E-M:/ Michigan Schools are doing a poor job adopting authentic IPM andMDA is doing a lousy job of enforcement.

[Praxis <praxis1986@triton.net>]

Title:

          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
 
 
 Originally Sent-
 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.
 
 Sincerely,
 
 Patrick D. McKown
 Samuel M. DeFazio
 Jean E. McKown
 
 Praxis  616-673-2793
  
 BMJ 2001;323:1317-1318 ( 8 December )
 
 Editorials
 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 
assumed association? 
 
 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 
and osteoporosis.13 
 
 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 
LE1 7DD
 
 
 
 
 
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 1.  Colborn T, Clement C, eds. . Chemically-induced alterations in sexual 
development: the wildlife/human connection. Princeton, NJ: Princeton Scientific 
Publishing, 1992.  
 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, 
1999:109-134.  
 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. 
http://ntp-server.niehs.nih.gov/htdocs/liason/LowDoseWebPage.html
(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.