Showing posts with label toxic chemicals. Show all posts
Showing posts with label toxic chemicals. Show all posts

Thursday, September 4, 2008

Part 9 Excitotoxins, Neurodegeneration and Neurodevelopment

Part 9 Excitotoxins, Neurodegeneration and Neurodevelopment
By Russell L. Blaylock, M.D

Conclusion

In this brief discussion of a most complicated and evolving subject I have had to omit several important pieces of the puzzle. For example, I have said little about the functional components of the receptor systems, the glutamate transporter and its relation to ALS and Alzheimer's dementia, receptor decay with aging and disease, membrane effects of lipid peroxidation products, membrane fluidity, effects of chronic inflammation on the glutamate/free radical cycle, stress hormones and excitotoxicity, the role of insulin excess on the eicosanoid system, or the detailed physiology of the glutamatergic system. I have also only briefly alluded to the toxicity of aspartame and omitted its strong connection to brain tumor induction.

But, I have tried to show the reader that there is a strong connection between dietary and indogenous excitotoxin excess and neurological dysfunction and disease. Many of the arguments by the food processing industry has been shown to be false. For example, that dietary glutamate does not enter the brain because of exclusion by the blood-brain barrier, has been shown to be wrong, since glutamate can enter by way of the unprotected areas of the brain such as the circumventricular organs. Also, as we have seen, chronic elevations of blood glutamate can breech the intact blood-brain barrier. In addition, there are numerous conditions under which the barrier is made incompetent.

As our knowledge of the pathophysiology and biochemistry of the neurodegenerative diseases increases, the connection to excitotoxicity has become stonger.94 This is especially so with the interrelationship between excitotoxicity and free radical generation and declining energy production with aging. Several factors of aging have been shown to magnify this process. For example, as the brain ages its iron content increases, making it more susceptible to free radical generation. Also , aging changes in the blood brain barrier, micovascular changes leading to impaired blood flow, free radical mitochondrial injury to energy generating enzymes, DNA adduct formation, alterations in glucose and glutamate transporters and free radical and lipid peroxidation induced alterations in the neuronal membranes all act to make the aging brain increasingly susceptible to excitotoxic injury.

Over a lifetime of free radical injury due to chronic stress, infections, trauma, impaired blood flow, hypoglycemia, hypoxia and poor antioxidant defenses secondary to poor nutritional intake, the nervous system is significantly weakened and made more susceptible to further excitotoxic injury. We known that a loss of neuronal energy generation is one of the early changes seen with the neurodegenerative diseases. This occurs long before clinical disease develops. But, even earlier is a loss of neuronal glutathione functional levels.

I included the material about the special function of ascorbic acid because few are aware of the importance of adequate ascorbate levels for CNS function and neural protection against excitotoxicity. As we have seen, it plays a vital role in neurobehavioral regulation and the dopaminergic system as well,which may link ascorbate supplementation to improvements in schizophrenia.

Our knowledge of this process opens up new avenues for treatment as well as prevention of excitotoxic injury to the nervous system. For example, there are many nutritional ways to improve CNS antioxidant defenses and boost neuronal energy generation, as well as improve membrane fluidity and receptor integrity. By using selective glutamate blocking drugs or nutrients, one may be able to alter some of the more devastating effects of Parkinson's disease. For example, there is evidence that dopamine deficiency causes a disinhibition (overactivity) of the subthalamic nucleus and that this may result in excitotoxic injury to the substantia nigra.95 By blocking the glutamatergic neurons in this nucleus, one may be able to reduce this damage. There is also evidence that several nutrients can significantly reduce excitotoxicity. For example, combinations of coenzyme Q10 and niacinamide have been shown to protect against striatal excitotoxic lesions. Methylcobolamine, phosphotidylserine, picnogenol and acetyl-L-carnitine all protect against excitotoxicity as well.

Of particular concern is the toxic effects of these excitotoxic compounds on the developing brain. It is well recognized that the immature brain is four times more sensitive to the toxic effects of the excitatory amino acids as is the mature brain.This means that excitotoxic injury is of special concern from the fetal stage to adolescence. There is evidence that the placenta concentrates several of these toxic amino acids on the fetal side of the placenta. Consumption of aspartame and MSG containing products by pregnant women during this critical period of brain formation is of special concern and should be discouraged. Many of the effects, such as endocrine dysfunction and complex learning, are subtle and may not appear until the child is older. Other hypothalamic syndromes associated with early excitotoxic lesions include immune alterations and violence dyscontrol.

Over 100 million American now consume aspartame products and a greater number consume products containing one or more excitotoxins. There is sufficient medical literature documenting serious injury by these additives in the concentrations presently in our food supply to justify warning the public of these dangers. The case against aspartame is especially strong.

References
1. Ikonomidou C and Turski L, Glutamate in Neurodegenerative Disorders, In, Stone TW ( Ed), Neurotransmitters and Neuromodulators: Glutamate, CRC Press, Boca Raton, 1995, 253-272.
2. Whetsell WO, Shapira NA. Biology of Disease. Neuroexcitation, excitotoxicity and human neurological disease. Lab Invest 68: 372-387, 1993.
3. Lucas DR and Newhouse JP. The toxic effect of sodium L-glutamate on the inner layer of the retina. Arch Opthalmol 58: 193-201, 1957.
4. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science 165: 719-721, 1969.
5. Pol ANV, Wuarin J-P, Dudek E. Glutamate, the dominate excitatory transmitter in neuroendocrine regulation. Science 250: 1276-1278, 1990.
6. Coyle JT, et al. Excitatory Amino Acid Neurotoxins: Selectivity, Specificity, and Mechanisms of Action. Neurosci Reseach Bull 19: #4, 1981.
7. Blackstone CD, Huganir RL. Molecular structure of Glutamate Receptor Channels. In, Stone TW, ed, CNS Neurotransmitters and neuromodulators: Glutamate. CRC Press, Boca Raton, 1995, 53-67.
8. Analysis of Adverse Reactions to Monosodium Glutamate ( MSG). Life Sciences Research Office. FASEB, July 1995.
9. Blaylock, RL. Excitotoxins: The Taste That Kills. Health Press, Santa Fe, NM, 1997, 248-254.
10. Olney JW. Glutamate: a neurotoxic transmitter. J Child Neurol 4: 218-226, 1989.
11. Choudhary P, Malik VB, et al. Studies on the effect of monosodium glutamate on hepatic microsomal lipid peroxidation, calcium, ascorbic acid and glutathione and its dependent enzymes in adult male mice. Toxicol Lett 89: 71-76, 1996.
12. Plaitakis A and Caroscio JT. Abnormal glutamate metabolism in amyotrophic lateral sclerosis. Ann Neuro 22: 575-579, 1987.
13. Blaylock RL. Neurodegeneration and aging of the central nervous system: Prevention and treatment by phytochemicals and metabolic nutrients. Integrative Med 1: 117-133, 1998.
14. Olney JW. Excitotoxic food additives: functional teratological aspects. Prog Brain Res 18: 283-294, 1988.
15. Parsons RB, Waring RH, et al. In vitro effect of the cysteine metabolites homocysteic acid, homocysteine and cysteic acid upon human neuronal cell lines. Neurotoxicology 19: 599-603, 1998.
16. Esskes TK. Neural tube defects, vitamins and homocysteine. Eur J Pediatr 157: Suppl 2: S139-S141, 1998.
17. McCaddon A, Daves G, et al. Total serum homocysteine in senile dementia of Alzheimer type. In J Geriatr Psychiatry 13: 235-239, 1998.
18. Banks JC, et al. Retinal pathology in Alzheimer's disease. I. Ganglion cell loss in foveal/parafoveal retina. Neurobiol Aging 17: 377- 384, 1996.
19. Onanow CW. A radical hypothesis for neurodegeneration. Trends in neurosci 16: 439-444, 1993.
20. Aisen PS, Davis KL. Inflammatory mechanisms in Alzheimer's disease: implications for therapy. Am J Psych 151: 1105-1113, 1994.
21. Murphey T, Parikh A, et al. Arachidonic acid metabolism in glutamate neurotoxicity. Ann NY Acad Sci 559: 474-477, 1989.
22. Smith MA, Richey Pl, et al. Widespread peroxynitrite-mediated damage in Alzheimer's disease. J Neurosci 17: 2653-2657, 1997.
23. Jenner P, et al. Oxidative stress as a cause of nigral cell death in Parkinson's disease and incidental Lewy body disease. Ann Neurol 32: 282-287, 1992.
24. Griffiths PD, Crossman AR. Distribution of iron in the basal ganglion and neocortex in Parkinson's disease and Alzheimer's disease. Dementia 2: 61-65, 1993.
25. Bolanos JP, Almeida A, et al. Nitric oxide-mediated mitochondrial damage in the brain: mechanisms and implications for neurodegenerative diseases. J Neurochem 68: 2227-2240, 1997.
26. Dexter DT, et al. Increased iron content in post-mortum Parkinsonian brain. Lancet ii: 219-220, 1987.
27. Hirsch EC, Brandel JP, et al. Iron and aluminum increase in the substantia nigra of patients with Parkinson's disease: an X-ray microanalysis. J. Neurochem 56: 446-451, 1991.
28. Logroscino G, Marder K, Graziano J, et al. Altered systemic iron metabolism in Parkinson's disease. Neurology 49: 714-717, 1997.
29. Schapira AHV, et al. Mitochondrial complex I deficiency in Parkinson's disease J. Neurochem 54: 823-827, 1990.
30. Bergerson C. Oxidative stress: Its role in the pathogenesis of amyotrophic lateral sclerosis. Neurol Sci 129: 81-84, 1995.
31. Gerlach M, Ben-Shachar D, et al. Altered brain metabolism of iron as a cause of neurodegenerative diseases. J Neurochem 63: 793-807, 1994.
32. Dawson VL, Dawson TM, et al. Mechanisms of nitric oxide-mediated neurotoxicity in primary brain cultures. J Neurosci 13: 2651-2661, 1993.
33. Williams LR. Oxidative stress, age-related neurodegeneration, and the potential for neurotrophic treatment. Cerebrovasc Brain Metab Rev 7: 55-73, 1995.
34. Domenico E, Pellegrini-Giampietro, et al. Excitatory amino acid release and free radical formation may cooperate in the genesis of ischemia-induced neuronal damage. J Neurosci 10: 1035-1041, 1990.
35. Mundy WR, Freudenrich TM, Kodavanti PR. Aluminum potentiates glutamate-induced calcium accumulation and iron-induced oxygen free radical formation in primary neuronal cultures. Mol Chem Neuropathol 32: 41-57, 1997.
36. Aarala JT, Loikkanen JJ, et al. Lead amplifies glutamate-induced oxidative stress. Free Radical Biol Med 19: 689-693, 1995.
37. Lipton SA, Nicotera P. Calcium, free radicals and excitotoxins in neuronal apoptosis. Cell Calcium 23: 165-171, 1998.
38. Murphey TH, et al. Immature cortical neurons are uniquely sensitive to glutamate toxicity by inhibition of cystine uptake. FASEB 6: 1624- 1633, 1990.
39. Fahn S. A pilot trial of high -dose alpha-tocopherol and ascorbate in early Parkinson's disease. Ann Neurol 32: S128-S132, 1992.
40. Niki E. Interactions of ascorbate and alpha-tocopherol. Third Conference of Vitamin C, Burns ET (Ed), NY Acad Sci 498: 186-199, 1987.
41. Beal MF, Hyman BT, Koroschetz W. Do defects in mitochondrial energy metabolism underlie the pathology of neurodegenerative diseases? Trends in Neurosci 16: 125- 131, 1993.
42. Pall HS, Blake DR, et al. Raised cerebrospinal-fluid copper concentration in Parkinson's disease. Lancet , Aug 1: 238- 241,1987.
43. Sorg O, Horn TF, et al. Inhibition of astrocyte glutamate uptake by reactive oxygen species: role of antioxidant enzymes. Mol Med 7: 431- 440, 1997.
44. Toth E and Lajtha A. Elevation of cerebral levels of nonessential amino acids in vivo by administration of large doses. Neurochem Res 6: 1309-1317, 1981.
45. Dowling P, Husar W, et al. Cell death and birth in multiple sclerosis brain. J Neurol Sci 149: 1-11, 1997.
46. Bennow K, et al. Blood-brain barrier disturbance in patients with Alzheimer's disease is related to vascular factors. Acta Neuro Scand 81: 323-326, 1990.
47. Zuccarello M, Anderson DK. Interactions between free radicals and excitatory amino acids in the blood brain barrier disruption after iron injury in the rat. J Neurotrauma 10: 397- 481, 1993.
48. Koenig H, et al. Capillary NMDA receptors regulate blood-brain barrier function and breakdown. 588: 297-303, 1992.
49. Novelli A, Reilly JA, et al. Glutamate becomes neurotoxic via the N- methyl-D aspartate receptor when intracellular energy levels are reduced. Brain Res 451: 205-207, 1988
50. Greenemyer JT. Neuronal bioenergetics defects, excitotoxicity and Alzheimer's disease: Use it or lose it. Neurobiol Aging 12: 334-336, 1991.
51. Parker WD, Boyson SJ, Parks JK. Abnormalities of the electron transport chain in idiopathic Parkinson's disease. Ann Neurol 26: 719- 723, 1989.
52.Schapira AHV, Mann VM, et al. Mitochondrial function in Parkinson's disease. Ann Neurol 32: S116-S124, 1992.
53. Beal MF, et al. Coenzyme Q10 and niacinamide are protective against mitochondrial toxins in vivo. Neuro 44 (Supp2) April 1994, A177.
54. Calvani M, Koverech A, Carurso G. Treatment of mitochondrial diseases. In, DiMauro S, Wallace DC, eds. Mitochondrial DNA in Human Pathology. Raven Press, New York,1993, 173-198.
55. Bucht G, et al. Changes in blood glucose and insulin secretion in patients with senile dementia of Alzheimer's type. Acta Medica Scand 213: 387-392, 1983.
56 Bucht,G, et al. Acta Medica Scand 213: 387-392, 1983.
57. Fujiasawa Y, Saki K, Akiyama K. Increased insulin levels after OGTT load in peripheral blood and cerebrospinal fluid of patients with dementia of the Alzheimer's type. Bio Psych 30: 1219-1228, 1991.
58. Gotoh F, Kitamura A, et al. Abnormal insulin secretion in amyotrophic lateral sclerosis. J Neurol Sci 16: 201-207, 1972.
59. Pettgrew JW, et al. The role of membranes and energetics in Alzheimer's disease. In, Terry RD, et al ( Eds) Alzheimer's Disease, Raven Press, New York, 1994.
60. Leibson CL, Rocca WA, et al. Risk of dementia among persons with diabetes mellitus: a population-based cohart study. Am J Epidemiol. 145: 301-308, 1997.
61. Kalaria RN, Harik SI. Reduced glucose transporter at the blood-brain barrier and in the cerebral cortex in Alzheimer's disease. J Neurochem 53: 1083-1088, 1989
62. Kaleria RN, et al.The glucose transporter of the human brain and blood brain barrier. Ann Neurol 24: 757-764, 1988.
63. Tannaka M, Kovalenko SA, et al. Accumulation of deletions and point mutations in mitochondrial genome in degenerative diseases. Ann NY Acad Sci 15: 102-111, 1996.
64. Spencer JP, Jenner A, et al. Intense oxidative DNA damage promoted by L-dopa and its metabolites. Implications for neurodegenerative disease. FEBS Lett 353: 246-250, 1994.
65.Ames BN, Shigenaga MK, Hagen TM. Oxidants, antioxidants, and the degenerative diseases of aging. Proc Natl Acad Sci 90: 7915-7922, 1993.
66. Raos KS. DNA-damage & DNA-repair in aging brain. Indian J Med Res 106: 423-437, 1997.
67. Boerrigter ME, Wei JY, Vijg J. DNA repair and Alzheimer's disease. J Gerontol 47: B177-B184, 1992.
68.Lyras L, Cairns NJ, et al. An assessment of oxidative damage to proteins, lipids and DNA in the brain from patients with Alzheimer's disease. J Neurochem 68: 2061-2069, 1997.
69. Mattson MP. Antigenic changes to those seen in neurofibrillary tangles are elicited by glutamate and Ca+2 influx in cultured hippocampal neurons. Neuron 2: 105-117, 1990.
70. Markey SP. MPTP: a new tool for understanding Parkinson's disease. Disc Neurosci 4: 1986
71. Olney JW, Wozniak DF, Farber NB. Excitotoxic neurodegeneration in Alzheimer's disease. New hypothesis and new therapeutic strategies. Arch Neurol 54: 1234-1240, 1997.
72. Gruenewald RA. Ascorbic acid distribution patterns in human brain. A comparison with nonhuman mammalian species. Ann NY Acad Sci 498: 1-12, 1987.
73. Grunewald RA. Ascorbic acid in the brain. Brain Res Rev 18: 123-133, 1993.
74. Boutelle MG, Svensson L, Fillenz M. Effect of diazepam on behavior and associated changes in ascorbate concentration in rat brain areas: striatum, N. Accumbens and hippocampus. Psychopharmacology 100: 230-236, 1990.
75. Tolbert LC, Thomas NT, et al. Ascorbate blocks amphetamine-induced turning behavior in rats with unilateral nigrostriatal lesions. Brain Res Bull. 4: 43-48, 1979.
76. Den Hartog Jager WA. Experminental amyotrophic lateral sclerosis in Guinea-pig. J Neurol Sci 67: 133-142, 1985.
77. Svenson L, Wu C, et al. Effect of aging on extracellular ascorbate concentration in rat brain. Brain Res 309: 36-40, 1993.
78. Suzuki K, Martin PM. Neurotoxicants and developing brain. In, Harry GJ, Ed, Developmental Neurotoxicology. CRC Press, Boca Raton, 1994, 9- 32.
79. Hirsch SR, Garey LJ, Belleroche J. A pivotal role for glutamate in the pathogenesis of schizophrenia, and its cognitive dysfunction. Pharmacol Biochem Behavior 56: 797-802, 1997.
80. Gong SL, Xia FQ, et al. Harmful effects of MSG on function of hypothalamus-pituitary -target gland system. Biomed Environ 8: 310-317, 1995.
81. Trocho C, Rardo R, et al. Formaldehyde derived from dietary aspartame binds to tissue components in vivo. Life Sci 63: 337-349, 1998.
82. Kenessey A, Yen S-H, et al. Detection of D-aspartate in tau proteins associated with Alzheimer paired helical filaments. Brain Res 675: 183- 189,1995
83.Fisher GH, D'Aniello AD, et al. Quantification of D-asparate in normal and Alzheimer brains. Neurosci Lett 143: 215-218, 1992)
84. Suzuki K, Martin PM, Neurotoxicants and The Developing Brain, In, Harry GT, ed, Developmental Neurotoxicology, CRC Press, Baco Raton, 1994, 9-32.
85.Olney JW. Excitotoxic food additives: functional teratological aspects. Progress Brain Res 73: 283-294, 1988
86.Brody JR, et al. Effect of micro-injections of L-glutamate into the hypothalamus on attack and flight behavior in cats. Nature 224: 1330, 1969
87. Wong PT, Neo LH, et al. Deficits in water escape performance and alterations in hippocampal cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice. Pharmacol Biochem Behav 57: 383-388, 1997.
88.Klingberg H, Brankack J, Klingberg F. Long-term effects on behavior after post-natal treatment with monosodium L-glutamate. Biomed Biochem ACTA 46: 705-711, 1987.
89. Freider B, Grimm VE. Prenatal monosodium glutamate ( MSG) treatment given through the mother's diet causes behavioral deficits in rat offspring.Intern J Neurisci 23: 117-126, 1984.
90.Frieder B, Grimm VE. Prenatal monosodium glutamate causes long- lasting cholinergic and adrenergic changes in various brain regions. J Neurochem 48: 1359-1365, 1987
91. Kubo T, Kohira R, et al. Neonatal glutamate can destroy the hippocampal CA1 structure and impair discrimination learning in rats. Brain Res 616: 311-314, 1993.
92. Bakke JL, Lawrence J, et al. Late endocrine effects of administering monosodium glutamate to neonatal rats. Neuroendocrinology 26: 220-228, 1978.
93. Maiter D, Underwood LE, et al. Neonatal treatment with monosodium glutamate: effects of prolonged growth hormone(GH)-releasing hormone deficiency on pulsatile GH secretion and growth in female rats. Endocrinology 128: 1100-1106, 1991.
94. Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway for neurologic disorders. New Eng J Med 330: 613-622, 1994.
95. Rodriguez MC, Obeso JA, Olanow CW. Subthalamic nucleus-mediated excitotoxicity in Parkinson's disease: a target for neuroprotection. Ann Neurol 44: ( Supp 1) S175-S188, 1998.
________________________________________
Article courtesy of Dr. Russell Blaylock and
The Medical Sentinel Journal
Authorized for replication as necessary to spread the truth.
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© 1996 DORway.com

Thursday, March 20, 2008

Spring Into Natural Cleaning

Spring is here and it's time to start thinking about spring cleaning. But what about the cleaners that you use. Well, here is a press release from one organization that wants people to learn about natural, safe cleaners. What a good idea!

For Immediate Release
March 20, 2008

Contact:
Sian Wu, sian@resource-media.org, 206-374-7795 x102

Ali Solomon, Women’s Voices for the Earth
ali@womenandenvironment.org, 406-543-3747

Concerned Consumers Spur Eco-Cleaning Movement
Nationwide Green Cleaning Parties Raise Awareness of Toxic Chemicals

MISSOULA, Mont.—Starting today, people across the country will host parties to teach friends and family how to make their own “green cleaners” from ingredients they know are safe and non-toxic. Women’s Voices for the Earth (WVE), a national environmental health group, is using the first day of spring and National Poison Prevention Week (March 16 – 22) to inform consumers that the cleaners they buy may not be as safe as they think.

“For many people, springtime means deep cleaning,” says Dori Gilels, executive director of Women’s Voices for the Earth. “But some of the products consumers rely on to create a clean, healthy environment can actually lead to long-term health problems.”

WVE released a report last summer, “Household Hazards” that found that several chemicals in common household cleaning products have been linked to reproductive and developmental problems, and even asthma, the most common serious chronic childhood disease, according to the National Heart, Lung and Blood Institute.

More than 100 people, from Florida to Hawaii, have already pledged to host green cleaning parties in their communities as part of a grassroots movement to reduce exposure to toxic chemicals in the home. The green cleaning party movement will go beyond the ritual of spring cleaning, with hundreds more parties expected in towns and cities across America through the rest of the year.

Alexandra Gorman Scranton, director of science and research at WVE says that a growing body of research shows that even minute traces of certain chemicals found in everyday products, like household cleaners, can potentially disrupt hormones, interfere with development and lead to disease. According to Gorman Scranton, “There’s no reason to include toxic ingredients, even in trace amounts, in products that consumers use on a daily basis when safe and equally effective alternatives exist.”

Several studies have shown that regular household vinegar, which is one of the main ingredients in WVE’s homemade recipes, is as effective or nearly as effective as commercial cleaners in eliminating microbes like E.coli from surfaces and sponges, effectively eliminating between 90-98 percent of bacteria.

Green cleaning party kits developed by WVE provide party hosts with everything they need to have a successful event, including recipe cards, environmentally friendly cleaning tips, an informational DVD, and advocacy information on how to contact local policy makers and cleaning product manufacturers. All homemade recipes have been tested by both consumers and professional cleaners and were found to be economical and just as effective as their branded counterparts.

"In my community, people are getting more and more concerned about exposure to toxic chemicals. The increase in allergies, especially among my family and friends has really made this a priority for me,” says Stephanie Kline, who is hosting a party in her home in Novato. “I think it's great that home made cleaners are so economical. It means they can be made available to anybody who wants to avoid using toxic chemicals in their homes."

Currently, household cleaning companies are not required by law to list ingredients on product labels. When asked by WVE in writing in July of 2007 to disclose this information, many of the leading manufacturers said they could not reveal trade secrets. Yet, food companies have to label ingredients despite their need to protect “secret recipes.” This system works well in alerting shoppers to ingredients they wish to avoid, for allergy reasons or otherwise.

“There’s so much excitement around green cleaning parties because people are concerned and confused about reports of toxic chemicals in products that they once trusted were safe,” says Gilels. “Until companies come clean about what they use in their products, we are encouraging people across the country to make their own.”

WVE works directly with cleaning product companies to promote full disclosure of ingredients on product labels, and advocates for better government regulation of toxic chemicals in consumer products. These green cleaning parties are part of their larger Safe Cleaning Products Initiative, a national effort to reduce exposure to hazardous chemicals in household cleaners.

Go to www.womenandenvironment.org for more information about party locations around the country, fact sheets and state-specific policies.

WOMEN’S VOICES FOR THE EARTH(WVE) is a national women centered environmental health and justice organization basedin Montana. WVE works toeliminate and reduce environmental toxins that impact human health and to increase women’s participation in environmental decision making.

# # #


WOMEN’S VOICES FOR THE EARTH (WVE)
is a national womencentered environmental health and justice organization based in Montana. WVE works to eliminate and reduce environmental toxins that impact human health and to increase women’s participation in environmental decision making.

EXECUTIVE DIRECTOR
Dori Gilels

WVE BOARD OF DIRECTORS
Lisa Woll - President

CEO, Social Investment Forum
Rockville, MD

Gloria Flora - Secretary
Director, Sustainable Obtainable Solutions
Helena, MT

Christine Kaufmann – Treasurer
Director, MT Human Rights Network
MT State Senator
Helena, MT

Aimee Boulanger
Program Director, Institute for Children’s
Environmental Health
Freeland, WA

Joyce Mphande-Finn
Private Counseling Practice
Stevensville, MT

Angela Park
The Kaleel Jamison Consulting Group
Hartland, VT

Anja Rudiger
National Economic and Social Rights
Initiative (NESRI) and the National
Health Law Program (NHeLP)
New York, NY

Lexi Shultz
Union of Concerned Scientists
Washington, DC
P.O. Box 8743
Missoula, MT 59807-8743

Phone: 406.543.3747
FAX: 406.543.2557

wve@womenandenvironment.org
http://www.womenandenvironment.org/