Cesium therapy CURE for Cancer – page 3-3

### Dr. SARTORI Cesium therapy cure for Cancer: page 3/3 http://www.mwt.net/~drbrewer/highpH.htm



The following methods are effective with virtually no adverse effects:

– (a) Nutrition and lifestyle of longevity populations that consume foods rich in the nutrients that are the basis of the high pH therapy discussed in “Nutrients and Cancer”, supra, and where high doses of these nutrients, especially if applied I.V., are by far the most effective treatment of cancer.

Also, their low stress/high physical activity lifestyle is important in cancer prevention as is the ozone-rich air in the high altitudes in which they live.

See “Cesium Therapy in Cancer Patients”, supra, as well as the Chapter “Ozone and Cancer” in the author’s book on “Ozone”, and his forthcoming book “NO More Cancers”.

– (b) Herbal treatments of cancer which were used worldwide since time immemorial including: Shark cartilage, Resistocell®, the thymus preparations Thymex L® and TFZ-Thymomodulin®, colostrum-derived transfer factor (TF) according to H. Hugh Fudenberg, Dr. Nieper¹s natural anticancer substances,
and herbal cancer treatments such as compounded Hoksey [Trifolium pratense, Rhammus cathartica, Berberis vulgaris, Arctium lappa, Stillingia sylvatica, Rhammus purshiana or Cascara amarga (Sweetia panamensis), Glycyrrhiza glabra, Zanthoxylum clava-herculis], compounded Echinacea [Echinacea spp, Ceanothus americanus, Baptisia tinctoria, Thuja occidentalis, Stillingia sylvatica, Iris versicolor, Zanthoxylum clava-herculis], Folia Thujae occidentalis (fresh),
Radix Astragali membranacei (Huáng Qí), Radix Rumicis crispi (fresh), and Renèe Caisse’s Essiac compound [Rumex acetosella, Arctium lappa (fresh root), Ulmus rubra, Rheum palmatum (root), etc.], PDR Cancer Formula [Larrea divaricata (folia), Sanguinaria canadensis (radix), Trifolium pratense (flores), Arcticum lappa (radix); Echinacea purpurea (radix), Hydrastis canadensis (radix); Symphytum officinale (folia),
Eleutherococcus senticosus (radix; eventually folia, radix, and flores), Chelidonium maius, combined with Artemisia absinthium, Yucca spp, and Commiphora molmol (gum), C. abyssinica (myrrh), or C. opobalsamum (bdellium-oleoresin)], Laetrile® et al. mandelonitriles,
immunostimulating mushroom extracts from Grifola frondosa (maitake), Ganoderma lucidum (reishi), and Lentinus edodes (shiitake), combined with herbs for specific cancers; e.g., herba Hedyotis diffusae (bái huo shé coo) combined with herba Scutellariae barbatae (bàn zho lían) for stomach, esophageal, & colon cancers , & the latter alone for lung cancers, & tuber Dioscoreae bulbiferae (huáng yào zo) for thyroid cancer & endemic goiter, and, especially, Haelan 851® Platinum Formula and Nature’s Blessing.

– (c) Oxidative Cancer Therapies are effective since the anaerobic cancer cells are highly sensitive to oxidants/electron donors. The most powerful of the naturally occurring electron donors is ozone that is found in clinically significant concentrations in the air in altitudes above 1800 m (6000 ft) and where cancer is virtually nonexistent in people living above 3000 m (10,000 ft).

The most effective herbal electron donors that restore the body to an alkaline balance can be found in plants containing high amounts of germanium (Ge), an ampholyte with four unstable electrons.

Medicinal plants that reputedly have anticancer activity and that contain high amounts of Ge include shelf fungus (Trametes cinnabarina; 800-2000 ppm), Ginseng (Panax ginseng; 250-350 Korean
Based on this concept, Kazuhiko Asai synthesized numerous non-toxic Ge compounds, most notably, propagermanium or biscarboxyethyl Ge sesquioxide [O3(Ge.CH2.CH2.COOH)2], which has been found effective in the prevention and treatment of numerous cancers and their metastases including cancers of the lungs, prostate, breast, liver, kidney, brain tumors, lymphomas and leukemias, and sarcomas such as chondro- and osteosarcomas. The recommended dosage for prevention is 100 to 200 mg/day and for treatment 1000 to 4000 mg/day for a 60 kg patient. Except for a Herxheimer-type “healing crisis” reaction, no other adverse effects have been observed with this compound. If no effect is seen, the treatment should be discontinued after 60 days.

– (d) Medical Ozone is the most powerful oxidative therapy, used in cancer treatment since the early 1920s, and where the DIRECT I.V. O3 Application has the following advantages:

= (1) EFFECTIVENESS of O3 in the treatment of all cancers, including leukemia, lymphomas and sarcomas. Direct I.V. O3 is particularly effective for lung cancers.

= (2) Consistently better results compared with the LAHT. Direct I.V. application produces much faster results and requires fewer applications than LAHT. This is particularly apparent in patients with lung cancer & sarcoids, allergies, & AIDS.

= (3) Prompt elimination of any allergic component contributing to cancer formation, e.g., by increasing the oxygen diffusion distance. This direct I.V. O3 effect is much more consistent than with LAHT. The same applies to removal of viruses, bacteria, and fungi that may be adjunctive cancer factors. Direct I.V. O3 consistently removes unwanted antibodies from the bloodstream, and seroconversions from HIV positive to HIV negative have been observed after only three to four consecutive administrations at the recommended dosage if patients are adequately supplemented, particularly with Zn, Se, vitamins A&E, & o-carotene.

= (4) Clean application of the ozone with simple syringes without the requirement of using disposable AHT bottles and other equipment that could be contaminated with blood-borne infectious agents, particularly, hepatitis C and B virus (HCV and HBV), syphilis-treponema (T. pallidum), Babesia spp (Babesiosis), Plasmodium spp (Malaria), Trypanosoma spp (Trypanosomiasis), cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV), human T-cell leukemia virus 1 & 2 (HTLV-1 & 2), the orbivirus of Colorado Tick Fever, etc.

= (5) Precise dosage since there is no reaction with the vitamin C that most German researchers suggest be added to the large autohemotransfusion (LAHT).

= (6) Homeopathic effect of direct I.V.ozone : The direct I.V. application of ozone (as contrasted to the LAHT) in a dosage of at least 0.1 mg/kg has a unique homeopathic effect that is not observed (and/or has never been described) with the LAHT. When ozone is injected into the bloodstream, it immediately starts to react with any available type of oxidizable substrate, most notably, the lipids of the cell membrane. Lipid peroxidation products of ozone include alkoxyl and peroxyl radicals, polyunsaturated fatty acid (PUFA) hydroxyperoxides, PUFA alcoxyl and peroxyl radicals, singlet oxygen, hydrogen peroxide (“peroxide burst”, the mechanism of killing viruses, bacteria and fungi of macrophages, microphages, and blood platelets), ozonides, carbonyls, alkanes and alkenes.

If all the different reaction products are taken into consideration, there may be perhaps 10,000 or more different oxidized species in minute (“homeopathic”) amounts, formed under conditions of considerable turbulence (simulating homeopathic “succussion”, or the vigorous shaking used in classic homeopathy to “potentiate” the effect of the remedy). This brings about a “healing crisis” that simulates milder versions of any hidden but still significant disease processes, that have not been completely resolved, including allergies, old drug toxicities, environmental pollution, old viral, bacterial or fungal infections, even physical traumas, migraines, and other conditions. After the “healing crisis” is brought about by the ozone administration, these conditions are resolved (analogous to the mechanism of action of homeopathic remedies) and people reach a new level of wellbeing that was unattainable before.

Particularly impressive is this effect in all chronic allergies, asthma, hay fever, “brain allergies”, and in chronic fatigue syndrome, as well as in all types of substance abuse & addiction including nicotine, alcohol, opiates, cocaine, etc

= (7) Direct IV Ozone oxidatively detoxifies any drugs or other toxic substances that have invariably accumulated in the bodies of patients with degenerative disease, especially cancer. This minimizes long-term detrimental effects and prevents late toxicity such as cardiac failure and death from doxorubicin or daunorubicin, permanent sterility from alkylating agents such as cyclophosphamide, melphalan, ifosfamide, etc., pulmonary fibrosis after bleomycin & nitrosureas such as carmustine & lomustine, and the myelosuppression seen after vitually all antineoplastic drugs, as well as carcinogenic environmental toxins such as dioxins, paraquat, polycyclic aromatic hydrocarbons, & other (non-/)halogenated aliphatic/aromatic/polycyclic hydrocarbons found in the air, water, or food taken in.

= (8) Hyperthermia effect of direct IV ozone is observed in most patients, especially the ones with extensive tumors and/or significant (concomitant) infections. The effectiveness of hyperthermia or fever in reversing malignancies was known since antiquity. Note that externally induced hyperthermia including immersion of the body in the hot healing waters of balneological cancer resorts, sitting in a sauna [especially, an infrared sauna] or steam bath, was used since antiquity against cancers [=.modern ways] and [Aquasizer baths with ultrapure ozonated water], or simply wrapping oneself in [space] blankets with a hot water bottle. The total body hyperthermia combined with potassium and glucose I.V. was developed in the 1940s by the late Professor Dr. med. Manfred von Ardenne in Dresden, Germany as his very successful low-pH therapy of cancer. This therapy was then superseded by the LSU (now ULS) ENHANCED HIGH-pH THERAPY of CANCER since the mid-1970s.


The “State of the Art” of Conventional Cancer Therapy

As stated previously in “Cesium and Cancer”, “(conventional) [t]reatment modalities of cancer include surgery, radiation and chemotherapy. In those cases where surgery was successful the body’s own immune system was able to counteract the reduced amount of tumor tissue. Surgery is likely to produce metastasis without stimulation of the immune system. Radiation may cause damages to the organism, e.g., carcinogenicity of x-rays and other radiations, and their depression of the immune system is well known. Prolonged chemotherapy may cause severe to lethal side effect in some instances, and the use of hormones and interferon are useful only for very few cases of cancer. Conventional treatments of cancer have produced 5-year survival rates which do not reflect the inexorable gradual deterioration of the cancer patients, no their suffering from various treatment-related adverse reactions, and where chemotherapy of, e.g., breast cancer may shorten the life by 18 to 36 months v. no treatments at all.”

Adverse Effects of Cancer Surgery may arise as anesthetic “accidents” and deaths, complications during surgery, & longterm surgical “aftereffects”.

– (1) Anesthesia: Over one half of all deaths attributed to anesthesia were caused by excessive blood loss during surgery; the remainder was from aspiration, overdose/misuse of anesthetics, & faulty technique. Brain damage from anesthesia was attributed in about 50% to faulty technique.
Other longterm effects of anesthesia include lasting immunodepression.

– (2) Surgery: Besides excessive blood loss and tissue trauma that is often unavoidable even for the most skilled surgeon, cancer surgery, in virtually all cases leads to dissemination of cancer cells and immunodepression. If there is enough immune function, the body may be ably to recognize and eliminate the spread cancer cells. Failure of tumor recognition, most prevalent in blood type A & AB, may lead to extensive metastasis.

– (3) Longterm Aftereffects: Lung surgery & massive abdominal resections may leave patients so crippled that they lose their will to live.
The same applies to many patients with colostomies, paralysis, or brain damage, and children who suffer an amputation of a limb or other severe mutilations.
Few surgeons are aware of the fact that there is a clinically significant immunodepression after almost any, but especially after (ultra)radical cancer surgery [less prevalent in the U.S. since about 2000](while radiologists are much more aware of the similar one after radiation), and which is manifested by a deficient antibody response to tumor & other antigens, cellular immunodeficiency with recurrent infections that, if severe, may include opportunistic pathogens, and phagocytic dysfunction (from operative stress) that interferes with removal of (pre)cancerous cells and contributes to bacterial/fungal infections.

Adverse Effects from Radiation include acute radiation syndrome, the hemopoietic, gastrointestinal, & CNS syndromes, & pneumonitis & pericarditis based on the location of the radiation, and late effects.

= (1) Acute Radiation Syndrome is characterized by nausea, vomiting, fatigue, loss of appetite & general malaise that may last for 48 to 72 hours [less prevalent in the U.S., as is (4), since about 2000].

= (2) Chest irradiation may cause granulocytopenia & thrombopenia from bone marrow depression, as well as radiation pneumonitis (insidious onset, cough, dyspnea, cyanosis, & fever 6-12 weeks after radiotherapy) & pericarditis.

= (3) Abdominal irradiation may cause profuse (& later chronic) diarrhea (unresponsive to conventional therapy), nausea, vomiting, lymphocyte depression, severe gastrointestinal upset, after a latency of 1 to 2 weeks bloody diarrhea & hematuria, and fistulas as late complications.

= (4) Cranial irradiation may cause after immediate nausea & vomiting, hypotension, apathy, ataxia, convulsions & coma, & delayed necrosis of the brain manifesting as headaches & a variety of neurological symptoms.

= (5) Late Effects: Inductions of secondary cancers of almost all types, as well as of leukemias & lymphomas, and where the female breast and the thyroid appear to be especially radiosensitive, and immunodepression worse than after surgery [see supra], especially, in addition, chronic depletion of lymphocytes, pancytopenia (especially if the bone marrow had been irradiated), & severe phagocytic dysfunction.


Of the about 75 presently used “anti-cancer” drugs, NONE has been proven effective, singly or in combinations, in properly controlled, let alone, double blind, clinical trials. On the contrary, since about 1975 to the present [2004], careful analysis of the results of cancer chemotherapy by Arlin J. Brown proved that these anti-cancer drugs are the MAJOR CAUSE of DEATH of cancer patients. Adverse effects of these drugs not only caused a severe life quality deterioration but also, in most cases, actually SHORTENED the life expectancy as compared to matched untreated controls.

The following gives some ideas about acute & delayed toxicity of these drugs, & where dose-limiting toxicity is listed in bold. Note that 35 pages, mostly tables, in “Ellenhorn’s Medical Toxicology”, 2d ed., Williams & Wilkins, Baltimore, 1997, are devoted to “Cancer Chemotherapeutic Agents/Cytotoxic Drugs”.

– (a) Acute Toxicity: Nausea & vomiting is found with almost all, except, perhaps, with aminoglutethimide, cladribine, GaNO3, gemcitabine, goserelin, the interferons, leuprolide, paxclitacel, tretinoin, & vincristine, & which is dose-limiting, e.g., with mechlorethamine (nitrogen mustard).

Anaphylaxis & other allergic reactions (A&A) may be encountered with many oft these drugs, e.g., amsocrine, asparaginase & pegaspargase, bleomycin, cisplatin, cytarabine (& acute respiratory distress), dacarbacine, dactinomycin, daunorubicin & doxorubicin, etoposide, fluorouracil (5-FU), methotrexate, paxclitel, etc.

Aldesleukin (IL-2): in addition (+), causes fever; fluid retention; hypotension; respiratory distress; rash, anemia, thrombopenia; diarrhea; erythema nodosum; neutrophil chemotactic defects, etc.

Daunorubicin & doxorubicin: (+), extravasation necrosis (EVN); acute cardiac toxicity (hours to days after) with EKG- changes including supraventricular arrhythmias, heart block, & ventricular tachycardia, major drop in ejection fraction, congestive heart failure (CHF), pericardial effusions (myocarditis-pericardiditis syndrome), GI toxicity, etc.

Ifosfamide: (+), cardiac toxicity; nephrotoxicity; confusion; metabolic acidosis & renal (de Toni-)Fanconi syndrome (proximal renal tubule dysfynction with hyperaminoaciduria, glycosuria, hyperphosphaturia, bicarbonate & water loss), etc.

Methotrexate: (+) hepatic necrosis; fever; diarrhea, etc.

Paclitaxel: A&A, dyspnea, hypotension, angioedema, urticaria, etc.

Asparaginase & pegaspargase: A&A, hypersensitivity; fever, chills; headache; abdominal pain; hyperglycemia leading to coma,etc.

Tretinoin: headache; xerosis; “retinoic acid syndrome” (i.e., fever, dyspnea, pulmonary infiltrates, pleural effusions, peripheral edema, hypotension); arthralgias, myalgias, etc.

– (b) Delayed Toxicity: Almost all nonhormonal anticancer drugs show dose-limiting (1) bone marrow depression or (2) delayed leukopenia & thrombopenia [the latter especially in carmustine, chlorozotocin, lomustine, et al.], as well as cutaneous reactions (sometimes severe), hyperpigmentation, & ocular toxicity, alopecia (which causes significant patient distress especially in women), & PERMANENT sterility after alkylating agents, e.g., cyclophosphamide, ifosphamide, & melphalan.

# Other dose-limiting toxicities include:

– (1) Pneumonitis & pulmonary fibrosis : bleomycin, busulfan, methotrexate, carmustine & lomustine, etc.

– (2) Renal damage: cisplatin, streptozocin, etc.

– (3) Stomatitis & oral ulcerations: dactinomycin, etc.; both oral & GI ulcerations: floxuridine, fluorouracil (5-FU), methotrexate, etc.

– (4) Cardiotoxicity (cumulative, dose-dependent cardiomyopathy/CHF; may be delayed for years): dauno- & doxorubicin, etc.

– (5) Hypophosphatemia: GaNO3

– (6) Hemorrhagic cystitis: ifosfamide, less in cyclophosphamide, etc

– (7) Teratogenicity; cheilitis: isotretinoin1* & tretinoin2*; & where 1*&2* cause rashes; pseudotumor cerebri; hypertriglyceridemia, & 1*, (+), causes anorexia; xerostomia, xerophthalmia & conjunctivitis; bone & joint pain; & 2*, (+), causes thrombophlebitis; & leukocytosis; whereas acute toxicity of vit. A (retinol & retinyl esters) can be almost completely avoided (up to 3 MU/day x 30 days) with concomitant vit. E (e.g., mixed tocopherols).

– (8) CNS depression: mitotane

– (9) Hemorrhagic diathesis: plicamycin

– (10) Peripheral neuropathy: vincristine

– (11) Mucositis: dauno- & doxorubicin, trimetrexate



Most naturally occurring dietary carcinogens are either “natural pesticides”(protecting plants against fungi, insects, & animal predators) or mycotoxins (metabolites produced by molds in food).

– (a) Natural Pesticides have been found carcinogenic if given in high doses to animals though there is no evidence of carcinogenicity in humans; allyl isothiocyanate ; in cabbage, cauliflower, Brussels sprouts, mustard, & horseradish is, in fact, clearly anti-carcinogenic. There is no evidence for human carcinogenicity of caffeic acid occurs in apples, pears, cherries, carrots, celery, lettuce, potatoes, endive, grapes, eggplant, thyme, basil, dill, caraway, rosemary, tarragon, & coffee beans,; of safrole in nutmeg, mace, pepper, cinnamon, natural root beer; estragole in basil, fennel, & tarragon; carvacrol in marjoram; furocoumarins in lime, citrus oils, carrots, celery, parsley, & parsnips; nor of pyrrolizidines in comfrey tea. The hepatic carcinogenicity of hydrazine, in mushrooms is linked to the hypo-methylation of organ DNA that occurs only in folic acid deficiency.
Note though that hydrazine overdosage (if used as “anticancer agent”) leads to ataxia, lateral nystagmus, loss of vibration sense, & seizures, & it is also hepatotoxic.

– (b) Mycotoxins proven highly carcinogenic in humans are aflatoxin B1 (AFB1) & natural mixtures of aflatoxins (B1, B2, G1, M1, M2, etc., & which are also mutagenic, teratogenic, & immunodepressive), as well as sterigmatocystin, while griseofulvin (antifungal) is moderately CAgenic.
Fumonisins and ochratoxin A are possible human carcinogens. Citrinin, patulin, penicillic acid, & zearalenone are carcinogenic for animals.

– (1) Aflatoxins, produced by Aspergillus parasiticus & A. flavus, occur in peanuts, maize, cotton seed, rye, barley, food grains, etc. Fowl & other farm animals fed infected ground nut meal may die of aflatoxicosis.
Aflatoxins cause liver & gallbladder cancers , & may increase lung cancer incidence via the AFB1-2,3-epoxide that forms the AFB1-N7-Gua adduct with the guanine of the DNA (which is also transferred transplacentally suggesting initiation of hepatocellular carcinoma in utero).
Aflatoxins also cause cirrhosis of the liver, including Indian childhood cirrhosis, acute hepatic failure & encephalopathy, Reye syndrome (acute severe encephalopathy with hepatic dysfunction in children after viral infection (influenza/varicella virus) treated with aspirin; also recurrent vomiting, elevated transaminases & ammonia, prolonged prothrombin time, fatty hepatomegaly; fever, diarrhea, abdominal pain, anorexia; followed by encephalopathy with acute brain swelling, coma within 24 – 48 hours, seizures, decerebrate rigidity &, eventually, death from acute hepatic & renal failure), & kwashiorkor (where aflatoxins contribute to etiology, increase childhood susceptibility to infections/parasitosis & cancers, retarded growth chronic diarrhea, anemia, hypalbuminemia, etc. primarily from protein, et al., malnutrition). Note that aflatoxin-contaminated heroin may contribute to the suppression of cell-mediated immunity (i.e., resulting from activation of T- lymphocytes) seen in AIDS patients.

– (2) Sterigmatocystin, from A. versicolor/flavus/ruber/luteum in wheat, peanuts, and rice, is highly carcinogenic in animals.

– (3) Fumosinins (esp. B1), in maize, are carcinogenic in rodents (liver & kidney cancers) & have been linked to esophageal cancer in humans.

– (4) Ochratoxin, from A. ochraceus, P. veridatum/cyclopium in wheat, oats, rice, & green coffee beans, has been implicated in renal adenomas & Balkan nephropathy.

– (5) Zearalenone, from Fusarium spp. in maize, wheat, sorghum, & feed grains, has been implicated in cervical cancer & premature thelarche.

– (6) T-2 toxin, in barley, maize, safflower seeds, & cereals, may contribute to pellagra (primarily caused by failure to convert tryptophan to niacin or niacin deficiency & characterized by dermatitis, mucositis, diarrhea, & psychic disturbances including depression, irritability, anxiety, confusion, disorientation, delusions, & hallucinations).


Food preparation & preservation are major sources of dietary carcinogens, including heterocyclic aromatic amines (HAAs), formed during frying, broiling, & grilling of high-protein foods and more prevalent in welldone meats; polycyclic aromatic hydrocarbons (PAHs), formed during broiling & smoking food, paticularly ground beef and steaks, less in pork & chicken; & N-nitroso compounds (NOCs), formed in smoked, salted, & pickled foods cured with nitrate or nitrite. Note that NOCs are also formed in the stomach from nitrites & amines in the diet. Acrolein, a decomposition product of glycerin from overheating fats, has been discussed in “Nutrients in Cancer”, supra [p. 9].

– (a) Heterocyclic Aromatic Amines (HAAs)
HAAs are potent mutagens & animal carcinogens causing cancers of the liver, colon, mammary gland, skin, prostate, lymphoid tissue, oral cavity, lung, etc. Of 20-some HAAs, 4 are possible human carcinogens, including 2 amino 3 methylimidazo [4,5-f] quinoline (IQ); 2 amino 3,4 dimethylimidazo[4,5-f]quinoline (MeIQ); 2-amino-3,8-dimethylimidazo [4,5-f] quinoxaline (8-MeIQx); and 2 amino 1 methyl 6 phenylimidazo[4.5-b] pyridine (PhIP). HAA-DNA form major adducts with C8, & IQ & MeIQx form minor adducts at N2 of guanine, and where the metabolic activation appear to occur via N-oxidation & O- acetylation to form N-acetoxy arylamines that bind to DNA, & where rapid oxidizers & acetylators may be at geater cancer risk.

– (b) Polycyclic Aromatic Hydrocarbons (PAHs), particularly benzo[a]- pyrene, less benzo[a]anthracene, dibenzo [a,h]pyrene, and chrysene, are animal carcinogens. There seems to be a correlation between PAH-DNA adducts & ras oncogene mutations & that the hGSTPI gene is an important factor in susceptibility to PAH-related cancers.

– (c) N-Nitroso Compounds (NOCs) are carcinogenic in animals, including primates, after oral ingestion. They may be a significant risk factor for human cancers of the stomach, esophagus, colon & rectum, nasopharynx, urinary tract, & liver. Note that ascorbic acid, tocopherols, retinoids,phenolic & sulfhydryl compounds, orange peel, and & other nutrients & specific foods mentioned in “Nutrients and Cancer”, supra, may inhibit the formation of endogenous NOCs.

# C. SYNTHETIC DIETARY CARCINOGEN (see also p.599 of “Cancer”, 6th ed., by DeVita, Hellman, & Rosenberg, Lippincott, Philadelphia, 2002]

– (a) Direct/Intentional Synthetic Additives include i.a., antioxidants, colorants, flavor ingredients, artificial sweeteners, solvents, & humectants.

– (b) Indirect/Unintentional Synthetic Additives include pesticides, solvents, and packaging-derived chemicals. These chemicals, which number more than 2000, enter the food supply during production, processing, packaging, and storage from a variety of sources. Of these, PESTICIDES are of major concern since most, if not all, pesticides have human toxicity potential, including carcinogenicity. Of these, arsenicals, benzal chloride, & fluoride insecticides are highly carcinogenic, while amitrole, benzotrichloride, carbon tetrachloride, chlorophenols, p-dichlorobenzene, ethylene dibromide & thiourea, formaldehyde, phenoxy acids, 2,3,7,8-tetrachlorodibenzo-p-dioxin, & 2,4,6-trichlorophenol are moderately CAgenic in humans, and where, because of bioaccumulation, the cancer & other longterm health risks from pesticides increase with repeated exposure over many years.[50 pages in “Ellenhorn’s Medical Toxicology”,2d ed., 1997, deal with “Pesticides”].
Note that the most effective insecticide, DDT (p,p’-dichlorodiphenyltrichloroethane, now: chlorphenotane), is anticarcinogenic & (properly used) virtually non-toxic to humans. Its ban in 1972, since it almost eradicated Anopheles spp., caused excess deaths from malaria alone of >90 million people by 2004.

Of packaging materials, vinyl chloride, is a human carcinogen, and several phthalate ester plasticizers (especially DEHP & its metabolite MEHP), are potential carcinogens. Note that extensive use of DEHPplasticized PVC blood tubing caused necrotizing dermatitis & plasticizerinduced hepatitis, & testicular atrophy with sterility in dialysis patients, & inhalation of DEHP & MEHP causes bronchial asthma; NBBS (in plastic resins & fungicides) may pose risk of amyotrophic lateral sclerosis,

– (c) Chemical Contamination of Water with carcinogens, principally, trihalomethanes (CHCl3, CHCI2Br, etc.), , which are disinfection by-products in public water supplies which do not occur with ozonation, industrial solvents trichloro-ethane & -ethylene, tetra- & 1,2 dichloroethylene, as well as arsenic & asbestos, and pesticides in wellwater are major public health concerns. Fluoride is a carcinogen, is THE aging factor, >1 ppm in drinking water increases risk of osteoporotic hip fracture, & ingestion of >10 mg/kg of F- (in toothpaste) may be lethal.

## APPENDIX IV: LIST OF CESIUM & RUBIDIUM ARTICLES that appeared in Pharmacology, Biochemistry & Behavior, Vol. 21, Suppl. I, 1984

Alkali Metals: An Update. Pharmacol Biochem Behav. 1984; 21 Suppl 1:1-135.

# 1: Brewer AK.
The high pH therapy for cancer tests on mice and humans. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 1-5.

# 2: Sartori HE..Nutrients and cancer: an introduction to cesium therapy. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 7-10.

# 3: Sartori HE.. Cesium therapy in cancer patients. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 11-3.

# 4: Neulieb R. Effect of oral intake of cesium chloride: a single case report. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 15-6.

# 5: Pinsky C, Bose R..Pharmacological and toxicological investigations of cesium. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 17-23.

# 6: Tufte MJ, Tufte FW, Brewer AK.. The response of colon carcinoma in mice to cesium, zinc and vitamin A. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 25-6.

# 7: Messiha FS.. Biochemical aspects of cesium administration in tumor-bearing mice. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 27-30.

# 8: Messiha FS, Stocco DM.. Effect of cesium and potassium salts on survival of rats bearing Novikoff hepatoma. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 31-4.

# 9: Messiha FS.. Effect of cesium and ethanol on tumor bearing rats. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 35-40

# 10: Yung CY.. A synopsis on metals in medicine and psychiatry. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 41-7.

# 11: Malek-Ahmadi P, Williams JA.. Rubidium in psychiatry: research implications. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 49-50.

# 12: Yung CY.. A review of clinical trials of lithium in medicine. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 51-5. Review.

# 13: Yung CY.. A review of clinical trials of lithium in neurology. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 57-64. Review.

# 14: Paragas MG.. Lithium adverse reactions in psychiatric patients. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 65-9. Review.

# 15: Yung CY.. Neuropsychiatric manifestations of alkali metal deficiency and excess. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 71-5. Review.

# 16: Pannell KH, La Neave CK, Rico E, Arkles B.. Concerning the relative non-toxicity of silacrown ionophores. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 77-80.

# 17: Roberts LA.. Chronotropic effect of alkali metals on spontaneously beating right atria. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 81-5.

# 18: Messiha FS.. Lithium, rubidium and cesium: cerebral pharmacokinetics and alcohol interactions. Pharmacol Biochem Behav. 1984; 21 Suppl. 1: 87-92.

# 19: Messiha FS, McGrath J.. Modulation of nitrogen dioxide toxicity by lithium. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 93-7.

# 20: McGrath JJ.. The effects of carbon monoxide on the heart: an in vitro study. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 99-102.

# 21: McGrath JJ, Leviseur C.. Cardiorespiratory responses to intestinal injection of carbon monoxide. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 103-7.

# 22: Baudhuin MG, Jefferson JW, Greist JH.. The Lithium Information Center: an efficient information service. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 109-11.

# 23: Messiha FS.. Cesium: a bibliography update. Pharmacol Biochem Behav. 1984; 21 Suppl 1: 113-29.

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