels."[ii]
We believe that seed treatment poses unacceptable health risks to workers, and
that the EPA risk assessment, despite efforts to obfuscate the truth by
separating dermal and inhalation exposures, demonstrates a serious health risk
that must be addressed.
NRDC is incorporates by reference all our prior comments on
the Lindane Draft Risk Assessment dated October 29, 2001, as we believe that EPA
has failed to address any of our concerns in the revised risk assessment.
Failure to include the major exposure pathways to lindane is an affront to the
scientific database on this chemical and is in contravention of the plain
language of the Federal Food, Drug and Cosmetic Act as amended by the Food
Quality Protection Act of 1996. On reviewing the literature on lindane’s
persistence, bioaccumulation in the environment and in human tissues, and
toxicity, we do not believe that this chemical can safely be registered for use
in the United States. We are particularly concerned about the disproportionate
risks to certain subpopulations, including fetuses, breastfeeding infants,
subsistence fishing communities, and workers. We will continue to monitor EPA
regulatory activities involving lindane and will not stand by while the Agency
tramples the clear requirements of FQPA.
[i]
Jensen, A.A. and S.A. Slorach, Chemical Contaminants in Human Milk. 1991, Boca
Raton Ann Arbor Boston: CRC Press, Inc.
[ii]
Ministry of Agriculture, Fisheries and Food, 1999. News Release: Review of the
Pesticide Lindane (206/99) June 18.
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