EPA recently began to "call in" data on developmental neurotoxicity (DNT) from manufacturers of pesticides already registered and considered to be neurotoxic-around 140 pesticides.
...studies indicate that neonatal exposure to pesticides--even in low doses--can potentiate and/or modify the reaction to adult exposure to xenobiotics, and thereby accelerate dysfunctional processes.
Read Comments
Subject: You Obviously Never Adequately Tested Your "Registered"
POISONS----
Date: Tue, 05 Sep 2000 14:46:10 -0400
From: Stephen Tvedten <steve@getipm.com>
Organization: Get Set Inc. (www.getipm.com)
To: Paul Helliker <phelliker@cdpr.ca.gov>
Director, State of
California, Department of Pesticide Regulation
Dear Mr. Helliker,
I thought you might find the following science interesting: 1: Toxicol
Appl Pharmacol 2000 Apr 1;164(1):1-14 - Testing methods for developmental
neurotoxicity of environmental chemicals. Claudio L, Kwa WC, Russell AL,
Wallinga, D
Mount Sinai School of Medicine, Division of Environmental
and Occupational Medicine, One Gustave Levy Place, New York, New York 10029,
USA.
Human brain development is slow and delicate, involving many unique, though interrelated, cellular events. The fetus and child are often more susceptible to chemical toxins that alter the structure and/or function of the brain, although susceptibility varies for individual neurotoxicants. Early exposure to neurotoxins has been implicated in neurological diseases and mental retardation. Pesticide exposures pose a particular concern since many are designed to be neurotoxic to pests and can also affect humans. Acknowledging the potential for vulnerability of the developing brain, EPA recently began to "call in" data on developmental neurotoxicity (DNT) from manufacturers of pesticides already registered and considered to be neurotoxic-around 140 pesticides. Chemicals are to be tested following the DNT testing guideline (OPPTS 870.6300). This paper assesses whether tests performed according to this guideline can effectively identify developmental neurotoxicants. We found the testing guideline deficient in several respects, including: It is not always triggered appropriately within the current tiered system for testing; It does not expose developing animals during all critical periods of vulnerability; It does not assess effects that may become evident later in life; It does not include methodology for consideration of pharmacokinetic variables; Methodology for assessment of neurobehavioral, neuropathological, and morphometry is highly variable; Testing of neurochemical changes is limited and not always required. We propose modifications to the EPA testing guideline that would improve its adequacy for assessing and predicting risks to infants and children. This paper emphasizes that deficiencies in the testing methodology for developmental neurotoxicants represent a significant gap and increase the uncertainty in the establishment of safe levels of exposure to developing individuals.
Copyright 2000 Academic Press.
------------------------------------------------------------------------------
------------------------------------------
1: Neurotoxicology 2000 Feb-Apr;21(1-2):67-73 -
Vulnerability to pesticide neurotoxicity is a lifetime issue. Weiss B Department
of Environmental Medicine, University of Rochester, School of Medicine and
Dentistry, NY 14642, USA.<A HREF="http://"> weiss@envmed.rochester.edu</A>
Early development is not the only life stage during which
which we see intensified responses to the adverse effects of chemicals.
Vulnerability to toxic processes rises again late in life, and in many ways
recapitulates the imperfect defenses deployed by the immature organism. One
feature common to both early and late phases is a reduced capacity to compensate
for impairment. In the first case, the functional mechanisms have yet to evolve.
In the second, they have passed into what might be called a post-mature decline.
Traced across the life cycle, this progression might be depicted as an inverted
U. The developing brain, however, is equipped with immense plastic potential;
the aging brain has lost much of its plasticity. The altered function of the
aging brain, however, is not simply an outcome of how long the organism has
lived. "Aging" is not a mechanistic explanation.
Events occurring during life must account for the changes. Older brains
are already high-maintenance properties, so that exposure to substances with
neurotoxic properties, such as pesticides, may accelerate the process, or
exploit its dwindling capacities to resist their effects. From this vantage
point, toxicants can act in three ways to depress function during advanced age:
they may interfere with brain development, leaving a legacy of diminished
redundancy not apparent until it is further compromised during aging; they may
hasten the progressive erosion of function observed with certain abilities; they
may exert greater effects in the aging brain because the aging nervous system
has already undergone a reduction in its ability to withstand toxic challenges.
PMID: 10794386, UI: 20252360
-------------------------------------------------------
1: Neurotoxicology 2000 Feb-Apr;21(1-2):37-47 - Neonatal
exposure to neurotoxic pesticides increases adult susceptibility: a review of
current findings. Eriksson P, Talts U
Department of Environmental Toxicology, Uppsala University,
Sweden. Per<A HREF="mailto:.Eriksson@Etox.uu.se">.Eriksson@Etox.uu.se</A>
An environmental mischance commonly occuring in nature is
the combination of neonatal exposure and later adult exposure to various toxic
substances. During neonatal life,
offspring can be affected by toxic agents either by transfer via mother's milk
or by direct exposure. In many mammalian species the perinatal period is
characterized by a rapid development of the brain--'the brain growth spurt'
(BGS). We have observed that exposure to pesticides, such as DDT and
bioallethrin, during the BGS in mice can potentiate susceptibility to
bioallethrin or paraoxon in adult life. This combined neonatal and adult
exposure caused spontaneous behavioural aberrations and changes in muscarinic
cholinergic receptors and led to impairment of the faculties of learning and
memory. Our studies indicate that neonatal exposure to pesticides--even in low
doses--can potentiate and/or modify the reaction to adult exposure to
xenobiotics, and thereby accelerate dysfunctional processes.
PMID: 10794383, UI: 20252357
-----------------------------------------------
1: Acad Emerg Med 1999 Dec;6(12):1295-7 - Topical use of
DEET insect repellent as a cause of severe encephalopathy in a healthy adult
male. Hampers LC, Oker E, Leikin JB
Section of Pediatric Emergency Medicine, The Children's
Hospital, Denver, CO, USA. PMID:
10609933, UI: 20076046
Well Mr. Helliker,
It seems true science is exposing some of the true dangers in the use of
your "registered" POISONS, when will it be "legal" (in your
opinion) for everyone, whether professional and/or amateur to use unregistered
alternatives to safely and far more effectively control their pest problems in
California?
Respectfully, Stephen L. Tvedten
TOP
If you would like to be included in our mailing list for continuing
information on pesticides, please email us at list@safe2use.com
with "subscribe" in the subject line.