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From the Canadian Environmental Protection Act, 1999
2. (1) In the administration of this Act, the Government of Canada shall� (a) exercise its powers in a manner that protects the environment and human health, applies the precautionary principle that, where there are threats of serious or irreversible damage, lack of full scientific certainty shall not be used as a reason for postponing cost-effective measures to prevent environmental degradation, and promotes and reinforces enforceable pollution prevention approaches; (http://laws.justice.gc.ca/en/C-15.31/29338.html) |
| The symptoms of the flu are also synonymous with the symptoms experienced when one is exposed to toxic levels of such poisons as pesticides, herbicides and fluoride. Granville Knight, MD, stated under oath at a Congressional Hearing in the 60s that �waves of so-called �Virus-X� and similar diseases �are caused by exposure to such agricultural chemicals; [and] that it is impossible for doctors to diagnose the difference between London flu, virus conditions and pesticide poisoning.� ~Immunization: The Reality Behind the Myth by Walene James, pp. 118-119 (http://www.vaclib.org/basic/flu_fact_sheet.htm) |
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Chemical: TRICHLOROETHYLENE
CAS Number: 79-01-6 http://www.scorecard.org/chemical-profiles/summary.tcl?edf_substance_id=79%2d01%2d6 Recognized: Carcinogen P65 Suspected: Cardiovascular or Blood Toxicant KLAA LADO RTECS Developmental Toxicant ATSDR EPA-HEN EPA-SARA JANK Endocrine Toxicant EPA-HEN Gastrointestinal or Liver Toxicant DIPA EPA-HEN LADO MALA RTECS Immunotoxicant EPA-HEN Kidney Toxicant EPA-HEN HAZMAP KLAA MERCK RTECS STAC Neurotoxicant ATSDR DAN EPA-HEN EPA-SARA EVAN FELD HAZMAP OEHHA-CREL RTECS Reproductive Toxicant EPA-SARA FRAZIER Respiratory Toxicant FOTH RTECS Skin or Sense Organ Toxicant OEHHA-CREL RTECS
Pesticide use: MOLE & GOPHER GET 51.1% |
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Dioxins and Coplanar PCBs
From http://www.epa.gov/waterscience/fish/forum/sectioned_pdfs/sections6-10.pdf �2,3,7,8-TCDD is considered to be a known carcinogen for humans, while other dioxin-like compounds and complex environmental mixtures of these compounds are considered likely to be carcinogenic. This based on unequivocal animal data studies demonstrating carcinogenicity and limited human studies. Cancer potency estimates are primarily based on recently published human epidemiological studies. EPA�s potency value has been revised upward by a factor of six compared to a value published by EPA in 1985 based on a rat study. Cancer risks to the general population may exceed 1 per 1,000 from normal (dietary) exposure. This is not the upper bound, though risks may be less. Non-cancer toxic effects of concern include developmental toxicity (affecting the immune system, nervous system and reproductive system), immunotoxicity, endocrine effects, chloracne and others. Information about non-cancer effects in animals and humans is sufficient to generate a level of concern similar to that for cancer. It is likely that part of the general population is at or near exposure levels where adverse effects can be anticipated. [�] This table summarizes the body burdens associated with adverse effects. The margins between current average body burden (5 nanograms per kilogram - ng/kg) and these effect levels are mostly less than an order of magnitude, so some people are at levels likely to result in adverse effects. Consequently, EPA will not develop an RfD for dioxin.� Adverse Effects Body Burden (Ng/Kg) Developmental neurotoxicity: 22 Developmental/reproductive toxicity: 0.7 - 42 Developmental immunotoxicity: 50 Adult immunotoxicity: 1.6 - 12 Endometriosis: 22 Biochemical Effects CYP1A1 Induction: 0.6 - 33 CYP1A2 Induction 2.1 � 83 The sources of US adult daily intake of dioxins, furans, and dioxin-like PCBs Dairy 21% Freshwater fish and shellfish 19% Milk 16% Beef 14% Marine fish and shellfish 7% Other meats 6% Pork 5% Poultry Eggs 4% Vegetable Fats Inhalation 1% Soil Ingestion Soil dermal contact�The sources and pathways involve discharges to air and water, transport through the air, deposition from the air, and re-entrainment to soil particles. The compounds bind to leaves that are consumed and then get into food supply. Releases have been greatly reduced in the last ten years. Municipal and medical waste incinerators have been greatly reduced. A major source remains backyard barrel burning. Some sources are poorly characterized. Reservoir sources are past releases of dioxin that are �stored� in the environment but that can be reintroduced. About 50% of population exposure is related to these sources. Most incorporation into food supply is in the corn belt, dairy states, and west. These are mostly upwind from major emission sources. Major reductions in emissions will not see proportional reduction in exposure because we are looking at complex exchanges between compartments. These need to be better understood.� |
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Toxicity Summary for METHYL MERCURY
From http://risk.lsd.ornl.gov/tox/profiles/methyl_mercury_f_V1.shtml "In Iraq, over 6000 individuals were hospitalized and 459 individuals died as a result of consuming bread prepared with flour made from wheat and barley treated with a methylmercurial fungicide (Bakir et al., 1973). Methyl mercury concentration in the wheat flour ranged from 4.8-14.6 �g/g (mean=9.1 �g/g). The clinical symptoms included paresthesia, visual disorders, dysarthria, and deafness. The most severe cases resulted in coma and death due to CNS failure. Based on data obtained during this incident, a dose-response relationship between blood mercury levels (<10 �g/dL to 500 �g/dL), and frequency and severity of symptoms showed that mild symptoms occurred at the lower blood mercury levels and that deaths occurred at levels >300�g/dL." 4.1.1. Human: Information on the carcinogenicity of methyl mercury in humans is not available. 4.1.2. Animal: Mitsumori et al. (1981) reported renal tumors (13/16; 2 adenomas and 11 adenocarcinomas) in male but not female mice fed methyl mercury chloride (15 ppm) for 53 weeks. No additional information was available regarding the carcinogenicity of methyl mercury. 4.4. EPA WEIGHT-OF-EVIDENCE: The potential carcinogenicity of methyl mercury has not been evaluated by the U.S. EPA and, therefore, does not receive a weight-of-evidence classification. |
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Although the following report is not quite clear to me since some of these amounts are calculated from 1990-2002, and some from 1978, you still may want to look at these stats from the FDA:
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Methyl Mercury is classified as a Proposition 65 hazard
From http://www.ScoreCard.org Chemical Profile for METHYL MERCURY (CAS Number: 22967-92-6) P65-MC CARCINOGEN: Hundreds of chemicals are capable of inducing cancer in humans or animals after prolonged or excessive exposure. There are many well-known examples of chemicals that can cause cancer in humans. The fumes of the metals cadmium, nickel, and chromium are known to cause lung cancer. Vinyl chloride causes liver sarcomas. Exposure to arsenic increases the risk of skin and lung cancer. Leukemia can result from chemically induced changes in bone marrow from exposure to benzene and cyclophosphamide, among other toxicants. Other chemicals, including benzo[a]pyrene and ethylene dibromide, are considered by authoritative scientific organizations to be probably carcinogenic in humans because they are potent carcinogens in animals. Chemically-induced cancer generally develops many years after exposure to a toxic agent. A latency period of as much as thirty years has been observed between exposure to asbestos, for example, and incidence of lung cancer. P65 DEVELOPMENTAL TOXICANT: Developmental toxicants are agents that cause adverse effects on the developing child. Effects can include birth defects, low birth weight, biological dysfunctions, or psychological or behavioral deficits that become manifest as the child grows. Maternal exposure to toxic chemicals during pregnancy can disrupt the development or even cause the death of the fetus. Exposure of pregnant women to mercury, lowers birth weight and can cause severe brain damage in children. While developmental toxicity usually results from prenatal exposures to toxicants experienced by the mother, it can also result from paternal exposures. For example, the occupational exposure of men to vinyl chloride has been associated with increased rates of spontaneous abortion in their wives. Early postnatal contact with toxicants can also affect normal development. Exposure to secondhand tobacco smoke, for example, increases an infant's risk of contracting respiratory infections or succumbing to sudden infant death syndrome. And suspected: immunotoxicant, kidney toxicant and neurotoxicant. |
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�Sources of Exposure Relevant to Children�
From http://www.parl.gc.ca/InfoComDoc/36/2/ENVI/Studies/Reports/envi01/13-ch6-e.html#B1
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"Congress is considering legislation to require schools to use safer pest controls. The law was killed in committee last Fall, and again this Spring. And while the Food Quality Protection Act has strictly limited the use of three toxic pesticides... there's no law that requires testing of thousands of new chemicals for effects on the developing brain. [...] Of the 3000 or so high production volume chemicals in use in this country today only 43% have been even minimally tested. Only about 10 percent have been thoroughly tested to examine their potential effects on children's health and development." (Bill Moyers, Now Transcript, May 10, 2002, http://www.pbs.org/now/transcript/transcript117_full.html)
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Total BDEs in contemporary human milk (ng/g lipid) [25]
From http://www.epa.gov/waterscience/fish/forum/sectioned_pdfs/sections6-10.pdf Country Number of samples Year Median Mean Sweden 93 1996-1999 3.2 4.0 Japan 12 2000? 1.4 1.3 Canada 50 2001-02 25 64 USA (adipose) 23 1998 41 86In view of BDES being detected in fish at 1-2 milligrams per kilogram (mg/kg) range, the state of Virginia developed guidance levels for the issuance of a fish consumption advisory for BDEs. Concentration (mg/kg or ppm) # of Meals per month 1 9.3 1.47 6.3 2 4.6 3 3.1 4 2.3 5 1.9 9 1 10 0.9Based on the calculations above, Virginia uses the following trigger levels for the issuance of a fish consumption advisory when fish is contaminated with BDEs. � Below 5 mg/kg or ppm - no advisory � 5 to below 10 mg/kg or ppm - two eight ounce meals per month � Above 10 mg/kg or ppm � no consumption Because data are limited and reproductive or developmental effects of BDEs have not yet been evaluated, the state concluded that it would be prudent for pregnant women, nursing mothers, and young children to avoid consumption of fish contaminated with BDEs above 5 mg/kg or ppm. Since reported concentrations in fish were below the trigger level, no advisory was issued. In issuing advisories Virginia tries to give the message that not every concentration is harmful. |
"Ikea do not use brominated flame retardants or other hazardous chemicals in any of their mattresses"
(http://www.greenpeace.org.uk/Products/Toxics/chemicalhouse.cfm?producttypeid=2&productid=12)
"Samsung is fully committed to phasing out hazardous chemicals, and is currently working on a phase out programme which sets dates for a ban on PVC, organotins and brominated flame retardants. Greenpeace applauds Samsung for introducing a corporate policy embracing the precautionary approach and sees Samsung as the trendsetter among electronics companies for their plan to phase out hazardous substances."
(http://www.greenpeace.org.uk/Products/Toxics/chemicalhouse.cfm?producttypeid=11&productid=156)