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E-M:/ Michigan Schools are doing a poor job adopting authentic IPM andMDA is doing a lousy job of enforcement.
- Subject: E-M:/ Michigan Schools are doing a poor job adopting authentic IPM andMDA is doing a lousy job of enforcement.
- From: Praxis <firstname.lastname@example.org>
- Date: Wed, 26 Mar 2003 16:35:10 -0500
- Delivered-To: email@example.com
- Delivered-To: firstname.lastname@example.org
- List-Name: Enviro-Mich
- Reply-To: Praxis <email@example.com>
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Michigan Schools are doing a poor job adopting authentic IPM and
MDA is doing a lousy job of enforcement.
This problem remains intact in Michigan today. Samuel DeFazio, Praxis 269-673-2793
Saturday, December 08, 2001 4:40 PM
Dear Mr. Wyant, Director Michigan Department of Agriculture
You do not have to be killed to be seriously injured by pesticide exposure
at even very low level equivalent to childhood exposure in schools. Authentic
IPM should have a goal of reducing harm to its lowest possible risk, clearly
based on the MDA's behavior to date regarding School IPM "Safe Schools" and
"Children First" are not embraced by the Pesticide and Plant Pest Management
Division under the leadership of Mr. Ken Rauscher.
The IPM Resource Manual, "IPM for schools and children's facilities" was
developed by Purdue entomology and by Purdue Extension with an EPA Grant.
Beyond encouragement of sanitation and reducing harborage it defaults to pesticide
use, safer alternatives like biological control are all but ignored in this
alleged IPM document. Please do not "sign on" and allow this to become any
part of School IPM management in Michigan. Below is a well documented peer
reviewed scientific document with web-ready links showing how extremely low
level (parts per billion-a quantity not long ago identified by university
toxicologists as so small as to be ignored .....to bulldoze public grave concern
about pesticide drift) exposure to pesticides harms children and women.
Putting a "spin" on pesticide use and absurd comments we have heard from
members of MDA's 3PM division, like "safe when used as directed" are not
factual or acceptable. Please share this with those members of your staff
that behave like pesticide fetishists, ignoring science, wisdom, and reason.
The ability to reproduce is a fundamental human right, it should not be diminished
by the actions of (promotion of pesticide use) or the failure to act (Lack
of enforcement of pesticide rules and regulation) by State of Michigan public
servants. The final insult to the common good being the repression, discouraging
and disparagement of pesticide alternatives like the Biotool Kit products
marketed by Praxis by MDA employee's. While apparently they have decided
to make pest management decisions for all of us, it is not their job. Please
take whatever action is necessary to make them stop.
Patrick D. McKown
Samuel M. DeFazio
Jean E. McKown
BMJ 2001;323:1317-1318 ( 8 December )
Endocrine disrupters and human health
Current research will establish baseline indices
Infertility is an emotive issue, and having children is a recognised "right,"
so any implication that environmental pollution affects reproduction has to
be taken seriously. When the putative causative agents might also be responsible
for various cancers and other diseases, then the level of interest that the
issue attracts is unsurprisinghence the calls in the early 1990s for action
in line with the "precautionary principle."1 In men hypospadias, cryptorchidism,
cancer of the prostate, testicular cancer, and semen quality and in women
breast cancer, cystic ovaries, and endometriosis have all been suggested as
indicators of adverse trends in reproductive health.2 The idea that these
trends are real and are connected with environmental pollution is gaining
credence internationally. The effect on human health of environmental chemicals
that are mediated through the endocrine systemendocrine disruptershas generated
huge interest and investment. Why is this, and what is the evidence for the
Changes in the sexual morphology of fish exposed to sewage effluent have
led some scientists to conjecture that humans also live in a "sea of oestrogens"
and that the apparent increases in the incidence of certain reproductive conditions
may be due to exposure to chemicals in the environment. The so called Sharpe-Skakkebaek
hypothesis offered a possible common cause and toxicological mechanism for
abnormalities in men and boysthat is, increased exposure to oestrogen in
utero may interfere with the multiplication of fetal Sertoli cells, resulting
in hormonally mediated developmental effects and, after puberty, reduced
quality of semen.3 It was postulated that synthetic chemicals in the environment
are the prime source of the excessive oestrogenic stimulation, with exposure
through food and water being the primary route. Further research has extended
the concern to the role of antiandrogens and has led to the recognition that
a range of systems and processes may be susceptible to hormonal modulation,
including immune function, behaviour, and learning and memory, as well as
reproduction. The term environmental oestrogen has given way to the more
encompassing term "environmental endocrine disrupter," defined as "an exogenous
substance that causes adverse health effects in an intact organism, or its
progeny, subsequent to changes in endocrine function."4
Endocrine disrupters are potentially present in food as natural "phytoestrogens"
and chemical contaminants, and there is a divide in the perception of natural
and synthetic substances.5 Hence the drive in some quarters to market "healthy"
bread that is rich in soya flour and linseed at the same time that other people
are warning against low levels of weak oestrogenic synthetic chemicals as
contaminants in food. Perhaps this reflects the common view of natural things
as good and synthetic things as necessarily bad.
Two questions need to be addressed. Do indicators of reproductive health
truly reveal a worsening situation? Can exposure to environmental chemical
contaminants conceivably be the cause of any such temporal changes? Baseline
data on many of the implicated conditions are so poor that it is not possible
to say for sure whether trends are occurring. There is also the issue of geographical
variability in the measured indices, which can be related to genetic differences
in the population or to climatic differences or changes in lifestyle, for
example. None the less, there is agreement that the incidence of testicular
and prostate cancer is increasing and that semen quality is probably worsening
in some regions of the world. There is also some evidence for an increasing
incidence of cryptorchidism and hypospadias; and in women endometriosis and
polycystic ovaries may be more common.4-6
Perhaps the most controversial issues in research on endocrine disrupters
are the possible disproportionate effects of low levels of exposure, as proposed
by Vom Saal et al and recently accepted by the US national toxicology programme,
at least for a limited number of chemicals7-9; the question of synergism in
mixtures, which has become something of a no go area since the withdrawal
of the much quoted paper by Arnold et al10; and the development of appropriate
test methods. Large amounts of resources have been invested in this last activity,
through the work of the endocrine disrupter screening and testing advisory
committee in the United States. Yet according to Ashby the developmental effects
of endocrine disruptors that are seen in rodent studies cannot be extrapolated
to humans. This is not only because of the uncertainty of applying such results
across species but also because of the absence of an agreed control database
in rodents and the variability in test protocols and in the developmental
effects in test animals.11
Among specific chemicals implicated as endocrine disrupters phthalates may
be of particular importance because of their ubiquity. Similarly bisphenol
A has been shown in both in vitro and in vivo assays to have high potential
for endocrine disruption and potential for exposure to humansfor example,
through its use in can linings. These are issues of major interest, not least
because of the possible exposure of infants to these chemicals at critical
stages of development. Sharpe has argued that, until appropriate in vivo experiments
are done, phthalates and similar chemicals will continue to cause concern
for testicular development.12 Meanwhile the debate about phytoestrogens and
women's health continues: on the one hand there is concern that any hormonally
active substance can induce or exacerbate breast and uterine cancer, and on
the other is the knowledge that these substances can be used as alternatives
to hormone replacement therapy in the treatment of postmenopausal symptoms
This is a fascinating area with important repercussions, and it is appropriate
to investigate environmental causes of disease. Research is now being undertaken
that will establish baselines for some key indices of reproductive health,
which should allow future researchers to resolve the current uncertainties
and determine the impact of endocrine disrupters on our health.
Paul T C Harrison, acting director and head of environmental toxicology.
MRC Institute for Environment and Health, University of Leicester, Leicester
1. Colborn T, Clement C, eds. . Chemically-induced alterations in sexual
development: the wildlife/human connection. Princeton, NJ: Princeton Scientific
2. Harrison PTC, Holmes P, Humfrey CDN. Reproductive health in humans and
wildlife: are adverse trends associated with environmental chemical exposure?
Sci Total Environ 1997; 205: 97-106[Medline].
3. Sharpe RM, Skakkebæk NE. Are oestrogens involved in falling sperm counts
and disorders of the male reproductive tract? Lancet 1993; 341: 1392-1395[Medline].
4. European Commission. European workshop on the impact of endocrine disrupters
on human health and wildlife: report of the proceedings. Brussels: European
Commission, 1997. (EUR 17549)
5. Holmes P, Phillips B. Human health effects of phytoestrogens. In: Hester
RE, Harrison RM, eds. Issues in environmental science and technology. , Vol
12. Endocrine disrupting chemicals Cambridge, UK: Royal Society of Chemistry,
6. Joffe M. Are problems with male reproductive health caused by endocrine
disruption? Occup Environ Med 2001; 58: 281-287[Full Text].
7. Vom Saal FS, Timms BG, Montano MM, Palanza P, Thayer KA, Nagel SC, et
al. Prostate enlargement in mice due to fetal exposure to low doses of estradiol
or diethylstilbestrol and opposite effects at high doses. Proc Natl Acad Sci
USA 1997; 94: 2056-2061[Abstract/Full Text].
8. Welshons WV, Nagel SC, Thayer KA, Judy BM, vom Saal FS. Low-dose bioactivity
of xenoestrogens in animals: fetal exposure to low doses of methoxychlor and
other xenoestrogens increases adult prostate size in mice. Toxicol Ind Health
1999; 15: 12-25[Medline].
9. National Toxicology Program. Endocrine disruptors low-dose peer review.
(accessed 24 May 2001).
10. McLachlan JA. Synergistic effect of environmental estrogens: report
withdrawn [retraction of Arnold SF, Klotz DM, Collins BM, Vonier PM, Guillette
LJ Jr, McLachlan JA. In: Science 1996;272:1489-92]. Science 1997; 277: 462-463[Medline].
11. Ashby J. Testing for endocrine disruption post-EDSTAC: extrapolation
of low dose rodent effects to humans. Toxicol Lett 2001; 120: 233-242[Medline].
12. Sharpe RM. Hormones and testis development and the possible adverse
effects of environmental chemicals. Toxicol Lett 2001; 120: 221-232[Medline].
13. Holmes P, Harrison PTC. Environmental and dietary endocrine disruptors
and women's health. J Brit Menopause Soc 2001; 7: 53-59.