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



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.