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). 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