Cancer Mortality Increase 2021. Jorma Jrykkanen

Antibiotics may increase risk of cancer and type 11 diabetes by increasing insulin secretion. 2021-07-21. Jorma Jyrkkanen

Antibiotic Use Linked to Increased Incidence of Type 2 Diabetes and probable promotion of cancer. Some antibiotics can also affect blood sugars. Fluoroquinolones such as levofloxacin and gatifloxacin stimulate insulin secretion and may cause hypoglycemia. Nov. 1, 2017 Because some antibiotics may icnrease insulin secretion and hyperinsulinemia has been linked to increased risk of cancer, its quite likely that another pathway to antibiotic induced cancers is via stimulating the increase in insulin which also favors cancer because of its high sugar demand in glycolysis production of ATP.

Proposal for a UN Police Force for Global Environment Sep. 7th, 2012 at 8:45 AM. Jorma Jyrkkanen

Proposal for a UN Police Force for Global Environment Sep. 7th, 2012 at 8:45 AM Proposal for a United Nations International Environment Law Dealing with Bio-Diversity and Species Extinction or Endangerment hereafter called the ‘Eco-Cide Law’ and its corollary, the Eco-Cide Act. Jan 23, 2002

The Global Eco-Cide Act Purpose of the Law and the Act The purpose of the Law and Act is to prevent the destruction of life forms and their habitats, which are essential to preservation of bio-diversity and the products of the creation of evolution, and to aggressively reverse the process of their decline. Its purpose is also to ensure that our Planet is inhabitable by all life forms indefinitely into the future and to that end, stop and aggressively reverse the destructive effects of pollution, land, air, forests, soil and water alteration, alienation and loss. This Law and Act recognizes the crucial value of land, air, water, soils, forests and other species, in ensuring the survival of life on earth. All of this is in clear recognition that crimes against nature are crimes against humanity. For example, CO2 related loss of Himalayan glaciers is a direct threat to the lives of half a billion people and to the nature they rely upon for life. Article I (I)Offenses It is an International Offense under this law by any country within the United Nations to: (I)(a). Cause the extinction of a species. (I)(b). Create rare or endangered species by neglect or willful acts. (I)(c). Cause the loss of bio-diversity. (I)(d). Fail to act to stop and reverse the decline of a species where it is caused by local human actions or impacts. (I)(e). Cause ecosystems to be altered faster than the member species can adapt. (I)(f). Fail to take effective measures to stop and reverse air pollution. (I)(g). Fail to take effective measures to stop and reverse water pollution. (I)(h). Put toxic substances in the food chain where they will bioconcentrate. (I)(i). Fail to prosecute polluters. (I)(j). Fail to protect and provide habitat for rare or endangered species. (I)(k). Fail to seek the advice of independent scientists in habitat protection. (I)(l). Destroy the atmospheric ozone with substances emitted because of failure to implement available technology. (I)(m). Fail to reduce greenhouse gas emissions to Kyoto Agreement by 2020 by a country. (I)(n). Fail to implement scientific advances in energy technology to replace fossil fuel combustion by 2020. (I)(o). Fail to control and reverse over-harvesting or illegal exploitation of fish and wildlife. (I)(p). Fail to protect ecosystems from harmful alteration. (I)(q). Fail to stop processes that contribute to harmful alteration, alienation, or destruction of ecosystems. (I)(r). Fail to create sanctuaries, preserves, parks, protected areas, and linkages between vital areas for corridors for gene flow to provide for species survival and prosperity and to fail to do so at the ecosystem level. (I)(s). Fail to participate in global efforts to save the life support capacity of planet earth. (I)(t). Fail to take measures to stop trafficking of illegal timber, fish and wildlife. (I)(u). Fail to harvest and manage renewable resources like forests and soils in a sustainable manner. Article II Culpability (II) The Minister of Environment or in the absence of such a person, the Persons or agencies appointed by Government for the purpose of Environmental Protection, or in the absence of such persons or agencies the Prime Minister shall be held accountable for crimes under the Eco-Cide Law, as will any subordinates under him responsible for any aspect of environmental governance down to and including the Deputy Minister of Environment. Article III (III) Penalties (III)(a). If found guilty of contravention of the Eco-Cide Act, the offending nation shall be assessed one million dollars per day for every day from the notice of violation to satisfactory corrective action, payable to the United Nations Habitat Protection and Ecosystems Conservation Fund and to be used to police the Act. (III)(b). If a nation's government ceases to have effective control over its resource base, and its ecosystesm, it shall become a ward of the United Nations Habitat Protection and Ecosystems Conservation Department. (III)(c)If found guilty of willful violation or repeat violation, membership to the United nations shall be revoked for twenty five years and readmission shall only be available upon payment of an appropriate levy, determined by the United Nations Habitat Protection and Ecosystem Conservation Fund. (III)(d)Additionally, the United Nations will arrest all persons responsible for commission of the offenses and they shall be tried as criminals under this act subject to personal fines and imprisonment. (III)(e)The United Nations special Environmental Management Office will assume control for a period of ten years over the environmental affairs of any nation, which is in violation twice in one calendar year. (III)(f)Any nation consistently unable to care for the environment, despite these punishments, shall become a ward of the United Nations Environmental Management Secretariat and shall have its rights to soveriegn nation status revoked permanently. It will be administered by an advisory body made up of five nations in good standing under the Act. © 2002 Jorma Jyrkkanen Tags: biodiversity, common law, criminal law, governments, joma jyrkkanen, justice for all

Imperialism is the Global Purveyor and Guarantor of the Capitalism that is Destroying Planet Earth. 2021-07-15. Jorma Jyrkkanen

Pesticide Carcinogens in Mothers’ Milk and Total Diet; An Issue of Motherhood; A Toxicology Review. Aug. 1997. Author. Jorma A. Jyrkkanen. Contact: jjyrkkanen76@outlook.com

EUREKA: mRNA vaccine being excreted in Mothers Breast Milk.

Pesticide Carcinogens in Mothers Breast Milk Nov. 3rd, 2010 at 10:41 AM Pesticide Carcinogens in Mothers’ Milk and Total Diet; An Issue of Motherhood; A Toxicology Review. Aug. 1997. Author. Jorma A. Jyrkkanen. Contact: jjyrkkanen76@outlook.com

Abstract A literature review assessed the carcinogenicity of pesticide and chemical residues found in mothers’ milk by various researchers, and determined their probable contamination route, source and carcinogenic effects. It was concluded that carcinogens were present and these were probably causing cancers in humans. The main source of exposure in women was diet but occupational exposure may play a role for many. The primary candidate cancers for pesticidal origin are melanoma, lymphatic cancers, blood cancers and multiple myeloma. Other cancers also have a highly suggestive correlation with pesticide carcinogenesis, including breast cancer. Articles were discussed which suggest that synergism and immune system compromise may increase mortality. The concept of safe level was found to be based on erroneous arguments, which do not represent the real world. Inerts and their contaminants have a potential to explain a large component of carcinogenicity but have not been researched because they have been in use covertly. Epidemiology is largely after the fact of exposure and can lead to the conclusion that a product is unsafe after it has been used for a long time, thereby endangering many populations. It was found that most carcinogens in Mother’s Milk were also endocrine and reproductive disruptors with hormonal impacts and involvement in development and carcinogenesis. Banning carcinogens at the source and using alternatives to pesticides are discussed as options to use of carcinogenic pesticides. Key Words: breast cancer, carcinogens, childhood cancers, contaminants, covert, endocrine, epidemiology, exposure, disruptors, hormonal, inerts, leukaemia, lymphoma, melanoma, Mother’s milk, multiple myeloma, pesticides, reproductive, residues, synergism, toxicology, unsafe Clean Milk/A Broken Trust The International Agency for the Research of Cancer (IARC, 1979) recognized that animal carcinogens are a cancer risk to humans and stated that for practical regulatory purposes they should be treated as if they are human carcinogens. Additionally, Uma Ram Nath (1978) of the World Health Organization (WHO) raised an alarm over their concern over chemicals in breast milk. In his report, he cites food as the main source of toxins, and environment as another; that the contamination poses an unkown risk to babies, and in some cases, breast feeding should be discontinued; that experts recommend alternative preventative measures for reducing environmental pollution. Keeping these comments in mind, I decided in 1989 to have a look at published literature worldwide to see how many pesticide residues were in Mothers’ Milk and how many of them were considered to be cancer causing. This exploration uncovered many surprises. Publishing in Residue Reviews, Volume 89, author Allan Astrup Jensen (1983) reports on a worldwide survey in an article titled "Chemical contaminants in human milk". The list of findings is substantial. I assessed the carcinogenicity from available peer reviewed literature (Saks, I., 1981) of the most common residues and found the following associations of pesticide to its reported carcinogenicity [published cancer causing ability] (see Tables I & II). The Breast Feeding Infants Diet Table 1. Carcinogenicity of Residues Found in Human Milk EXPOSURE SPECIES CARCINOGENICITY PESTICIDE ROUTE TESTED FINDING DDT®; oral-mouse(mus)-conclusive (concl) carcinogen (carc), subcutaneous(scu)-mus-concl, animal (anim)-suspected(susp)-International Agency for Research on Cancer(IARC) PCB's®; conclusive human and mouse liver carcinogen DDE®; oral-mus-concl, etc.etc. hexachlorobenzene (HCB)®; oral-hamster (ham)-concl hexachlorocyclohexanes (HCH)®; (includes Lindane)-oral-mus-concl, anim-positive (pos)-IARC dieldrin®; oral-rat-suggest (sugg), oral-mus-concl, anim-pos-IARC heptachlor epoxide®; oral-mus-concl-potent experimental carc aldrin; mus-National Cancer Institute(NCI)-bioassay-pos, oral-rat-suggestive (sugg) heptachlor®; oral-mus-concl DDD (TDE); oral-rat-sugg, oral-mus-sugg, questionable (quest), anim-pos-IARC, NCI bioassay; results indefinite (indef) mirex®; oral-mus-concl, anim-pos-IARC oxychlordane®; oral-mus-concl trans-nonachlor®; no references in Sax (1981) pentachlorobenzene; "benzene is a high volume chemical and presents a serious and imminent threat to public health"Sax. PCT; oral-mus-concl PBB; oral-rat-quest, indef-IARC TCDD®; Discussed below hexachlorophene; negative (neg) perchloroethylene; oral-mus-concl, NCI bioassay-mus-pos halothane; note-1,2-dibromoethane used as a fumigant for apples-oral-rat-concl,oral-mus-concl, IARC-pos, also related 1,2-dichloroethane-mus-concl, rat-concl, bioassay-pos carbon disulphide; note that bisdiethylthiocarbamoyl, disulfide is oral-mus-concl, scu-mus-sugg, NCI bioassay-neg nicotine; oral-rat-sugg, intraperitonially (ipr)-mus- sugg, scu-ham-sugg, ipr-mus-concl, human suspected (susp) ®Reproductive and endocrine disrupters as of 1995. Clearly this is a diet that will make males less masculine and females less feminine and accounts for the homosexuals and lesbians in our society. Pellizzari et al.(1982) found several hundred volatile chemicals in Mother’s' milk from four different areas of the USA indicating a much broader contamination than expected. His list included the following chemicals. Volatile Organics in Mothers’ Breast Milk I mention that numerous purgeable organic compounds have been found in Mother’s' milk. The carcinogenicity and endocrine disruptivity of these is of great interest due to the widespread nature of the contamination, and the potential ramifications of this to nursing infants later in life, as well as to the contaminated parents. Exposure to multi-chemical carcinogens through nursing can be expected to induce mutations which may contribute to increased cancer incidence at a later date. Toxic chemicals can of course have other effects including neurological, reproductive, immunological, developmental and cognitive. The list is long but I will grind through it for the sake of science to show that multi-chemical exposure is highly multi, when taken together with the multitude of pesticides, inerts and residues I also mention in this review article. 26 HALOGENATED cpds; chlorodifluoromethane, chlorotrifluoromethane, dichlorodifluoromethane, chloromethane, chloroethane, trichlorofluoromethane, dichloroethylene, Freon 113, methylene chloride, chloroform, 1,1,1-trichloroethane, carbon tetrachloride, tetrachloroethylene, chloropentane, dibromochloromethane, tetrachloroethylene, dichloropropene, chlorobenzene, chlorohexane, iodopentane, 3-methyl-1,1-iodobutane, chloroethylbenzene, dibromodichloromethane, dichlorobenzene, chlorodecane, trichlorobenzene. This class of compounds tends to be carcinogenic and many induce cancers of the stomach, blood vessels, skin, breast, lung, uterus, liver and biliary tract in experimental animals. Some have proven to be human carcinogens of the lung, skin, liver and blood forming tissues. (N. I. Sax, 1983. Cancer Causing Chemicals. Van Nostrand Reinhold}. 17 ALDEHYDES; acetaldehyde, methyl propanal, n-butanal, methylbutanal, **Crotonaldehyde {Insecticide and CHEMICAL WARFARE AGENT (CAS: 4170-30-3)}, n-pentanal, n-hexanal, Furaldehyde {Insecticide, fungicide, germicide, irritates mucous membranes and acts on CNS, lacrimation and acts on eyes}, n-heptanal, benzaldehyde, n-octanal, phenyl acetaldehyde, n-nonanal, methyl furaldehyde, n-decanal, n-undecanal, n-dodecanal. 20 KETONES; acetone, methyl ethyl ketone, methyl propyl ketone, methyl vinyl ketone, ethyl vinyl ketone, 2-pentanone, methyl pentanone, methyl hydroxyfuranone, 2-methyl-3-hexanone, 4-heptanone, 3-heptanone, 2-heptanone, methyl heptanone {narcotic in high doses}, furyl methyl ketone, octanone, acetophenone, 2-nonanone, 2-decanone, alkylated lactone, phthalide. 26 other OXYGENATED cpds; C4H6O, C4H8O, C5H10O, C6H8O, C6H10O, C4H6O2, C6H12O, C7H12O, C7H10O, C7H14O, C6H6O2, C8H14O2, C8H16O, C7H8O2, C7H10O2, C9H18O, C8H6O2, C10H12O2, C10H14O, C10H16O, C10H18O, C10H20O, C10H.22O, C9H8O2, C11H20O, C10H10O2; {Note: C4H6O can be either vinyl ether, an explosive anesthetic, or methyl vinyl ketone, an alkylating agent, plastic, steroid and vitamin A precursor, with high absorbtion, irritancy to mucous membranes and respiratory system (Asthma link?), and high general systemic toxicity in mammals, or Crotonaldehyde which is already confirmed}. 10 ALCOHOLS; methanol, isopropanol, 2-methyl-2-propanol, n-propanol, 1-butanol, 1-pentanol, alpha-furfuryl alcohol, 2-ethyl-1-hexanol phenol, 2-ethyl-1-hexanol phenol, 2,2,4-trimethylpenta-1,3-diol, alpha terpineol. 2 ACIDS; acetic acid, decanoic acid. 4 SULFUR cpds; sulfur dioxide {Linked to increased heart disease, many cancers but especially lung cancer, respiratory diseases including Asthma, infant mortality} carbon disulfide, dimethyl disulfide, carbonyl sulfide. 7 NITROGEN cpds; nitromethane {Solvent, rocket fuel, coating industry}, C5H6N2 {this is either alpha or beta aminopyridine [Dye or anithistaminic] or Glutaronitrile [trimethylene cyanide]}, C5H8N2, C4H4N2O, methyl acetamide, benzonitrile, methyl cinnoline. 6 ESTERS; vinyl propionate, ethyl acetate, ethyl-n-caproate, isoamyl formate, methyl decanoate, ethyl decanoate. 2 ETHERS; dimethyl ether {Refridgerant}, dihydropyran. 1 EPOXIDES; 1,8-cineole. 14 FURANS; furan {Vapors anesthetic, absorbed through skin}, methyl furan, tetrahydrofuran, methyltetrahydrofuran, ethylfuran, dimethylfuran, 2-vinylfuran, furaldehyde, 2-n-butylfuran, 2-pentylfuran, methylfuraldehyde, furyl methyl ketone, alpha-furfuryl alcohol, benzofuran. 13 ALKANES; C3H8, C4H10, C5H12 {Pentane or neopentane}, C6H14, C7H16, C8H18, C9H20, C10H.22, C11H24, C12H26, C13H28, C14H30, C15H32. 12 ALKENES; C3H6 {Cyclopropane [explosive anesthetic], propylene [plastic, simple asphyxiant [Asthma?] and anesthetic at high concs]} , C4H8, C5H10, C6H12, C7H14, C8H16, C9H18, C10H20, C11H.22, C12H24, C13H26, isoprene {skin and mucous irritant, and in high concentrations, narcotic}. 7 ALKYNES; C5H8 {Isoprene again??}, C6H10 {Norcarane}, C7H12, C8H14, C9H16, C10H18, C12H.22, 11 CYCLIC cpds; cyclopentane, methyl cyclopentane, cyclohexane, ethyl methyl cyclohexane, C10H14 isomers, C10H16 isomers, limonene, methyl decalin, alpha pinene, camphene, Camphor {Plasticiser, pyrotechnics, moth repellents, preservative in pharmaceuticals and cosmetics, topical anti-infective, topical antipruritic, internally as stimulant and carminative, counter-irritant and antiseptic: causes nausea, vomiting, vertigo, mental confusion, delerium, clonic convulsions, coma, respiratory failure, death}; benzene {Leukemia}, toluene {Cancer promoter}, ethyl benzene, xylene, phenyl acetylene, styrene, benzaldehyde, C3 alkylbenzene isomers, C4 alkylbenzene isomers, C5 alkylbenzene isomers, C6 alkylbenzene isomers, methyl styrene {Styrene is a carcinogen}, dimethyl styrene, napthalene. Clearly, Pellizzarri et al. has much to tell us about how we are getting our pollutants into human tissues and into our children, pollutants which will do virtually nothing to improve health and almost everything to degrade it. He cites (IARC) 1979 and mentions that some of the most often detected contaminants seem to be carcinogenic or cocarcinogenic in laboratory animals. This concurs with these findings on the above chemicals. It cries out for action. Lance A. Wallace et al. (1989) followed this work up and the interested reader might find their work helpful. Infants and Fetus at Higher Risk " Jensen, says that "...In general, newborns are particularily sensitive to toxic chemicals citing Quinby et. al. (1965) .. because their kidneys, liver enzyme systems, and blood -brain barriers are not fully developed (Knoll and Jayarman 1973 a and b). " "..Furthermore, the newborn has very little body fat for storage; consequently, the fat soluble chemicals are circulated in the blood throughout the body for a longer period and may interfere more intensely with the normal enzyme activity (Kroger 1974). " Jerry M. Rice (1982) in his paper on exposure to chemical carcinogens during pregnancy and the consequences for mother and conceptus, says that transplacental transfer of carcinogens can cause cancer in the developing infant. The developing fetus is apparently exposed to pesticide residues in utero as well as at the breast. The BC Province Newspaper ran a story, Dec. 20, 1987, on Arnold Schecter, New York Scientist, who analysed the cancer risk to infants from just one of these compounds, tetrachlorodibenzo-p-dioxin (TCDD), one form of dioxin. Schecter is purported to have said; " We have calculated that the current exposure of nursing infants are 27 times greater than EPA's one in a million cancer risk level." But Schecter added that the lifetime risk is much higher. He said; " If it is assumed that infants in the United States nurse for one year, then during this year the child will have consumed 189 to 858 times the lifetime (70 yr ) Environmental Protection Agency (EPA) recommended intake." [1300 x in another source] This leads naturally to the question of what happens when you add the risk from all of the other chemicals and pesticides, taken singly and in combination? But first, lets look at routes or exposure and quantities. Routes of Exposure So where are these contaminants coming from and how is it getting into the milk? A report at the Third International Conference on Pesticides held in Helsinki, 3-9th July 1979 which made the link clear. V. M. Adamovic, et al. (1979) gave a report titled " Daily Pesticides Intake through food in the Population of Serbia". He reported finding DDT, alpha BHC, gamma-BHC and Dieldrin. Thus food is one avenue of contamination. Linda R. Pim (1981) cites H.F. Kraybill (1969) who was writing in the Canadian Medical Association Journal about pesticide exposure in the general population. Kraybill estimates that 30 mg of DDT and DDE are absorbed from food, 4.96 mg are inhaled and 0.03 mg are absorbed from air and 0.01 mg from water, per annum. He says that 90% of the contamination is from food. He estimated that average daily intake of chlorinated organic pesticides was .0013 mg/kg body weight per day in the general population in the period 1965-67. 2,4-D, 2,4,5-T, (Agent Orange was a mixture of these two) PCP, MCP, and others amounted to 0.00013 mg/kg/day of which 2,4-D formed 1/3 while MCP and PCP formed 1/2. 2,4,5-T isn’t legally sold anymore but many related isomers are still on the market covertly as Inert ingredients. Organophosphates (OP’s), chiefly malathion, but also parathion, diazinon, ethion, ronnel formed .00013 mg/kg body wt/ day. Carbamate daily dietary intake was .0009 mg/kg body weight. Adipose tissue retained 6 ppm DDT and 8.6 ppm DDE. Though banned in Canada and the USA, DDT is widely used in tropical regions. Meats, fish, poultry and dairy products were the main sources of persistent pesticides. Hair dressing, lipstick, hair lotion and sprays, and eye shadows provided 3.5 mg/person/year. White Americans averaged 8 ppb while non-whites averaged 16 ppb, indicating greater exposure in non-whites. His most important statement was that chlorinated organic pesticides have been found in all diet samples and all food classes within samples. That was in 1965-1967. Of course the variability could be very large depending on what a person ate, what their occupation was, and where they lived, and so on. Pesticides in the Canadian Diet Pesticide residues in the total diet in Canada were reported by Harry A. McLeod et. al. (1980). His list included along with average daily dietary intake in micrograms/kg (ug/kg) during the period 1976-1978, the following 24 different residues at that time representing organochlorines (OC’s), OP’s, sulfur, nitroanaline, phthalonitrile, and carbamate compounds. He reported for the first time; chlordane, methidathion, phosalone, toxaphene, chlorothalonil, dichloran, quintozene, sulfur, chlorpropham, and PCB (see Table II). Many could have been missed due to crude detection limits or by limiting the scope of the assay. Table II. Carcinogenicity of Pesticide Residues in the Canadian Diet EXPOSURE SPECIES CARCINOGENICITY PESTICIDE ROUTE TESTED FINDING =(avg Intake in ppb/day) INSECTICIDES BHC®=.01; oral-mus-concl, anim-pos-IARC (benzene hexachloride). Contaminant of corn, oats, rice. Chlordane®=<.001; oral-mus-concl., hepatocellular carcinomas (technical grade has 3 isomers incl. heptachlor). Garden fruits. DDT®=.023; oral-rat-sugg/or-mus-concl/scu-mus-concl/anim-susp-IARC, NCI-bioass-neg. Wide range of foods. Diazinon=.001; NCI-neg: final. Cereals. Dieldrin®=.002; oral-rat-sugg/or-mus-concl/anima- pos/NCI bioassay-neg:final. Wide range of foods. Endosulfan®=.007; oral-mus-sugg/NCI-neg:final Fruits, veggies. Endrin=.001; EPA Farm Worker Field Re-entry/NCI-neg Ethion=<.001; no data; Fruits. Heptachlor® epoxide=<.001; oral-mus-concl/potent experimental carc in animals; Dairy products. Malathion®=.012; oral-rat-quest/ NCI-neg/neg; Cereal contam. Methidathion=.012; No data; Regist. for potatos only Canada, contaminant on citrus fruits and apples imported from S. Africa, Chili, NZ, Australia, USA. Parathion=.003; oral-rat-quest/farm worker field re-entry NCI-Indefinite; Leafy vegetables and fruits. Parathion methyl; farm worker field re-entry/NCI-neg Phosalone=.007; (Zolone) No data; Winnipeg, Vancouver, Fruits. Toxaphene®=.012; oral-rat-quest, oral-mus-concl/oral-mus-concl/oral-mus-concl/NCI-bioassay-pos-mus; Halifax-leafy vegetables and legumes. FUNGICIDES Captan=.004; oral-mus-sugg/scu-mus-sugg/NCI-mus pos (Orthocide); Fruits. Chlorothalonil=<.001; oral-rat-sugg/NCI- rat pos (Daconil-2787, Bravo, Termil, Bravo-w-75); Garden fruits- Montreal. Dichloran=.01; (Dichloramine??)-intravenous (intrav)-rat- conc/skin-mus-quest/IARC-indef. (Batran); Not registered for fruits in Canada, USA. Minor foods pest use contaminant. Folpet; scu-mus-sugg (phaltan) HCB®=<.001; oral-mus-sugg/oral-ham-sugg/oral- ham-sugg; Dairy, meats, potatos, oils and fats. Quintozene=<.001; oral-mus-concl/skin-mus- sugg/IARC-anim-pos/NCI bioassay-neg; Leafy veggies. Sulfur=<.001; (Orthoflotox, Magnetic 6) No data MITICIDES Chlorobenzilate=.006; oral-rat-quest/oral-mus- concl/oral-mus-concl/IARC-anim-pos/NCI- mus-pos; Fruit. Dicofol®=.002; oral-mus-concl/oral-mus-concl/NCI-mus-pos; Leafy veggies, fruits. HERBICIDES Chlorpropham=.016; oral-mus-sugg/IARC indef; Potatos. OTHER PCB's®=.001; CONCLUSIVE HUMAN CARCINOGEN; meats, fish? Note: {1 ug/kg = 1 ppb}.® Reproductive and endocrine disrupters as of 1995. Note how many carcinogens are also endocrine disrupters suggesting a mechanism for carcinogenesis. Endocrine receptors probably deliver the toxins to the genes. The American Diet For an accounting of chemical pollution of the American diet the reader is encouraged to consult Marcia J. Gartell, et. al. (1985). The authors discuss daily dietary intake of pesticides, industrial chemicals, and the elements. They list the following pesticides and chemicals and toxic heavy metals. The total package Gartell and co-workers uncovered in the American diet included the following pesticides: alpha,beta, gamma, delta BHC®; captan, carbaryl, chlordane®, octachlor epoxide, chlorobenzilate, 2-chloroethyl caprate, 2-chlorethyl laurate, 2-chloroethyllinoleate, 2-chloroethyl myristate, 2-chloroethyl palmitate,chlorpropham, chlorpyrifos, DCPA, DDT®, DDE, TDE, DEF, Demeton-s-sulfone, diazinon, dichloran, dicofol®, dieldrin®, dimethoate, endosulfan I®, endosulfan II®, endosulfan sulfate, endrin, ethion, 2-ethylhexyl diphenyl phosphate, fenitrothion, fenthion, fonofos, heptachlor® epoxide, hexachlorobenzene,® leptophos, linuron, malathion®, methidathion, methoxychlor®, nitrofen®, trans -nonachlor®, parathion, parathion methyl, pentachloroanisole, pentachlorobenzene, pentachlorobenzonitrile, pentachlorophenol®, perthane, o-phenylphenol, phosalone, polychlorinated biphenyls, quintozene, pentachloroaniline, pentachlorothioanisole, ronnel, tecnazene, tetrachloroaniline, tetrachloroanisidine, tetrachloroanisole, tetrachlorobenzene, tetrachlorothioanisole, toxaphene®, tri-n-butyl phosphate, vinclozolin®, arsenic, cadmium®, lead®, mercury®, zinc.[Note:®Endocrine and reproductive disrupters, 1995; vinclozolin is an antiandrogen linked experimentally with hermaphrodism] The reader is encouraged to assess the carcinogenicity of the American diet. The source and the route of the breast contamination is thus clear. It is from contamination of the environment, entering our bodies by food, domestic products, air and water. McLeod said that all residues detected were within the United Nations Food and Agriculture Organization (FAO) and World Health Organization (WHO) proposed acceptable daily intakes but what does that mean. Safe Levels or Not? Does this mean that it is safe and nobody will be affected? There are many assumptions for this to be true worthy of examination. There is an argument circulating around amongst the proponents that thresholds exist and effects are dose dependent and if there is a sufficient safety factor in the amount of contamination, that it will not have any significant effect. There are others that believe that a safe level cannot be established for a carcinogen (Becker and Coye, 1984-cites NIOSH and OSHA; Surgeon General of the USA). A sample of one corporate Scientist’s viewpoint follows. George Paget, Director of the Biomedical program for Monsanto (Tim Padmore, Vancouver Sun, Sat. June 20, 1981) expressed a view more common to proponents of pesticides. He is reported to have told the Canadian Federation of Biological Societies that some people may die from environmental pollution is a price society should be willing to pay, and that people should just be told the risk, and make their own decisions. However, human data hasn't been and probably will never be collected on sufficient numbers of chemicals and pesticides to fully corroborate either detailed dose dependency for carcinogenicity or threshold hypotheses for humans specifically for each residue. Greim et. al. (1981) reports his findings on the relevance of high doses used in animal studies to the question of human carcinogenicity. He concluded that between species extrapolation and high to low dose extrapolation of chemicals undergoing metabolic activation and inactivation is most complicated. Greim's comments about inactivation and activation and species differences suggests that a great deal of detailed biochemical study is required, in the subjects who will be exposed, before we can state with assurance, that deactivating mechanisms exist in humans for any particular chemical. Are there individual differences in carcinogen metabolizing and excretion mechanisms? Cytochrome p-450 enzyme systems which do precisely that do vary significantly between individuals (Davis, L. 1986). , Genetic polymorphisms exist in genes that govern capacity to metabolize environmental contaminants (MS Wolff et. al. 1997). Predicting a safe level for all is imossible because of this. How then do we get this complex data, is the technical, moral and ethical question raised, except by making guinea pigs of us all? Safe or Not? Cancer Incidence Change Have cancers changed in incidence since the chemical era really began? Cancer deaths have doubled in Canada since the turn of the century (Statistics Canada Report, 1983) but some unkown proportion of this may be due to longevity and improvements in detection. In males all neoplasms increased from 1923 to 1973 according to J. Cartwright (1984). In the USA, amongst males, cancer of the bronchus, pancreas and leukemia increased during this period. Cancers in females decreased slightly during the first period but began a gentle increase again. Leukemia and bronchial cancers increased significantly during this period. Melanoma's which have been increasing (Swerdlaw. A. J. 1979), can be caused by solar radiation, x-rays, or pesticide pollution (see epidemiology below). Non-Hodgkin's lymphomas (NHL) (Smith, P.G. 1978) and multiple myelomas (Cuzick, J. Unpublished Data, cited in Cartwright, 1984) are also increasing and these have strong pesticide links (see epidemiology below). Childhood malignancies varying worldwide are brain tumor, Ewing's sarcoma, lymphomas and leukemias (Munoz, N. 1976) so that it is possible and prudent to conclude that they have an environmental component and certainly have strong associations with pesticide studies (see epidemiology below). Others may show a similar pattern if studied closely or may vary on a smaller geographical scale leading to a similar interpretation. To complicate epidemiological findings is the fact that people may change their life-styles and occupations several times in a lifetime, so that while they may be at one risk, say from being exposed to a cancer initiator chemical at the one job or chemical use area, that they will be at a significantly increased risk at one or more of the other arenas of exposure to cancer promoters or carcinogens which start the cancers developing. Safe or Not? Variability in Susceptibility One needs to consider that some people are more vulnerable to cancer than others (Rawis, 1983) and they may not need much exposure to carcinogens so that if their carcinogensis has a pesticide causality, prevention in these types of people would require complete banning of the pesticide. This might be especially true of people with genetic predisposition to cancer and those with weakened immune systems from disease, physical or psychosocial factors or those possibly contaminated with immune suppressors like TCDD (Raloff, J. 1986), PCB or DDTcontamination which is widespread and affects the immune systems of all animals studied, or those affected by poor nutrition and especially those with HIV. Safe or Not? The Epidemiology Story Epidemiological studies are very slow to shed light on the matter of human carcinogenicity. Conclusive epidemiological findings are extremely difficult to obtain, especially for cancers that normally have a low frequency of occurrence. For example, for n-nitroso-diethylamine, there is an enormous body of evidence that it is a conclusive carcinogen in numerous animal species when administered numerous ways, and it is almost certainly a human carcinogen; yet IARC lists it as `a Suspected Human Carcinogen'. A large number of carcinogenic chemicals lack epidemiological data (see Cartwright, 1984, pg 32.) and their recommendations always come after the fact of significant exposure and if positive, significant human mortality. It is useful to review some of the studies and see what is consistent and what is not. A brief survey of the literature follows. There is evidence from California that pesticide use in the home can lead to increased leukemias in children (Science News, 1988). In an epidemiological study in Sweden, testicular, endocrine, CNS and Hodgkins cancers were increased (Wiklund, K. 1989). E. A. Barthel (1986) in a retrospective cohort study of the cancer incidence in pesticide-exposed male pest control workers found elevated standardized mortality ratios (SMR’s)of 133 for all malignant neoplasms and high SMR’s for stomach (180), esophagus (430)! and melanoma (588)! which was anomalously high, and we are being told its the sun. A study on OC’s pesticides exposure in the human body (Wang X.Q. et.al. 1988) provides strong evidence of a correlation between beta-HCH and cancer mortality. The accumulation levels of beta-HCH in the populations studied were highly significantly correlatedwith the mortality rates from liver cancer, colon/rectum cancer, and lung cancer in males as well as colon/rectum cancer in females (P< 0.01), suggesting that the effect of HCH on the above cancers should be studied further. C. Wesseling et. al. (1996) found the following standardized incidence ratios for four cancers among pesticide exposed banana workers: SIR were observed for melanoma (SIR = 197, 95% CI: 94-362) and penile cancer (SIR = 149, 95% CI: 55-324); among women for cervix cancer (SIR = 182, 95% CI: 1.22-241)and leukaemia (SIR = 274, 95% CI: 86-639). P. Torchio (1994) working in Italy found increasing risks for melanoma, eye cancer, connective tissue and lymphomas. M. C. Allavanja et.al. (1987) studied pesticide exposed grain mill workers and found elevated cancers of the lymphatic systems and the blood forming systems. In particular they found elevated lymphosarcoma and reticulum cell sarcoma, other neoplasms of lymphoid tissue (i.e., giant follicular lymphoma and other primary malignant neoplasms of lymphoid tissue), and multiple myeloma. L.F. Burmeister (1990) found elevated multiple myeloma in Iowa farmers. It appears that melanoma, cancers of the lymphatics, lymphomas, and lymphosarcomas, and blood, leukaemia, multiple myeloma are clearly most consistent. Other cancers are also implicated but not so consistently but this may be due to a different mix of pesticides in the study cohort exposure history. The variability inherent in exposure history, genetic diversity, geographical location, migratory patterns, dietary preferences, synergism potentials and local natural carcinogen interactions, means that finding a consistent dose dependent relationship using epidemiology is very difficult and in many cases probably impossible even if it exists. Thus all of the above findings may be in fact real effects of pesticides. Waiting for epidemiological conclusiveness may subject many people to exposure before a safe or unsafe verdict is reached. But what if an unsafe verdict is reached as is emerging for the blood and lymphoid cancers above? A lot of people have now died from this large International experiment which could have been prevented and more are dying every day. Safe or Not? Multiple Chemical Exposure Thus, the public at large are part of a large and increasing experiment, to see if they and their children can survive multiple chemical pollution into the future, and the children are, due to the relatively recent findings of new pesticides in total diet in Canada, via their Mother's milk, at the front line of the experiment. One cannot help wondering what the increased lifetime risk is from all of these contaminants combined, plus that which might result from the enormous number of combinations of interactions that are also possible. These are called synergy’s, multiplicative effects, a well known phenomenon used in pesticide formulations and called `potentiation’ by toxicologists -where several chemicals exhibit greatly increased toxicity when used in a mixture together. An analogous example that we are more familiar with is smoking and alcohol exposure (Selikoff, I. et. al. 1968; Selikoff, I., et. al. 1980). Pharmacologists and the general public are familiar with this phenomena as drug interactions and these can be fatal (Sternon J., Gilles C. 1996). The concept of safe levels are based on the experimental presence in test animals of only one pesticide or pollutant. In the real world there are hundreds known, probably thousands that are not yet assayed for in each living organism. Pesticides are capable of interaction with various entities, which include formulating agents, solvents and carriers, impurities in formulation, and isomeric forms of active ingredients (Iyanimura, T.T. 1990) and of course the same things in all other pesticides. It is thus not even logical or ethical to speak of safe levels when extrapolating from experimental trials of single pesticides due to the existence of multiple chemical exposures and potentiation, and endocrine and synergistic effects in the real world. Estimates of `safe levels' based on single chemical exposure trials with animals therefore doesn't accurately describe the real world for humans, either in number and types of chemicals, chemical carcinogenic mechanisms, or potential interactions multiplying impacts. Safe or Not? Pesticide & Pathogens Multiply Mortality Pesticides may also make viral infections more serious. A common familiar example of a virus drug interaction magnifying impacts are Reye’s Syndrome in humans, where aspirin and flu in children can kill. M. Friend and D. O. Trainer (1970) found that young ducks exposed to PCB’s were more vulnerable to hepatitus virus. Crocker et. al. (July 6, 1974) found that mice given mixtures of the pesticides DDT and fenitrothion and injected with a sublethal encephalomyocarditis virus that normally doesn’t lead to much mortality had a greatly increased incidence of mortality (33-60%) than those given pesticides DDT (6-17%) singly or fenitrothin (4-9%) singly compared to viral infected controls which had no mortality. Fatty livers and kidneys were found and these mice died in paralysis and convulsions (epilepsy?). Crocker et. al. (1976) also reports that Canadian children exposed to DDT and fenitrothin had CNS and liver pathology symptoms [the same as in the mice]. Clearly, the immune system is compromised in some way by this interaction and support for this hypothesis comes from the work of P.R. McConnachie and A. C. Zahalsky (1991) who report that 38 humans exposed to pentachlorophenol, a wood preservative, had activated T-cells in females, autoimmunity, functional immunosuppression, and B-cell dysregulation. Other accounts of immune effects can be found in the literature. A. Betta et. al. (1989) reviewed published data and found that pesticide exposure is often associated with depressed humoral and cellular responses in mammals. The immunomodulating effects are affected by the route of administration and can also occur without general toxic effects, with a clear dose-effect correlation and for different dose levels. These findings hint at the possibility that people who are more vulnerable to infectious vectors may also be afflicted by simultaneous pesticide immunosuppression. Note also that this viral interaction effect makes the concept of safe levels of pesticide meaningless. The only safe level was none in the experiment. Pesticides’ Secret Companions; the Inerts There is another enormous source of unassayed residues including toxic chemicals, and that is from the secret inert igredients most pesticides are mixed with for field use. The inerts can form a larger part of the spray than the pesticide so the potential contamination is very high. I have revisited this issue recently with Joe Cole (Jyrkkänen J. A. & J. Cole, 1997) and have made the following findings reported in a story to the Globe and Mail. See also J. Jyrkkänen & J. Cole, (June 10) A Nation At Risk; Bravo Veterans Outlook (June/July 1997 Issue, pages 14, 60). “Active Agents Classified as Non-Active by the Canadian Government- ExtensiveToxicological Ramifications. Covert Use; Ramifications Toxic chemicals labeled as `non-active’ (inerts) in a lengthy { >=75 pages) federal pesticide ingredients list, pose a hazard to unsuspecting users and the environment. It has been discovered by the Researchers from the tables examination that a long list of active and toxic ingredients are in covert use in Canada without user knowledge and have the potential to harm persons and the environment. The list includes chemicals with long and exotic names like, 2,4,6-Trichlorophenoxyacetic acid (2,4,6-T), 2,4-Dichlorophenoxyacetic acid (2,4-D), Benzene Formaldehyde, Chlorofluorocarbon 11 & 12, Chromium oxide, Dioxane®, Nickel acetate , Polyoxyethylene amine (POEA), Polyvinyl chloride®, Toluene. Also present in the Canadian Inert List are chemicals found in the USA EPA 1989 list of Inerts of toxicological Significance that they were aware of: 2-ethylhexyl phthalate®, acrylic copolymer possibly, asbestos fiber, benzene, dichlorebenzene, dimethyl formamide, hexane, isophorone, lead compounds, malachite green, methyl chloride, methyl ethyl ketone, nonylphenol®, perchloroethylene, ethyelene glycol monethyl ether, rhodamine B compounds, trichloroethylene. These health effects may include: gender bending and reduced fertility effects, neurotoxicity, fetotoxicity, mutagenesis, carcinogenicity, teratogenicity, tumor promotion, immunotoxicity, or synergicity between these classes. These ingredients or numerous similar products are in use widely without public awareness because they have been classified as non-active ingredients and are therefore also Trade Secrets which are not subject to public disclosure. The precise heading on these ingredients is `Non-Actives in Registered Products; Non-Active Names (Chemical or Trade)’. Another level of cover-up is nested within this group as well since within Trade named products, there can be many non-listed ingredients and contaminants. A detailed look at what peer reviewed published studies have found about just a few of these non-actives regarding cancer causing potential follows; (2,4,6-T), (closely related to 2,4,5-Trichorophenoxyacetic acid used in production of Agent Orange). 2,4-6 T carcinogenicity was conclusive in rats and mice in 4 studies, positive in NCI bioassay and questionable in only 1 study. (2,4-D), a known carcinogen, linked to NH Lymphoma, soft tissue sarcoma, also used in agent orange; 2,4-D has been found to have the following contaminants contained within; octachlorobisfirone, xanthen-9-ones, mono, di, tri, and tetradioxins and probably furans, n-nitrosomethylamines and n-nitrosodiethylamines, ortho and para monochlorophenol isomers, (2,6-Di, 2,4,6 tri-) chloromethoxy phenol isomers, n-nitrosodiethanolamine, 3 chlorophenoxymethanes. These contaminants are thus part of the Non-Active package delivered and most are toxic. Benzene-a well studied cause of human leukemia. Formaldehyde-human cancer initiator and probable promoter. (CFC’s ) 11 & 12, now banned for use because of their harmful effects on ozone but included in the list. Chromium oxide-closely related chromium dioxide was found to be a conclusive carcinogen in rats in two studies and suspected in another. Dioxane-six conclusive carcinogenicity studies in rats and mice, 2 positive findings and one suggestive; discovered by J. Jyrkkänen and Dr. D. Monroe in 1989 in Vision herbicide. Nickel acetate-three conclusive cancer studies in rats and mice. (POEA)-a suspected human carcinogen. POE sorbitan monooleate and sorbitan monolaureate have been linked to human cancers of lung, skin, alimentary tract and bladder. (PVC’s)-human carcinogen which oxidizes in low heat to dioxins. Toluene-cancer promoter. One can see readily from perusal of the toxicology sample above that these substances are far from non-active, and may in fact be highly dangerous. Inert ingredients are defined as: Non-Active against the Targeted Pest, in Canada and the United States. Because of the potentially serious harmful effects of these toxic chemicals, the consumer has to wonder what the Canadian government has been up to in the Health Protection Branch to allow these dangerous chemicals to go unreported in commercial and domestic products. The ramifications for Canadian Federal liability are enormous if these toxins are exported in pesticide products or consumer goods and can be linked to diseases in the end users. There is also a serious jeopardy to Trade relations with Green countries or States who presently import Canadian goods. The reason given to the lead investigator by one official for classifying substances as Trade Secrets was that proprietary information in development would be disclosed to competitors. It now appears that there was a more insidious purpose to the Secrecy.” Contaminants Add to Residue Burden A good example is 2,4-D which has been found to have the following contaminants contained within; octachlorobisfirone, xanthen-9-ones, mono, di, tri, and tetradioxins and probably furans, n-nitrosomethylamines and n-nitrosodiethylamines, ortho and para monochlorophenol isomers ,(2,6-Di, 2,4,6 tri-) chloromethoxy phenol isomers, n-nitrosodiethanolamine, 3 chlorophenoxymethanes. Pesticide contaminants are thus part of the Non-Active (active in reality in the human body) package delivered to the environment and most are toxic. Conclusion This review has demonstrated the existence of chemical carcinogens in Mother’s milk and that the problem is widespread. Epidemiology has been largely ineffective at providing answers fast enough to keep pace with the growing use and distribution of pesticides as evidenced by the contamination with numerous carcinogens and it exposed people to danger before finding out if it is safe, and in many cases, unsafe. Evidence was brought forward that other potentially carcinogenic substances might be present that have not been disclosed or assayed for ie. amongst the inerts, and contaminants. Unknown isomers and formulants may also be present. There is the long list of anthropogenic chemicals which N. Irving Sax (1981) and others like The Merck Index, an Encyclopedia of Chemicals, Drugs and Biologicals, list as potential human exposure hazards. It appears that the concept of safe levels is meaningless in the multichemical milieu that we find ourselves due to interactions. There was evidence to suggest that the infant and fetus are at greatest risk from exposure. Most of the contamination is through food, though not all. Chlorinated organic pesticides have been found in all diet samples and all food classes within samples. What appears to be a distinct possibility from the above world-wide data, is that there is world-wide a large number of cancers induced by these chemicals because of their known experimental carcinogenicity and because of the enormous numbers of infants being exposed in milk, and the many years that they continue to be exposed through the dietary intake throughout life. Supporting this proposition are Erving J. Selikoff, MD. and E. Cuyler Hammond, SC.D. (1979) who estimated that from 75-85 % of cancers have an environmental origin. These percentages are however hotly debated by scientists working on risk models. However, most of these ignore synergy, potentiation, immunosuppression, individual susceptibility and the total load. Regarding breast cancer; accepted risk factors ie; unsaturated fat intake, socio-economic status, obesity, etc., are implicated in less than half of all cases.... halogenated hydrocarbons [to which group many pesticides belong]--acting as either co-carcinogens or promoting agents.... may play a role in breast cancer risk; elevated levels of polychlorinated biphenyls, bis (4-chlorophenyl)-1,1 dichloroethene, and bis(4-chlorophenyl)-1,1,1 trichloroethane were found in fat samples from women with cancer, suggesting a role for environmentally derived suspect carcinogens in the genesis of mammary carcinoma (Falck F. Jr et. Al. 1992). Also, MS Wolff et. al. 1997, found studies linking OC’s and DDT to breast cancer in four different countries. Ramamoorthy K. et. al. (1997) found that 10(-4)M endosulfan caused a 2000 fold increase in activity in the Beta Galactosidase reporter gene in yeast which had estrogen receptor inserts, suggesting that it is a steroid analogue. Estrogen substitution therapy hs been linked to increased risk of breast cancer. Endosulfan is part of the Canadian and American diet, and is used on fruits and vegetables. However, 10(-4)M is a very high concentration. This review has focused primarily on carcinogenicity. My review of epidemiology studies and cancer trends has concluded that modern childhood cancers are linked to pesticides and also the following cancers in all age groups: melanoma, cancers of the lymphatics, lymphomas, and lymphosarcomas, and blood, leukaemia, are clearly most consistent and multiple myeloma. Assuming that there was accurate reporting of viewpoints, opposing the viewpoint that breast feeding is potentially harmful according to the writer Rebecca Burnham (Nov. 1990), are Dr. Verity Livingston of the Vancouver Breast Feeding Clinic, Dr. John Blatherwick, the Vancouver Medical Health Officer and most Scientists. However, a full five percent of papers given this summer at a Reproductive Symposium in Portland Oregon were dedicated to chemical and pesticide toxicology suggesting real concern by high level scientists for the effects of these substances. This review has shown that the suspicion that cancer causing pesticides found in the breast and in its milk and probably also in utero, mostly derived from food contaminated with residues, probably causes significant increases in childhood cancers, and later in adults as well due to time lags before onset and continued ingestion of residues from food. Other avenues of contamination are probably minor except for those occupationally exposed. Melanoma, blood cancers, sarcomas, and lymphomas and multiple myeloma are clear contenders for breast milk linked cancers. It saddens me to reach the conclusion, based on this review of scientific evidence, that many people have already died and many more are doomed world-wide from these preventable cancers. The strong pesticide association of melanoma and the widespread nature of its occurrence amongst north temperate caucasians suggests an interaction of solar radiation and chemical pollution as causal, and it would be interesting to find out what proportion is due to which venue in a restrosective synergism study. The problem is of course an International one because of the export and import of food items, and varying regulations and pesticide usage patterns between countries (Table III) . Table. III Average (avg) Total Pesticide Residues in Mother's Milk From Around the World & Canada; (DATA in ppb's) PESTICIDE COUNTRY/AVG RESIDUE CANADA ( avg(range)) (avg/(range) ( Yr)) ALDRIN; FRG=50 PPB. 1+/(1978/79) DDT; Guatemala= 3100(410-12,200). 154+/(1967/68) DIELDRIN; Lisbon Portugal= 18-31. 5+/(<1-60)(1967/68) HCB; Melbourne=2-330. 2/1(<1-21)(1975) HCH; Punjab=14-820. 1(1975) BETA-HCH; Griefswald DDR=0-900. <21(1975) GAMMA-HCH; Spain=73. <(1-35)(1967/8) HEPTACHLOR AND HEPT. EPOXIDE; Spain=39. OXYCHLORDANE AND CHLORD; USA<=20. 1 PCB; USA=50-4091. MEDIAN=4(1979) TRANS-NONACHLOR; USA=<10. 1(1975) What Should We Do? This review supports the proposition that there is enough evidence to conclude that action to prevent chemical carcinogenesis is warranted and prudent and could save many lives from disease, keeping in mind the social costs of potentially reduced quantity of foods. In North Termperate regions quanity of food is not a problem so much as distribution and access to food varying according to income level and education. In the tropics, and in poor countries in general, exposure through dermal and inhalation routes due to ignorance and poverty are probably higher. It concurs with and supports fully the alarm sounded by WHO in 1987. If it is chosen to eliminate these carcinogens from mother's milk, this will require a coordinated effort on the part of citizens and governments amongst all trading partners. Organic gardening, biological pest control, and Integrated Pest Management (IPM) offers a means to reduce pollution and keep food production up. Soils may actually increase in quality through application of these procedures. IPM however still uses suspected pesticides and undisclosed inerts. Regulatory measures offer a means to reduce exposure. Italy has already registered lower levels, in Mother’s' milk, of conclusive animal carcinogens HCB, alpha-HCH, beta-HCH, lindane, DDE and DDT due to tougher Italian and European restrictions of 1982 (Dommarco, et al. 1987). So has Norway (Brundtland, Gro, 1989). However, governments cannot as we have seen all be trusted. Banning them at the source, along with toxic inerts would be the only way to get rid of all residues completely, but this would have to be by international agreement. Governments will have to come under scrutiny by independent auditors to ensure they do not use toxic inerts. There are those who will oppose tougher legislation. They may argue that the exponential growth of resistance to pesticides by pest species (Georgia, G. 1981) argues for an increase in the number of pesticides to deal with them, if that route of control is not effectively replaced by alternative methods. They may argue that agricultural production requires pesticides. One cannot but wonder at what kind of milk future generations of infants will be consuming if the demonstrated trend continues. I believe strongly that strides to improve the quality of our chemical environment will be made by those that become aware of what is in our environment, in Mother’s' milk, because protection of our children and the future of life itself is, after all, a motherhood issue. What I have identified above hints strongly that chemical carcinogenesis is the probable cause of breast cancer in most women. It seems highly unlikely that such a collection of carcinogens passing into and through the breast, cannot at some point turn on that breast tissue itself and cause cancerous transformation. One needs only a brief look at how fats are turned into milk to realize how intimately these lipophilic pesticides are associated with crucial cellular metabolic pathways. In Israel, studies suggest that the dramatic drop in breast cancer mortality rates is associated with a ban on alpha-BHC and lindane (Westin J. B. 1993). DDT was also present but had already been banned, implying a causal connection for any or all of these pesticides for breast cancer. They are a different set of pesticides than those identified as linked to breast cancer by Falck F. Jr. et. al. 1992, who report an association of polychlorinated biphenyls, bis (4-chlorophenyl)-1,1 dichloroethene, and bis(4-chlorophenyl)-1,1,1 trichloroethane in cancerous breast tissue. Clearly these seven pesticides/contaminants need immediate attention. We must keep in mind that other effects may be present as well; teratogenicity, fetotoxicity, gender bending, fertility effects, neurotoxicity, and immunotoxicity and a chemical role in cancer promotion. There may also be exotic diseases of unknown origin caused by or linked to pesticides. For example, bovine Kreutzfeld Jacobs disease (BSE) has been linked to the (OP) Phosmet (Purdey, M. 1996). This raises the possibility that OP’s may also cause it in humans. Parkinsons disease has been linked to dieldrin (a mitochondrial poison) exposure and Altzhiemers disease has a highly suggestive link to pp-DDT though he doesn’t mention it in his abstract (Fleming, et. al. 1994). Some epilepsy may turn out to be linked to DDT and or fenitrothion and viral infections since we saw the mice die in siezures and children similarly exposed had similar gross pathological symptoms. Autoimmune diseases like MS, some diabetes, and some forms of arthritis may turn out to be linked to cyclic halogens (pentachlorophenol?-see McConnachie et. al. above) or other autoimmune triggers acting synergistically with ordinary pathogen infections. Of these other effects, the greatest risk to life and natural selection processes are those affecting reproduction and the immune system. The immune system is of course under assault from loss of ozone as well, and so should have a great amount of funding for research. Chemically diminishing the effectiveness of the immune system will make organisms more vulnerable to all manner of diseases including cancer. Other species are often at greater risk than we humans because they are more often exposed to the direct toxicity as well as these side effects of our pesticide use and many species are assaulted from combined habitat loss, alienation, physical and chemical alteration of their environment. Footnote When discussing this issue, I am often confronted by anxious women who worry about continuing breast feeding. Everything in this article and my analysis cries out; “Stop Breast Feeding!” However, we are in a Catch .22. We are damned if we do and more damned if we don’t, but for the infant, the chance to get a normal immune system depends upon being exposed to human milk. This leaves us no choice except to conclude that for practical purposes, benefits of limited breast feeding might outweigh the harmful potential. A poisoned immune system is better than no immune system at all. The duration or length of time spent breast feeding is the issue which does need detailed examination until such time as we clean up the pollution of Mother’s milk. The infant needs human milk to prime the immune system and to transfer antibodies when its own are as yet undeveloped. Mother’s milk has human specific fats and proteins vital to the infants development. The child needs its Mother’s touch to ensure normal physiological and psychological development and the mother needs it too to bond properly. If one is still concerned about a potential risk, then get tested although this is a worrisome and expensive procedure, which would probably only return what we already know. Reducing life-time burden or exposure by eating organic foods and washing foods thoroughly and by peeling fruits, can help. Most importantly, lobby for change in pesticide and inert management to eliminate those that are capable of affecting the health of humans and the environment. Demand labels with full disclosure of active, inert and contaminant ingredients on all products used. Boycott serious polluters. Do not stop early breast feeding unless you have reason to believe that you are seriously polluted. If seriously concerned still, reduce the time spent breast feeding or find an unpolluted Wet Nurse. My personal bias is to go the above route while eliminating carcinogens and those chemicals affecting the endocrine systems and reproduction and the immune system at their point of origin. Health and Welfare Canada should also answer an important question. Do Material Safety Data Sheets (MSDS) have allowance for the toxicities of the inert ingredients and contaminants and where are these toxicity databases kept? I want a copy. Also, whose idea was it to create the secret inert database? Literature Cited Adamovic, V. M., J.A. Burke, B. Sokic, O Petrovic. 1979. Daily Pesticides Intake through Food in the population of Serbia. Pesticides: Third International Conference. Helsinki, 3-9 July. Alavanja MC, Rush GA, Stewart P, Blair A J 1987. Proportionate mortality study of workers in the grain industry. Natl Cancer Inst. 78(2):247-252. Feb. Barthel E A 1986. Retrospective cohort study of the cancer incidence in pesticide-exposed male pest control workers [1214 who worked 5 yrs or more]. Z Erkr A-ungsorgane;166(1):62-68. Becker, Charles E. and Molly Joel Coye. 1984. Recent advances in occupational cancer. Clinical Toxicology. .22(3):195-208. Betta A, Maranelli G, Dal Ri C 1989. Pesticide immunotoxicity Med Lav. 80(5):381-389 Sep. [Article in Italian] Brundtland, Gro. 1989. Personal communication. [Responding to my global concerns about carcinogenic pesticides in Mother’s Milk via Minister of Health]. Burmeister LF (1990) Cancer in Iowa farmers: recent results. Am J Ind Med 18(3):295-301 Burnham, Rebecca, (1990). Crying Wolf once too often. BC Report, p: 24. Nov. Cartwright, J. 1984. Cancer Epidemiology. In Chemical Carcinogens. Vol. 1. Charles E. Searle, Editor. ACS Monograph 182. Crocker, J.F.S., K.R. Rozee, R.L. Ozere, S.C. Digout, O. Hutzinge. 1974. Insecticide and viral interaction as a cause of fatty visceral changes and encephalopathy in the mouse. The Lancet, p:.22. July 6. Crocker J. F.S. et al. 1976. Pesticides/Virus/DDT/Fenitrothion On Humans. Science (192):1351-1353. Cuzick, J. Unpublished Data, cited in Cartwright, 1984. Davis, L. 1986. One Man's Poison: Genetic Vulnerability. Science News (129) Dommarco, Roberto, Alphonso De Muccio, Ivano Camoni, and Beniamino Gigli. 1987. Organochlorine Pesticide and Polychlorinated Biphenyl Residues in Human Milk from Rome (Italy) and Surroundings. Bull. Environ. Contam. Toxicol. (39):919-925. Falck F Jr, Ricci A Jr, Wolff MS, Godbold J, Deckers P .1992. Pesticides and polychlorinated biphenyl residues in human breast lipids and their relation to breast cancer. Depar-ent of Ophthalmology, University of Michigan, Ann Arbor. Arch Environ Health47(2):143-146. Mar. Fleming L, Mann JB, Bean J, Briggle T, Sanchez-Ramos JR 1994 . Parkinson's disease and brain levels of organochlorine pesticides. Depar-ent of Epidemiology and Public Health, University of Miami School of Medicine, FL 33136. Ann Neurol;36(1):100-103 .July . [Epidemiological studies have suggested an etiologic relationship between pesticide exposure and Parkinson's disease (PD). Organochlorine pesticides were assayed in pos-ortem brain samples from 20 PD, 7 Alzheimer's disease (AD), and 14 nonneurological control cases. The three groups were similar in age at death, sex, and demographic variables. Only two of 16 pesticide residues screened were detected. A long-lasting residue of DDT(pp-DDE) was found in the majority of cases of PD and AD, as well as in all the control cases; pp-DDT was significantly more likely to be found in AD controls than the PD cases (Fisher's exact two-tailed, p = 0.04). Dieldrin was detected in 6 of 20 PD brains, 1 of 7 AD, and in none of 14control samples. Despite the relatively small number of brains assayed, the association between Dieldrin and the diagnosis of PD was highly significant (p = 0.03). Dieldrin, a lipid-soluble, long-lasting mitochondrial poison, should be investigated as a potential etiological agent of Parkinsonism]. Friend, M. and D. O. Trainer (1970). Science (170):1314. Gartell, Marcia J., John C. Craun, David S. Podrebarac, Ellis L. Gunderson. 1985. Pesticides, Selected Elements, and Other Chemicals in Total Adult Diet Samples, October 1979- September 1980. J. Assoc. Off. Anal. Chem. 68(6):1184-1197. Georgia, George P. and Roni B. Mellon. 1981. Pesticide resistence in time and space. Pesticide Resistance to Pesticides. Plenum Press: New York. p:1-48. Grem, H., U. Andrea, S. Hesse, L.R. Schwarz. 1981. How relevant are high doses in mutagenicity and carcinogenicity studies in animals? Progress In Mutation Research, Vol.2, p:129-147. Hardell, Lennart, 1977. Malignant mesenchymal tumors and Exposure to Phenoxy Acids: A Clinical Observation. Lakarttidningen. (74):2753-2754. Iyanimura, T.T. 1990. Mammalian toxicity and combined exposure to pesticides. Laboratory for General Toxicology, Institute of Public Health and Environmental Hygiene, Bilthoven, The Netherlands Vet Hum Toxicol; 32(1):58-62. Feb. IARC. 1979. Chemicals and industrial processes associated with cancer in humans. IARC Monographs, Suppl. 1. Lyon: International Agency for Research on Cancer. Jensen, Allan Astrup, 1983. Chemical contamination in human milk. Residue Reviews (89):1-128. Jyrkkänen J. A. & D. Monroe. 1989. New concerns about potential contamination of forestry herbicide Vision by the probable human and confirmed animal carcinogen and liver and kidney toxin, 1,4-dioxane. Unpublished paper. Jyrkkänen, J. A. & J. Cole, 1997. Active Agents Classified as Non-Active by the Canadian Government-ExtensiveToxicological Ramifications. 7 August Press Release to the Globe and Mail. p:1-3. See also J. Jyrkkänen & J. Cole, (June 10) A Nation At Risk; Bravo Veterans Outlook. Active Agents Classified as Non-Active by the Canadian Government-ExtensiveToxicological Ramifications (June/July 1997) (p: 14, 60). Knoll and Jayarman [Cited in Jensen] Kraybill, H. F. 1969. Significance of Pesticide Residues in Food in Relation to Total Stress. Can. Med. Assn. Journal. Vol. 100:204-215. Jan 25. Kroger 1974 [Cited in Jensen] McConnachie, P.R. and A. C. Zahalsky (1991). Immunological Consequences of Exposure to Pentacholorphenol. Archives of Environmental Health. 46(4):249-253. July/August. McLeod, Harry A., Dorothy C. Smith, and Nathan Bluman, 1980. Pesticide residues in the total diet in Canada, v: 1976 to 1978. Journal of Food Safety (2):141-164. Munoz, N. 1976. In "I Tumor Infantale"; Bucabssi, P. et. al.; Eds.; Casa Editrice Ambrosiana: Milan, p:5-15. Nath, Uma Ram. 1987. WHO sounds alarm over chemicals in breast milk. New Scientist. p:30. June 25. Pim, Linda R. 1981. The Invisible Additives. Pollution Probe. p:1-269. Pellizzerri, E. D., T. D. Hartwell, B. S. H. Harris, R. D. Waddell, D. A. Whitaker, and M. D. Erickson. 1982. Purgeable organic compounds in mother's milk. Bull. Environ. Contam. Toxicol. (28):3.22 Purdey M. (1996), The UK epidemic of BSE: slow virus or chronic pesticide-initiated modification of the prion protein? Part 2: An epidemiological perspective. High Barn Farm, Somerset, UK. Med Hypotheses. 46(5):445-454. May. [An alternative hypothesis is proposed that cites exposure of the bovine embryo to various specific high-dose lipophilic formulations of organophosphates, such as the high-dose phthalimide containing organophosphate phosmet, (which were applied compulsorily and exclusively in the UK during the 1980s/early 1990s) as the primary trigger that initiated the deformation of prion protein and the onset of the bovine spongioform encephalopathy epidemic.] Quinby, E., J. F. Armstrong, W. F. Durham. 1965. DDT in Human Milk. Nature (207):726. Raloff, J. 1986. Dioxin: Is everyone contaminated? Science News. 128(2):26-29. Ramamoorthy K, Wang F, Chen IC, Norris JD, McDonnell DP, Leonard LS, Gaido KW, Bocchinfuso WP, Korach KS, Safe S .1997. Estrogenic activity of a dieldrin/toxaphene mixture in the mouse uterus, MCF-7 human breast cancer cells, and yeast-based estrogen receptor assays: no apparent synergism. Veterinary Physiology and Pharmacology, Texas A&M University, College Station 77843-4466, USA. Endocrinology 138(4):1520-1527 Apr. [10(-4) M endosulfan caused a 2000-fold increase in beta-gal reporter gene activity.] Rawis, Rebecca L. 1983. Dioxin's Human Toxicity is Most Difficult Problem. C&EN. Washington, June 6. Rice, Jerry M. 1982. Exposure to chemical carcinogens during pregnancy: consequences for mother and fetus. First World Congress on Trophoblastic Neoplasms, Nairobi, Kenya, Oct. 25-27. Saks, N. Irving. 1981. CANCER CAUSING CHEMICALS. Van Nostrand Reinhold. p:1-466. Science News, 1988. Pesticide Link to Leukemia. Selikoff, I. J. MD. and E. Cuyler Hammond, SC.D. 1979. Cancer and the Environment. In Understanding Cancer. Bull Publishers. p:1-135. Selikoff, I, J. Hammond, E. C. Chung, J. Jama. 1968. J. American Medical Association. (204):106-112. Selikoff, I., J. Seidman, H. Hammond, E. C. 1980. JNCI, J. Natl. Cancer Inst. (65):507-513. Selikoff, I. J. MD. and E. Cuyler Hammond, SC.D. 1979. Cancer and the Environment. In Understanding Cancer. Bull Publishers. p:135. Smith, P.G. 1978. In "Lymphoma". UICC Workshop, Geneva. Statistics Canada, 1983.-mortality in Canada-. The Queen's Printer. Sternon J., Gilles C. 1996. Poly-medication and drug interaction in geriatrics. [Article in French] Service de Medecine Interne, Hopital Erasme, Bruxelles. Rev Med Brux Dec;17(6):389-396 [the authors focus on 9 families of drugs potentially dangerous to the health and 5 interactions with deadly consequences ] Swerdlaw. A. J. 1979. British Medical Journal. (2):1324-1327. Torchio P, Lepore AR, Corrao G, Comba P, Settimi L, Belli S, Magnani C Sci Total Environ 1994. Mortality study on a cohort of Italian licensed pesticide users., di Orio F Center of Epidemiology, University of L'Aquila, Italy. 149(3):183-191 Jun . 20 Wallace Lance A. et al. (1989). The Influence of Personal Activities on Exposure to Volatile Organic Compounds. Environmental Research (50):37-55. Wang XQ, Gao PY, Lin YZ, Chen CM. 1988. Studies on hexachlorocyclohexane and DDT contents in human cerumen and their relationships to cancer mortality Institute of Nutrition and Food Hygiene, Chinese Academy of Preventive Medicine, Beijing. Biomed Environ Sci 1(2):138-151. Aug. Wesseling C, Ahlbom A, Antich D, Rodriguez AC, Castro R 1996 Cancer in banana plantation workers in Costa Rica. Pesticide Program, Universidad Nacional, Heredia, Costa Rica. Int J Epidemiol; 25(6):1125-1131. Dec. Westin JB. 1993. Carcinogens in Israeli milk: a study in regulatory failure. Int J Health Serv; 23(3):497-517. Wiklund K, Dich J, Holm LE, Eklund G 1989. Risk of cancer in pesticide applicators in Swedish agriculture. Department of Cancer Epidemiology, Karolinska University Hospital, Stockholm, Sweden. Br J Ind Med. 46(11):809-814. Nov. Wolff MS, Weston A.1997. Breast cancer risk and environmental exposures. Division of Environmental and Occupational Medicine, Mount Sinai School of Medicine, New York, New York 10029-8574, USA.Environ Health Perspect;105 Suppl 4:891-896 June. Copyright 1997. Jorma Jyrkkanen. All rights reserved. Tags: pesticides, carcinogens, endocrine disrupters, residues, diet, mothers milk, infants, pediatrics, Jorma Jyrkkanen Tags: carcinogens, diet, endocrine disrupters, infants, jorma jyrkkanen, mothers milk, pediatrics, pesticides, residues

Amyotropic lateral sclerosis ALS and dioxin 2,3,7,8-TCDD may be causally linked. Mar. 4th, 2010 Supported by Later Studies. Jorma Jyrkkanen

Amyotropic lateral sclerosis and dioxin may be causally linked. Validated by later studies. Mar. 4th, 2010 at 5:34 AM. Jorma Jyrkkanen

In fish exposed to dioxins, the first symptom is finrot. Degeneration of periferal extremities. It is irreversible and begins with an extremely small exposure. We see in ALS a similar degeneration of the extremities. This leads me to suspect that dioxins and possibly furans and PCB's are involved ALS causality. I should like to do a statistical test to affirm this. Gallagher found elevated neurodegenerative disease in School Districts in BC with Pulp Mills, which incidentally emit dioxins, furans and a host of other organochlorines supporting my hypothesis. I believe that a proper epidemiological test could put the matter of ALS to rest. ©2010 Jorma Jyrkkanen. All rights reserved. Tags:ALS, dioxin, causality, Jorma Jyrkkanen, epidemiology Tags: als, causality, dioxin, epidemiology, jorma jyrkkanen Dioxins and related environmental contaminants increase TDP-43 levels Peter E. A. Ash, Elizabeth A. Stanford, Ali Al Abdulatif, Alejandra Ramirez-Cardenas, Heather I. Ballance, Samantha Boudeau, Amanda Jeh, James M. Murithi, Yorghos Tripodis, George J. Murphy, David H. Sherr & Benjamin Wolozin Molecular Neurodegeneration volume 12, Article number: 35 (2017) Cite this article 2539 Accesses 16 Citations 13 Altmetric Metricsdetails Abstract Background Amyotrophic lateral sclerosis (ALS) is a debilitating neurodegenerative condition that is characterized by progressive loss of motor neurons and the accumulation of aggregated TAR DNA Binding Protein-43 (TDP-43, gene: TARDBP). Increasing evidence indicates that environmental factors contribute to the risk of ALS. Dioxins, related planar polychlorinated biphenyls (PCBs), and polycyclic aromatic hydrocarbons (PAHs) are environmental contaminants that activate the aryl hydrocarbon receptor (AHR), a ligand-activated, PAS family transcription factor. Recently, exposure to these toxicants was identified as a risk factor for ALS. Eureka ALS cause found. Pulp mills carcinogens and mutagens and some EDs. I suggested dioxin caused ALS in 2010 and this is supported by subsequent research. I presented details of this list as Intervenor at Al Pac hesrings. It is Found in BKME effluent. Agent Orange and other sources.

s 2,3,7,8-TCDD.

Climate Change Predictions at 2002. Posted 8 Jan 2010. Jorma Jyrkkanen Revisited 2021.

Climate Change Predictions by Jorma Jyrkkanen Jan. 8th, 2010 at 1:01 AM Climate Change Predictions; Published previously in now defunct geocities.com/Jormabio jjyrkkanen76@outlook.com

Some of the best brains in the world have put the following sites up for us all to examine what is happening and what is likely to happen. My review of these sites is cursory and I have formed an opinion which is that there is serious cause for concern. The predictions raise serious questions; will the post-glacial era have post-glacial rebound and accelerated plate techtonic activity with increased volcanism and earthquake activity; will methane clathrates melt and release their contents to the oceans and atmosphere resulting in a run-away greenhouse global disaster; if so how much time do we have; can we reverse global warming or is it all ready too late. Please examine these sites and others that you may be interested in and form your own conclusions. Norwegian Predictions http://www.grida.no/soeno97/climate/ Canadian Model Projections CCMA Temperature Online http://www.cccma.bc.ec.gc.ca/diagnostics/cgcm1/animation1.shtml CCMA Precipitation Model http://www.cccma.bc.ec.gc.ca/diagnostics/cgcm1/animation4.shtml CCMA Soil Moisture Model http://www.cccma.bc.ec.gc.ca/diagnostics/cgcm1/animation5.shtml USGS Climate Change on Glacier National Park http://nrmsc.usgs.gov/research/glacier_model.htm Climate Change Projections for Alaska for 2100 http://www.usgcrp.gov/usgcrp/Library/nationalassessment/overviewalaska.htm NWS Climate Predictions Center http://www.cpc.ncep.noaa.gov/ GIMMS time Series and Mapping http://ltpwww.gsfc.nasa.gov/gimms/htdocs/timeseries/timeseriesGIMMS.html Carbon Dioxide Information Center http://cdiac.ornl.gov/ Global Change Data and Information http://cdiac.ornl.gov/by_new/bysubjec.html#landuse Global Data Banks; International http://www.eman-rese.ca/eman/ecotools/datasets/intro.html

Very disturbing development. Oxygen decline suggesting photosynthesis is decreasing.

Is it due to dropping photosynthesis from high temoperature???

© 2002 Jorma Jyrkkanen. All rights reserved. Current Mood:awake Tags: climate, ghg, jorma jyrkkanen, predictions

Is Capitalism the Next Chicxulub. 27 March 2013. Jorma Jyrkkanen

Is Capitalism the Next Asteroid That Dooms Our Planet March 27, 2013 What is Capitalism by JormaJyrkkanen 8 March 2013 Capitalism is an absolute kleptocratic cannibalistic Monarchy of corporate Plutocrats that converts the blood, sweat, tears, dreams and slavery of the masses into personal fortunes by devouring the energy, ingenuity, lives, resources, biodiversity and common property of Planet Earth via puppet mafias called government. It matters not if those governments are communist, theocratic, democratic or tribal, they are all puppet vehicles for that cannibal cabal. They dupe the masses into believing they too can become rich beyond their wildest dreams and that this is the road to freedom and happiness. They do this with a spin machine called hollywood and commercials that peddles the lie that growth has no limits and every girl can be a princess who finds a prince with a castle and a dungeon full of gold. Spice this toxic cocktail up with criminal mafias, laundry money, offshore accounts and corrupt officials and government leaders and you get what we have globally, 1% rich beyond belief and 99% Serfs paying homage to them and our planet going to hell at an accelerating rate. Must Read http://www.kingworldnews.com/kingworldnews/Broadcast/Entries/2013/3/24_Dr._Paul_Craig_Roberts.html http://www.ft.com/intl/cms/s/2/43e7da5c-917d-11e2-b4c9-00144feabdc0.html#axzz2OXdeXYr5 http://rense.com/general33/fd.htm Copright 2013 All rights reserved. Jorma Jyrkkanen

How Municipal Incinerators Make Dioxins from Chlorophenols and Remediation. 1987. Karasek, FW and LC Dixon. and More. JEC Consulting.

Mechanism of formation of polychlorinated dibenzo-p-dioxins produced on municipal incinerator flyash from reactions of chlorinated phenols{Fly ash had 600 different organic molecues adsorbed onto it}

Richmond Incinerator was aditted by Feds to produce dioxins and I pointed out to them that these were dispersed over the lower Fraser River market garden croplands. Author links open overlay panelL.C.DicksonF.W.Karasek https://doi.org/10.1016/S0021-9673(01)94417-6Get rights and content Abstract All incinerators burning municipal waste produce chlorinated dioxins. The mechanism by which these compounds are formed is unknown. Experiments were performed that show these compounds can be produced from known precursors by surface catalysed reactions on the flyash particulates present in the incineration process. A full range of the tetra- through octachlorinated dibenzo-p-dioxins were produced from 13C-labelled pentachlorophenol and two trichlorophenols on the surface of flyash from an Ontario municipal incinerator that had been previously freed from organic material. A simple flow-tube apparatus at 300°C under a 10-ml/min nitrogen flow was used for the experiments. The use of 13C-labelled pentachlorophenol gave a direct measure of the extent of the catalytic reactivity of the flyash surface. Much lower amounts of chlorinated dioxins were produced in similar experiments with flyash from a modern Japanese incinerator whose effluents are normally extremely low in these compounds. Only small amounts of octachlorodioxin, the thermal condensation product expected, were formed using ground firebrick or an empty flow-tube for the reactive surface. These results indicate that the flyash surface has constituents and properties that promote the production of chlorinated dioxins from chlorinated phenols and support the catalysed surface reaction mechanism previously proposed. Remediation. https://www.sciencedirect.com/science/article/pii/S0301479718307473 Abstract Rapid urbanization and industrialization of anthropogenic activities have exerted immense pressure on the environment. Polyhalogenated organic compounds, especially dioxins and furans are regarded as ubiquitously persistent environmental pollutants in the ecosystem. The recalcitrant nature of dioxins and furans induce toxicity in both humans and wildlife. Dioxins and furans are generated by defective technological chemical processes that occur during the manufacture of herbicides and pesticides, use of fertilizers, bleaching of paper and wood pulp and incomplete combustion process. However, incineration and incomplete combustion of solid waste are the main cause for the discharge of dioxins and furans to the environment. During incineration and incomplete combustion, noxious flue gas and ashes are released into the atmosphere and contaminate the soil and water systems; thereby affecting the ecology. According to World Health Organization fact sheet 2016, more than 90% of human exposure to dioxins is through the food chain, especially from dairy products, seafood and meat. These pollutants are mutagenic, carcinogenic, immunotoxic and teratogenic for lower and higher forms of life i.e. microorganisms to humans. This review describes the sources of dioxins and furans pollution, hazardous effects on the ecosystem and recent techniques to minimize and treat dioxins and furans contaminants in the environment. This paper also previews the significance of conventional and latest remediation techniques prevailing around the globe for treating dioxins and furans entry into the ecosystem.

Do Cell Phones Cause Cancer. Evidence Suggests there is a “high probability” that radiofrequency radiation emitted by cellphones causes gliomas and acoustic neuromas, two types of brain tumors..

Moskowitz: Cellphone radiation is harmful, but few want to believe it By Anne Brice, Berkeley News| JULY 1, 2021. jjyrkkanen76@outlook.com This agrees with conclusions reached in 1990 by me, 2209 by others and again in 2021. Brain cancer a high pr9obability. The vast majority of American adults — 97% — own a cellphone of some kind, according to the Pew Research Center. (Photo by Susanne Nilsson via Flickr) For more than a decade, Joel Moskowitz, a researcher in the School of Public Health at UC Berkeley and director of Berkeley’s Center for Family and Community Health, has been on a quest to prove that radiation from cellphones is unsafe. But, he said, most people don’t want to hear it. “People are addicted to their smartphones,” said Moskowitz. “We use them for everything now, and, in many ways, we need them to function in our daily lives. I think the idea that they’re potentially harming our health is too much for some people.” Since cellphones first came onto the market in 1983, they have gone from clunky devices with bad reception to today’s sleek, multifunction smartphones. And although cellphones are now used by nearly all American adults, considerable research suggests that long-term use poses health risks from the radiation they emit, said Moskowitz. portrait of joel moskowitz Joel Moskowitz is a researcher in the School of Public Health and director of the Center for Family and Community Health at UC Berkeley. (School of Public Health photo) “Cellphones, cell towers and other wireless devices are regulated by most governments,” said Moskowitz. “Our government, however, stopped funding research on the health effects of radiofrequency radiation in the 1990s.” Since then, he said, research has shown significant adverse biologic and health effects — including brain cancer — associated with the use of cellphones and other wireless devices. And now, he said, with the fifth generation of cellular technology, known as 5G, there is an even bigger reason for concern. Berkeley News spoke with Moskowitz about the health risks of cellphone radiation, why the topic is so controversial and what we can expect with the rollout of 5G. Berkeley News: I think we should address upfront is how controversial this research is. Some scientists have said that these findings are without basis and that there isn’t enough evidence that cellphone radiation is harmful to our health. How do you respond to that? Joel Moskowitz: Well, first of all, few scientists in this country can speak knowledgeably about the health effects of wireless technology. So, I’m not surprised that people are skeptical, but that doesn’t mean the findings aren’t valid. A big reason there isn’t more research about the health risks of radiofrequency radiation exposure is because the U.S. government stopped funding this research in the 1990s, with the exception of a $30 million rodent study published in 2018 by the National Institute of Environmental Health Sciences’ National Toxicology Program, which found “clear evidence” of carcinogenicity from cellphone radiation. In 1996, the Federal Communications Commission, or FCC, adopted exposure guidelines that limited the intensity of exposure to radiofrequency radiation. These guidelines were designed to prevent significant heating of tissue from short-term exposure to radiofrequency radiation, not to protect us from the effects of long-term exposure to low levels of modulated, or pulsed, radiofrequency radiation, which is produced by cellphones, cordless phones and other wireless devices, including Wi-Fi. Yet, the preponderance of research published since 1990 finds adverse biologic and health effects from long-term exposure to radiofrequency radiation, including DNA damage. More than 250 scientists, who have published over 2,000 papers and letters in professional journals on the biologic and health effects of non-ionizing electromagnetic fields produced by wireless devices, including cellphones, have signed the International EMF Scientist Appeal, which calls for health warnings and stronger exposure limits. So, there are many scientists who agree that this radiation is harmful to our health. I first heard you speak about the health risks of cellphone radiation at Berkeley in 2019, but you’ve been doing this research since 2009. What led you to pursue this research? I got into this field by accident, actually. During the past 40 years, the bulk of my research has been focused on tobacco-related disease prevention. I first became interested in cellphone radiation in 2008, when Dr. Seung-Kwon Myung, a physician scientist with the National Cancer Center of South Korea, came to spend a year at the Center for Family and Community Health. He was involved in our smoking cessation projects, and we worked with him and his colleagues on two reviews of the literature, one of which addressed the tumor risk from cellphone use. At that time, I was skeptical that cellphone radiation could be harmful. However, since I was dubious that cellphone radiation could cause cancer, I immersed myself in the literature regarding the biological effects of low-intensity microwave radiation, emitted by cellphones and other wireless devices. After reading many animal toxicology studies that found that this radiation could increase oxidative stress — free radicals, stress proteins and DNA damage — I became increasingly convinced that what we were observing in our review of human studies was indeed a real risk. While Myung and his colleagues were visiting the Center for Family and Community Health, you reviewed case-control studies examining the association between mobile phone use and tumor risk. What did you find? Our 2009 review, published in the Journal of Clinical Oncology, found that heavy cellphone use was associated with increased brain cancer incidence, especially in studies that used higher quality methods and studies that had no telecommunications industry funding. Last year, we updated our review, published in the International Journal of Environmental Research and Public Health, based on a meta-analysis of 46 case-control studies — twice as many studies as we used for our 2009 review — and obtained similar findings. Our main takeaway from the current review is that approximately 1,000 hours of lifetime cellphone use, or about 17 minutes per day over a 10-year period, is associated with a statistically significant 60% increase in brain cancer. Why did the government stop funding this kind of research? The telecommunications industry has almost complete control of the FCC, according to Captured Agency, a monograph written by journalist Norm Alster during his 2014-15 fellowship at Harvard University’s Center for Ethics. There’s a revolving door between the membership of the FCC and high-level people within the telecom industry that’s been going on for a couple of decades now. The industry spends about $100 million a year lobbying Congress. The CTIA, which is the major telecom lobbying group, spends $12.5 million per year on 70 lobbyists. According to one of their spokespersons, lobbyists meet roughly 500 times a year with the FCC to lobby on various issues. The industry as a whole spends $132 million a year on lobbying and provides $18 million in political contributions to members of Congress and others at the federal level. The telecom industry’s influence over the FCC, as you describe, reminds me of the tobacco industry and the advertising power it had in downplaying the risks of smoking cigarettes. Yes, there are strong parallels between what the telecom industry has done and what the tobacco industry has done, in terms of marketing and controlling messaging to the public. In the 1940s, tobacco companies hired doctors and dentists to endorse their products to reduce public health concerns about smoking risks. The CTIA currently uses a nuclear physicist from academia to assure policymakers that microwave radiation is safe. The telecom industry not only uses the tobacco industry playbook, it is more economically and politically powerful than Big Tobacco ever was. This year, the telecom industry will spend over $18 billion advertising cellular technology worldwide. You mentioned that cellphones and other wireless devices use modulated, or pulsed, radiofrequency radiation. Can you explain how cellphones and other wireless devices work, and how the radiation they emit is different from radiation from other household appliances, like a microwave? Basically, when you make a call, you’ve got a radio and a transmitter. It transmits a signal to the nearest cell tower. Each cell tower has a geographic cell, so to speak, in which it can communicate with cellphones within that geographic region or cell. Then, that cell tower communicates with a switching station, which then searches for whom you’re trying to call, and it connects through a copper cable or fiber optics or, in many cases, a wireless connection through microwave radiation with the wireless access point. Then, that access point either communicates directly through copper wires through a landline or, if you’re calling another cellphone, it will send a signal to a cell tower within the cell of the receiver and so forth. The difference is the kind of microwave radiation each device emits. With regard to cellphones and Wi-Fi and Bluetooth, there is an information-gathering component. The waves are modulated and pulsed in a very different manner than your microwave oven. What, specifically, are some of the health effects associated with long-term exposure to low-level modulated radiofrequency radiation emitted from wireless devices? Many biologists and electromagnetic field scientists believe the modulation of wireless devices makes the energy more biologically active, which interferes with our cellular mechanisms, opening up calcium channels, for example, and allowing calcium to flow into the cell and into the mitochondria within the cell, interfering with our natural cellular processes and leading to the creation of stress proteins and free radicals and, possibly, DNA damage. And, in other cases, it may lead to cell death. In 2001, based upon the biologic and human epidemiologic research, low-frequency fields were classified as “possibly carcinogenic” by the International Agency for Research on Cancer (IARC) of the World Health Organization. In 2011, the IARC classified radiofrequency radiation as “possibly carcinogenic to humans,” based upon studies of cellphone radiation and brain tumor risk in humans. Currently, we have considerably more evidence that would warrant a stronger classification. Most recently, on March 1, 2021, a report was released by the former director of the National Center for Environmental Health at the Centers for Disease Control and Prevention, which concluded that there is a “high probability” that radiofrequency radiation emitted by cellphones causes gliomas and acoustic neuromas, two types of brain tumors. Let’s talk about the fifth generation of cellphone technology, known as 5G, which is already available in limited areas across the U.S. What does this mean for cellphone users and what changes will come with it? For the first time, in addition to microwaves, this technology will employ millimeter waves, which are much higher frequency than the microwaves used by 3G and 4G. Millimeter waves can’t travel very far, and they’re blocked by fog or rain, trees and building materials, so the industry estimates that it’ll need 800,000 new cell antenna sites. Each of these sites may have cell antennas from various cellphone providers, and each of these antennas may have microarrays consisting of dozens or even perhaps hundreds of little antennas. In the next few years in the U.S., we will see deployed roughly 2.5 times more antenna sites than in current use unless wireless safety advocates and their representatives in Congress or the judicial system put a halt to this. How are millimeter waves different from microwaves, in terms of how they affect our bodies and the environment? Millimeter wave radiation is largely absorbed in the skin, the sweat glands, the peripheral nerves, the eyes and the testes, based upon the body of research that’s been done on millimeter waves. In addition, this radiation may cause hypersensitivity and biochemical alterations in the immune and circulatory systems — the heart, the liver, kidneys and brain. Millimeter waves can also harm insects and promote the growth of drug-resistant pathogens, so it’s likely to have some widespread environmental effects for the microenvironments around these cell antenna sites. What are some simple things that each of us can do to reduce the risk of harm from radiation from cellphones and other wireless devices? First, minimize your use of cellphones or cordless phones — use a landline whenever possible. If you do use a cellphone, turn off the Wi-Fi and Bluetooth if you’re not using them. However, when near a Wi-Fi router, you would be better off using your cellphone on Wi-Fi and turning off the cellular because this will likely result in less radiation exposure than using the cellular network. Second, distance is your friend. Keeping your cellphone 10 inches away from your body, as compared to one-tenth of an inch, results in a 10,000-fold reduction in exposure. So, keep your phone away from your head and body. Store your phone in a purse or backpack. If you have to put it in your pocket, put it on airplane mode. Text, use wired headphones or speakerphone for calls. Don’t sleep with it next to your head — turn it off or put it in another room. Third, use your phone only when the signal is strong. Cellphones are programmed to increase radiation when the signal is poor, that is when one or two bars are displayed on your phone. For example, don’t use your phone in an elevator or in a car, as metal structures interfere with the signal. Also, I encourage people to learn more about the 150-plus local groups affiliated with Americans for Responsible Technology, which are working to educate policymakers, urging them to adopt cell tower regulations and exposure limits that fully protect us and the environment from the harm caused by wireless radiation. For safety tips on how to reduce exposure to wireless radiation from the California Department of Public Health and other organizations, Moskowitz recommends readers visit his website, saferemr.com, Physicians for Safe Technology and the Environmental Health Trust.