Vaccine Ingredients


IDENTIFICATION AND USE: Glutaraldehyde is a colorless liquid. It is registered for pesticide use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. It is used as algaecide, bactericide and fungicide. Glutaraldehyde is used as a tissue fixative in histology and electron and light microscopy, generally as a 1.5-6% aqueous solution. Glutaraldehyde is used, generally in conjunction with wetting agents, to control viruses and other micro-organisms in fish farming.

Glutaraldehyde based products are effective sterilant and disinfectants for medical devices that cannot be steam sterilized, are particularly heat-sensitive, for lensed instruments that are commonly subjected to high-level disinfection between patient uses. It is a colorless, oily liquid with a pungent odor. As a cold sterilizer, it is commonly used as a 2%-4% aqueous solution, and it is found in Ultizyme. Glutaraldehyde has also been used as a preservative in chemical products such as fabric softeners, antiperspirants and fixatives for biological specimens.”

Glutaraldehyde is allowed as a preservative in cosmetics in Europe at concentrations up to 0.1%. It is not allowed in aerosols and sprays. Glutaraldehyde is a biocide commonly used in a 2% concentration for cold sterilization of surgical and dental equipment. Biocides, such as glutaraldehyde, are added to eliminate bacterial growth in fracturing fluids.

HUMAN EXPOSURE AND TOXICITY: Exposure to concentrations < 1 ppm by inhalation or skin contact may cause irritation of the skin and/or mucous membranes. The critical effects of glutaraldehyde exposure are eye, skin, and respiratory irritation, skin sensitization and occupational asthma. Nose and throat irritation has been observed in humans at vapor concentrations below 0.2 ppm. Occupational asthma has also been reported in workers exposed to dilute solutions of glutaraldehyde.

Contact dermatitis and eye irritation have been reported in workers using glutaraldehyde solutions, usually 2% or higher. Skin sensitization has been confirmed in workers using dilute solutions.

Other symptoms that may be brought on by glutaraldehyde exposure include heart palpitations and tachycardia. The incidence of death and incidence of cancer deaths in 186 male employees at a glutaraldehyde production unit were compared to those of US white males and to 29,000 other chemical workers during the period 1959 – 1978. All subjects were observed for 10 yr. The number of deaths was less than expected, as was the incidence of cancer deaths.

ANIMAL STUDIES: Glutaraldehyde was corrosive to the skin and eyes of rabbits at high concentrations, with signs of skin irritation evident at 2%, and eye irritation at 0.2%. In an inhalation study where mice were exposed to glutaraldehyde at concentrations of 33 or 133 ppb for 24 hours, the animals exhibited panting and increased grooming, mice that inhaled the highest concentration developed toxic hepatitis.

Following a single whole-body inhalation exposure at 1 ppm for 1 day, rats and mice developed coagulation pathology of the upper respiratory tract squamous epithelium. After 4 days of such exposures, inflammatory granulocytic infiltrate into the squamous epithelium and lamina propria with thickened epithelium of the nasal lumen ensued. In those animals inhaling 0.5 or 1 ppm glutaraldehyde for four days, the nasal passages became obstructed with intraluminal debris; degenerative/hyperplastic erosions with epithelial abscesses extended as far as the nasopharyngeal meatus in the 1-ppm exposure group.

A study of male and female rats given glutaraldehyde in drinking water at concentrations of 0, 50, 250, or 100 ppm through two generations indicated a dose-related decrease in parental waterconsumption and body weight (attributed to adverse taste) and decrease in offspring (1000-ppm group) body weights. No adverse reproductive effects were observed. In other study, there was a significant dose-dependent reduction in the average of maternal body weight gain and a significant increase in the number of stunted (body weight) and malformed fetuses at the 5 mL/mg/day dose level.

Early mutagenicity studies were negative, but more recent studies have indicated that glutaraldehyde is mutagenic in vitro in bacterial assays and tests in mammalian cells. In vivo genotoxicity tests to date have proven negative. Groups of 50 male and 50 female rats and mice were exposed to glutaraldehyde vapor at concentrations of 0, 0.25, 0.50, or 0.75 (rats) and 0, 0.062, 0.12, or 0.25 ppm (mice) 6 hr/day, 5 days /week.

The incidences of non-neoplastic lesions of the nose were reported to be significantly increased in the 0.50 and 0.75-ppm exposed rats and in the 0.12 and 0.25-ppm exposed male and female mice.

ECOTOXICITY STUDIES: Available chronic toxicity data for glutaraldehyde indicate that continuous exposure results in measurable effects on cold-water fish at a concentration of 5.1 mg a.i./L. A second study on cold-water fish resulted in measurable effects at 2.5 mg a.i./L. Measurable effects on freshwater invertebrates were noted at concentrations of 8.5 mg/L product and 4.9 mg a.i./L.




IDENTIFICATION AND USE: Medium 199 was originally developed for nutritional studies of chick embryo fibroblasts. It has broad species applicability, particularly for cultivation of non-transformed cells. Medium 199 is widely used in virology, vaccine production, and in vitro cultivation of primary explants of mouse pancreatic epithelium, and rat lens tissues.

Medium 199 contains unique components, including adenine, adenosine, hypoxanthine, thymine, and additional vitamins. Medium 199 is available with Earle’s salts for use in a CO2 incubator, or with Hank’s salts for use without CO2.




IDENTIFICATION AND USE: Minimum Essential Medium (MEM), developed by Harry Eagle, is one of the most widely used of all synthetic cell culture media. Early attempts to cultivate normal mammalian fibroblasts and certain subtypes of HeLa cells revealed that they had specific nutritional requirements that could not be met by Eagle’s Basal Medium (BME). Subsequent studies using these and other cells in culture indicated that additions to BME could be made to aid growth of a wider variety of fastidious cells.

MEM, which incorporates these modifications, includes higher concentrations of amino acids so that the medium more closely approximates the protein composition of mammalian cells. MEM has been used for cultivation of a wide variety of cells grown in mono-layers.

Optional supplementation of non-essential amino acids to the formulations that incorporate either Hanks’ or Eagles’ salts has broadened the usefulness of this medium. The formulation has been further modified by optional elimination of calcium to permit the growth of cells in suspension.




IDENTIFICATION AND USE: the procedure involves the use of a variant and somewhat unstable strain of Clostridium Tetani and a culture medium containing a pancreatic digest of casein with additional cystine and tyrosine, beef heart infusion, glucose and inorganic salts. A high concentration of iron must be provided. The “modified” makes it more stable. Casein is a milk protein. Cystine and tyrosine are amino acids. Glucose is the sugar that cells burn. “Pancreatic digest” means that enzymes from the pancreas of an animal are used to break down the soup so the tetanus bacterium can eat it. A basic medium constituted as follows served this purpose: Pancreatic digest of casein, 150.0mg; glucose, 75.0mg; cysteine, 1.25mg; tyrosine, 2.5mg; NaCl, 25.0mg; Na2HPO4, 5.0mg; KH2PO4, 1.75mg; MgSO4.7H20, 0.5mg; reduced iron powder, 2.5 to 5.0mg; H2O to 10ml.




IDENTIFICATION AND USE: a simple chemically defined medium for the production of phase 1 Bordetella Pertussis described consisting of sodium glutamate, proline, cystine, salts, and growth factors, which is suitable for the large-scale production of phase 1 bordetella pertussis. The cultures were detoxified by the addition of 0.14% formalin. The acellular pertussis antigens (PT, FHA, and pertactin) are isolated from Bordetella pertussis culture grown in modified Stainer-Scholte liquid medium. PT and FHA are isolated from the fermentation broth; pertactin is extracted from the cells by heat treatment and flocculation. The antigens are purified in successive chromatographic and precipitation steps. PT is detoxified using glutaraldehyde and formaldehyde. FHA and pertactin are treated with formaldehyde. Each antigen is individually adsorbed onto aluminum hydroxide. Each 0.5-mL dose is formulated to contain 5 Lf of tetanus toxoid, 2.5 Lf of diphtheria toxoid, 8 mcg of inactivated PT, 8 mcg of FHA, and 2.5 mcg of pertactin (69 kiloDalton outer membrane protein). For more information on effects on the body see formaldehyde and glutaraldehyde.




IDENTIFICATION AND USE: only three vitamins (pantothenate, p-amino benzoic acid, nicotinic acid) and two amino acids (serine, glutamine) were required in the growth medium for Gluconobacter oxydans which allowed the concentration of yeast extract to be reduced to 5–10% of the previous concentration.

When compared with data from cultivations with complex media, the new medium gave a lower yield (about 0.02 g biomass per g glycerol) and comparable growth rate (0.24 to 0.38 h−1) but a higher productivity (10.3 g dihydroxyacetone/gh).

A semisynthetic medium, containing yeast extract as the only non defined component and glucose, glycerol, Tween 80 and mineral salts, has been developed to grow the strains of Propionibacterium acnes Beck 2037, Gerrath 2038 and Vogel 2039, at a rate comparable to that of complex media.

An average of 10(12) cells per 1 (equivalent to approximately 1.5 g/l dry weight) was usually achieved. These yields are appropriated for biochemical and immunological studies, e.g. cell wall preparation, polysaccharides isolation, etc. In this work, some properties of the cell walls (sugar and amino acid composition) and the antigenic polysaccharides (neutral and amino sugar components) are described.




IDENTIFICATION AND USE: Used in the management of porphyria attacks, particularly in acute intermittent porphyria. It may also be used for other conditions as determined by your doctor. Hemin is an enzyme inhibitor made from red blood cells. It works by correcting certain types of heme deficiency in the liver. Iron deficiency induces heme deficiency and anemia due to the lack of iron for ferrochelatase to incorporate into protoporphyrin IX. Iron deficiency is present in ∼ 2 billion women and children and causes oxidative damage and loss of function in mitochondria and mitochondrial DNA

HUMAN EXPOSURE AND TOXICITY: May cause mild fever; pain, redness, or swelling at the injection site. Seek medical attention right away if any of these severe side effects occur: Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); change in the amount of urine; unusual bleeding; unusual tiredness.

Hemin chloride, a heme oxygenase 1 inducer, is a porphyrin complex that is derived from erythrocytes. At a concentration of 20 mM Hemin chloride demonstrated the significance of heme in myotube maturation by increasing size, number, cross-striations, and contraction frequency and strength of myotubes.

The compound has been observed to induce cGMP formation through induction of guanylate cyclase. Hemin chloride has been noted to stimulate calcium-dependent K+ channels and modulate fluid transport and Na+ in the loop of Henle in rat studies. Hemin has also been documented to give rise to active chloride secretion in Caco-2 cells. In cadmium injured rat testes, hemin chloride demonstrated anti-apoptotic, anti-inflammatory and antioxidant properties. Derived from procine. Porcine: Having to do with swine. From the Latin “porcus” meaning “pig.” Historically, Porcine insulin is obtained from pig pancreas. A porcine skin graft is one in which pig skin is used, such as in surgical treatment of burns or other serious skin injuries.




IDENTIFICATION AND USE: used for treating a variety of conditions, including shock due to blood loss in the body, burns, low protein levels due to surgery or liver failure, and as an additional medicine in bypass surgery. It may be used for certain conditions as determined by your doctor. Human Albumin is a concentrate of plasma proteins from human blood. It works by increasing plasma volume or serum albumin levels.

Human Albumin is prepared from human pool plasma by alcoholic precipitation [12]. For pathogen inactivation albumin is pasteurized for at least 10 h at 60 °C (see also European Pharmacopoeia).

QUALITY CRITERIA: human albumin solutions for transfusion are obtained from human plasma proteins as sterile preparations which, according to the monograph ‘Human Albumin Solutions’ of the European Pharmacopoeia, must contain a minimum of 95% albumin. Aside from human albumin, preparations currently available have a sodium concentration between 87 and 160 mmol/l and a potassium concentration below 2 mmol/l. Because of variable electrolyte concentrations contained in albumin preparations, it is required to monitor the balance of water and electrolyte, especially when administering large amounts. Up to 3.2 g/l sodium octanoat and up to 4.29 g/l acetyltryptophan are added as stabilizers. All albumin preparations currently available contain less than 200 μg/l of aluminum.

Albumin solutions do not contain isoagglutinins or blood group substances and can thus be administered independent of the recipient’s blood group. They do not contain oxygen carriers, coagulation factors, or antibodies. Based on the manufacturing process and the pathogen inactivation involved, albumin preparations are considered to carry no risk of transmitting infections.

IMPROVING TRANSPORT CAPACITY FOR DRUGS: human albumin serves as a transport protein for many substances (e.g. bilirubin, drugs). It is doubtful whether in the case of hypoalbuminemia there may also be an increase in the ‘free’ unbound (biologically active) fraction of drugs (e.g. coumarin derivatives). Since an increase in the free fraction of a substance is most often followed by a more rapid metabolism or an increased elimination of this substance, no critical increase in the concentration of the free substance in plasma is to be anticipated in case of low levels of albumin. There is no risk of acute toxic effects resulting from hypoalbuminemia because of rapid migration of the unbound fraction of drugs from the intravascular to the extravascular space, so that a (low-level) balance is reached. In addition, apparently binding sites for drugs are lost in the production process of human albumin solutions. Administration of human albumin to improve the transport capacity for drugs is not recommended.

FREE RADICAL SCAVENGER AND FOR BINDING TOXIC SUBSTANCES: physiologically, albumin is assumed to serve as free radical scavenger and is able to bind toxic substances (e.g. free fatty acids). Therefore, albumin seems to be indicated in particular in patients with sepsis because toxic oxygen radicals play a role in pathogenesis and maintenance of sepsis. Allegedly albumin can also bind toxins in large-scale burns. Therefore, albumin solutions could have a beneficial effect in these patients. However, to date there are no confirmed factual data on the benefit of human albumin therapy regarding morbidity or mortality in humans. It is uncertain whether human albumin preparations currently commercially available have the same (radical scavenger) properties as natural albumin or whether they are altered by the manufacturing process.

ADVERSE REACTIONS: anaphylactoid reactions, fever, chills, rash, nausea, vomiting, tachycardia, hypotension.

DERMATOLOGIC SIDE EFFECTS: urticaria, skin rash, pruritus, edema, and erythema. Nervous system side effects have included headache, chills, and febrile reactions.


GASTROINTESTINAL SIDE EFFECTS: nausea, vomiting and increased salivation.





HUMAN FETAL TISSUE: some vaccines are grown in cell cultures that were originally obtained from two human fetuses. Two different strains of human diploid cell cultures made from fetuses have been used extensively for vaccine production for decades:

  • WI-38 HUMAN DIPLOID CELLS – Winstar Institute 38, human diploid lung fibroblasts derived from the lung tissues of a female fetus aborted because the family felt they had too many children in 1964 in the United States.
  • MRC-5 HUMAN DIPLOID CELLS – Medical Research Council 5 (cells containing two sets of chromosomes) derived from the normal lung tissues of a 14-week-old male fetus aborted for “psychiatric reasons” in 1966 in the United Kingdom.
  • IMR-90 and 91 HUMAN DIPLOID CELLS – Institute of Medical Research 90 and 91 Derived from lung tissue of a 16-week-old female Caucasian fetus. The cells have a virus susceptibility similar to WI-38 and MRC-5 cells.

WI-38 and MRC-5 have become the most used cell lines to make vaccinations. Labs currently use these 2 cell lines, as well as new sources (a.k.a new aborted infants) to create new vaccines.

DEOXYRIBONUCLEIC ACID (DNA): is a self-replicating material present in nearly all living organisms as the main constituent of chromosomes. It is the carrier of genetic information. DNA is harvested from aborted infants. It is used as an adjuvant in vaccines. In vaccines, 100,000,000 bits and strands of human DNA are allowed per dose.

ADVERSE REACTIONS: in a recent study, Dr. Helen Ratajczak, reports that about the same time the vaccine manufacturers took thimerosal out of most vaccines, they began making some vaccines using human tissue. Ratajczak says human tissue is currently used in 23 vaccines. She discusses the increase in autism incidences corresponding with the introduction of human DNA to MMR vaccine, and suggests the two could be linked. Ratajczak also says an additional increased spike in autism occurred in 1995 when chicken pox vaccine was grown in human fetal tissue. Dr. Helen Ratajczak explains that foreign DNA can cause brain damage, because it’s human DNA and the recipients are humans, there is homologous recombination. Homologous recombination is a form of genetic recombination in which two similar DNA strands exchange genetic material. That DNA is incorporated into the host DNA, and now it’s changed, altering itself and the body kills it. Where is this most expressed? The neurons of the brain. Now you have the body killing the brain cells and it is an ongoing inflammation. It doesn’t stop, it continues through the life of that individual.




IDENTIFICATION AND USE: Hydrolyzed Porcine Collagen refers to enzymatically or chemically processed collagen derived pig skin, and bone. It is water soluble and contains peptides like amino acids as well as glycine, proline, hydroxyproline, and glutamic acid. Hydrolyzed collagen is normally used to benefit nails and skin due to the presence of the amino acids. It is also used to regenerate cells for the body’s lean muscle mass, benefit arthritis, and even help the body burn off fat and enhance weight loss.

HUMAN EXPOSURE AND TOXICITY: There is no documented evidence of a deleterious nature to humans from the ingestion of collagen, other than a rare allergenic response, when the diet has provided an adequate amount of the amino acid tryptophan and is deficient in several others, and thus is of low nutritive value.

ANIMAL STUDIES: Collagen is used in various pharmaceutical formulations. The incidence of tumors in experimental animals (mice) injected subcutaneously with gelatin in various strength solutions, did not differ from that in untreated control animals.

ADVERSE EFFECTS: Hydrolyzed porcine collagen side effects from topical use may trigger dermatitis or inflammation of the skin. Initially, a mild rash may develop. Since dermatitis is an allergic reaction, the reaction may therefore depend on the person using the cream and doesn’t affect every user. Before taking any supplement orally, you should check with your physician for any allergies to animal products. While marine collagen is very much safe, people might have allergic reactions to animal or plant hydrolyzed collagen. Some hydrolyzed collagen supplements are now being made from chicken. While no studies yet show any bad effects from chicken based hydrolyzed collagen, other chicken based supplements aside from collagen have been known to cause mild cases of nausea, heartburn, diarrhea, constipation, drowsiness, skin reactions, and headache. No significant adverse findings other than rare hypersensitivity have been found in the examination of data from feeding and biochemical experiments.


  • Runny nose. Those who have collagen allergy can suffer from a runny nose after exposure or consumption of products that contain collagen
  • Hives. One of the most common reactions to collagen is hives
  • Diminished blood pressure level
  • Anaphylaxis




IDENTIFICATION AND USE: Insect cells (IC) and particularly lepidopteran cells are an attractive alternative to mammalian cells for biomanufacturing. Insect cell culture, coupled with the lytic expression capacity of baculovirus expression vector systems (BEVS), constitutes a powerful platform, IC-BEVS, for the abundant and versatile formation of heterologous gene products, including proteins, vaccines and vectors for gene therapy. Such products can be manufactured on a large scale thanks to the development of efficient and scalable production processes involving the integration of a cell growth stage and a stage of cell infection with the recombinant baculovirus vector.

Insect cells can produce multimeric proteins functionally equivalent to the natural ones and engineered vectors can be used for efficient expression. Insect cells can be cultivated easily in serum- and protein-free media. Insect cell culture is a common choice for heterologous protein expression. For large scale production or basic research, insect cells are able to express large quantities of protein with complex post-translational modifications. Sf9 (Cat. no. B825-01) and Sf21 (Cat. no. B821-01) cell lines are the traditional cell lines used with baculovirus and originated at the USDA Insect Pathology Laboratory. The cell lines are also suitable for use in the InsectSelect™ System. These two cell lines originated from the IPLBSF-21 cell line, derived from the pupal ovarian tissue of the fall armyworm, Spodoptera frugiperda (O’Reilly et al., 1992; Vaughn et al., 1977). When working with recombinant or wild-type viral stocks (e.g.,infecting cells), always maintain separate media bottles for cell culture and for virus work. Baculovirus particles can survive and be maintained in media at 4°C, and will contaminate your stock cultures if introduced to culture plates or flasks during passaging

COMMON PROBLEMS ASSOCIATED WITH INSECT CELL CULTURE: morphological changes in the cells or changes in the growth rate can indicate an underlying problem with the culture. Baculoviruses are arthropod‐specific, enveloped viruses with circular, supercoiled double‐stranded DNA genomes. They infect Lepidoptera (butterflies and moths), Hymenoptera (sawflies) and Diptera (mosquitoes). While many viruses are studied because of their damaging effects, the study of baculoviruses was stimulated by their potential utility to control insect pests. Later, the utility of baculovirus as gene expression vectors was evidenced and a new research area emerged. A major step forward was the development of bacmid technology (the construction of bacterial artificial chromosomes containing the genome of the baculovirus) which allows the manipulation of the baculovirus genome in bacteria. With this technology, foreign genes can be introduced into the bacmid by site‐directed recombination or by transposition.

HUMAN STUDIES: Baculoviruses have been used to explore fundamental questions in molecular biology such as the nature of programmed cell‐death. Moreover, the ability of baculoviruses to transduce mammalian cells led to the consideration of their use as gene therapy and vaccine vectors. Strategies for genetic engineering of baculoviruses have been developed to meet the requirements of new application areas, and the establishment of new genetic modification systems is still necessary when an unexplored experimental system is to be addressed.

A new vaccine for influenza has hit the market, and it is the first ever to contain genetically-modified (GM) proteins derived from insect cells. According to reports, the U.S. Food and Drug Administration (FDA) recently approved the vaccine, known as Flublok, which contains recombinant DNA technology and an insect virus known as baculovirus that is purported to help facilitate the more rapid production of vaccines.

According to Flublok’s package insert, the vaccine is trivalent, which means it contains GM proteins from three different flu strains. The vaccine’s manufacturer, Protein Sciences Corporation (PSC), explains that Flublok is produced by extracting cells from the fall armyworm, a type of caterpillar, and genetically altering them to produce large amounts of hemagglutinin, a flu virus protein that enables the flu virus itself to enter the body quickly. So rather than have to produce vaccines the “traditional” way using egg cultures, vaccine manufacturers will now have the ability to rapidly produce large batches of flu virus protein using GMOs, which is sure to increase profits for the vaccine industry.

ADVERSE EFFECTS: serious side effects, including the deadly nerve disease Guillain-Barre Syndrome (GSB), which is listed on the shot as a potential side effect. If Guillain-Barre Syndrome (GBS) has occurred within six weeks of receipt of a prior influenza vaccine, the decision to give Flublock should be based on careful consideration of the potential benefits and risks,” explains a section of the vaccine’s literature entitled “Warnings and Precautions.” Other potential side effects include allergic reactions, respiratory infections, headaches, fatigue, altered immunocompetence, rhinorrhea, and myalgia. According to clinical data provided by PSC in Flublok’s package insert, two study participants actually died during trials of the vaccine, but the company still insists Flublok is safe and effective, and that it is about 45 percent effective against all strains of influenza in circulation, rather than just one or two strains.




IDENTIFICATION AND USE: L-histidine is an essential amino acid that is required for the production of HISTAMINE. Histidine is a semi-essential amino acid (children should obtain it from food) needed in humans for growth and tissue repair, Histidine is important for maintenance of myelin sheaths that protect nerve cells and is metabolized to the neurotransmitter histamine. Histamines play many roles in immunity, gastric secretion, and sexual functions. Histidine is also required for blood cell manufacture and protects tissues against damage caused by radiation and heavy metals.

HUMAN STUDIES: Histidine is an alpha-amino acid with an imidazole functional group. It is one of the 22 proteinogenic amino acids. Histidine was first isolated by German physician Albrecht Kossel in 1896. Histidine is an essential amino acid in humans and other mammals. It was initially thought that it was only essential for infants, but longer-term studies established that it is also essential for adults. Infants four to six months old require 33mg/kg of histidine.

It is not clear how adults make small amounts of histidine, and dietary sources probably account for most of the histidine in the body. Histidine is a precursor for histamine and carnosine biosynthesis. Inborn errors of histidine metabolism exist and are marked by increased histidine levels in the blood. Elevated blood histidine is accompanied by a wide range of symptoms, from mental and physical retardation to poor intellectual functioning, emotional instability, tremor, ataxia and psychosis. Histidine and other imidazole compounds have anti-oxidant, anti-inflammatory and anti-secretory properties. The efficacy of L-histidine in protecting inflamed tissue is attributed to the capacity of the imidazole ring to scavenge reactive oxygen species (ROS) generated by cells during acute inflammatory response. Histidine, when administered in therapeutic quantities is able to inhibit cytokines and growth factors involved in cell and tissue damage.

Histidine in medical therapies has its most promising trials in rheumatoid arthritis where up to 4.5g daily have been used effectively in severely affected patients. Arthritis patients have been found to have low serum histidine levels, apparently because of very rapid removal of histidine from their blood. Other patients besides arthritis patients that have been found to be low in serum histidine are those with chronic renal failure. Urinary levels of histidine are reduced in pediatric patients with pneumonia. Asthma patients exhibit increased serum levels of histidine over normal controls. Serum histidine levels are lower and are negatively associated with inflammation and oxidative stress in obese women. Histidine supplementation has been shown to reduce insulin resistance, reduce BMI and fat mass and suppress inflammation and oxidative stress in obese women with metabolic syndrome. Histidine appears to suppress pro-inflammatory cytokine expression, possibly via the NF-κB pathway, in adipocytes. Low plasma concentrations of histidine are associated with protein-energy wasting, inflammation, oxidative stress, and greater mortality in chronic kidney disease patients. Histidine may have many other possible functions because it is the precursor of the ubiquitous neurohormone-neurotransmitter histamine. Histidine increases histamine in the blood and probably in the brain. Low blood histamine with low serum histidine occurs in rheumatoid arthritis patients. Low blood histamine also occurs in some manic, schizophrenic, high copper and hyperactive groups of psychiatric patients. Histidine is a useful therapy in all patients with low histamine levels.

ADVERSE EFFECTS: Histidine might be safe for most people. Doses of up to 4 grams per day have been used in research without causing noticeable side effects.

SPECIAL PRECAUTIONS AND WARNINGS: not enough is known about the use of histidine during pregnancy and breast-feeding. Stay on the safe side and avoid use.

FOLIC ACID DEFICIENCY: if you have this condition, don’t use histidine. It can cause an unwanted chemical called formiminoglutamic acid (FIGLU) to build up in the body. Formiminoglutamic acidemia (FIGLU) is an inherited condition in which the body is unable to break down and process certain building blocks of protein, called amino acids. Individuals with FIGLU are also unable to produce a specific form of the vitamin folate, which has many important functions in the body. There are two forms of FIGLU which are classified in terms of severity. Both are associated with varying degrees of physical and mental disability.




IDENTIFICATION AND USE: Lactalbumin Hydrolysate is a pancreatic digest of lactalbumin recommended for use in culture media for tissue culture, production of lactobacilli, virus, vaccines, fermentations and special diets. Additional uses include preparation of baculovirus medium and as an agar overlay for protein expression. Lactalbumin Hydrolysate (LAH) is a supplement utilized with Grace’s Insect Cell Culture Medium for Baculovirus protein expression systems to assist in increasing biomass production.





IDENTIFICATION AND USE: The sugar found in milk. Lactose is a large sugar molecule that is made up of two smaller sugar molecules, glucose and galactose. In order for lactose to be absorbed from the intestine and into the body, it must first be split into glucose and galactose. The glucose and galactose are then absorbed by the cells lining the small intestine. The enzyme that splits lactose into glucose and galactose is called lactase, and it is located on the surface of the cells lining the small intestine.

HUMAN STUDIES: Lactose intolerance is the inability to digest significant amounts of lactose, the predominant sugar of milk. This inability results from a shortage of the enzyme lactase, which is normally produced by the cells that line the small intestine. Lactase breaks down the lactose, milk sugar, into glucose and galactose that can then be absorbed into the bloodstream. When there is not enough lactase to digest the amount of lactose consumed, produce some uncomfortable symptoms. Some adults have low levels of lactase. This leads to lactose intolerance. The ingested lactose is not absorbed in the small intestine, but instead is fermented by bacteria in the large intestine, producing uncomfortable volumes of carbon dioxide gas. While not all persons deficient in lactase have symptoms, those who do are considered to be lactose intolerant.

ADVERSE REACTIONS: nausea, cramps, bloating, gas, and diarrhea, which begin about 30 minutes to 2 hours after eating or drinking foods containing lactose. The severity of symptoms varies depending on the amount of lactose each individual can tolerate. Lactose intolerance that occurs after age 21 (genetically-determined lactase deficiency usually occurs between ages 5-21) is rarely due to genetic lactase deficiency; it suggests another process is interfering with lactose digestion.




IDENTIFICATION AND USE: Lipids are molecules that contain hydrocarbons and make up the building blocks of the structure and function of living cells. Examples of lipids include fats, oils, waxes, certain vitamins, hormones and most of the non-protein membrane of cells.

Lipids are molecules that can be extracted from plants and animals using nonpolar solvents such as ether, chloroform and acetone. Fats (and the fatty acids from which they are made) belong to this group as do other steroids, phospholipids forming cell membrane components etc.

All Lipids are hydrophobic: that’s the one property they have in common. This group of molecules includes fats and oils, waxes, phospholipids, steroids (like cholesterol), and some other related compounds.




IDENTIFICATION AND USE: Mineral salts are necessary for the correct functioning of the human body. In particular, they are a source of cations, trace elements often present in very small quantities in the body, but which are essential to cell activity. They are involved in tissue formation (organs, muscles, etc.), hormone synthesis, protecting the body, enzyme systems, osmotic balance of body fluids

The body is not capable of synthesizing these minerals. The necessary intake is acquired naturally through the foods that we eat. If this does not happen (due to foods lacking in trace elements, deficiency or poor assimilation) medicinal intake is effective for avoiding some complications or illnesses.





IDENTIFICATION AND USE: monkey kidney cells come from African Green monkeys. They are known to contain SV40 (simian virus 40) which is a monkey virus that grows in monkey tissue (particularly kidneys). In two separate studies, there were reports of SV40 in non-Hodgkin’s lymphoma tumors. It is used in polio and rotavirus vaccines. The Vero epithelial cell line was established in 1962 by Y. Yasumura and Y. Kawakita at the Chiba University in Chiba, Japan. The tissue from which the line was derived was obtained from the kidney of a healthy adult African green monkey.

HUMAN EXPOSURE AND TOXICITY: widely used in transfections and vaccine production, Vero cells are also often utilized in the detection of verotoxins, a group of interrelated toxins produced by some strains of Escherichia coli that are a key cause of hemorrhagic colitic and hemolytic uremic syndrome in humans.

The array of viruses that Vero cells are susceptible to is broad and includes polioviruses, simian virus 5 (SV5), simian virus 40 (SV40), rubeola, rubellavirus, reoviruses, simian adenoviruses, Getah, Ndumu, Pixuna, Ross River, Semliki Forest, Paramaribo, Kokobera, Modoc, Murutucu, Germiston, Guaroa, Pongola, and Tacaribe. The Vero cell line is negative, however, for reverse transcriptase and is resistant to Stratford, Apeu, Caraparu, Madrid, Nepuyo, and Ossa viruses.

The polyomavirus simian virus 40 (SV40) is a known oncogenic DNA virus which induces primary brain and bone cancers, malignant mesothelioma, and lymphomas in laboratory animals. Persuasive evidence now indicates that SV40 is causing infections in humans today and represents an emerging pathogen.

A meta-analysis of molecular, pathological, and clinical data from 1,793 cancer patients indicates that there is a significant excess risk of SV40 associated with human primary brain cancers, primary bone cancers, malignant mesothelioma, and non-Hodgkin’s lymphoma.




IDENTIFICATION AND USE: The molecular formula of potassium phosphate monobasic is KH2PO4. Potassium phosphate monobasic is a white, odourless, granular or crystalline powder, or colourless crystals. It is freely soluble in water and practically insoluble in alcohol. Apart from its essential role in bone structure, phosphate is also important in many metabolic and enzymatic pathways. It is involved in energy storage and transfer, the utilization of B-complex vitamins, the buffering of body fluids, and in the renal excretion of hydrogen ions.

HUMAN EXPOSURE AND TOXICITY: To avoid potassium or phosphorus intoxication, infuse solutions containing potassium phosphate slowly. In patients with severe renal or adrenal insufficiency, administration of potassium phosphate may cause potassium intoxication. Infusing high concentrations of phosphorus may cause hypocalcemia and calcium levels should be monitored.

Solutions which contain potassium ions should be used with great care, if at all, in patients with hyperkalemia, severe renal failure and in conditions in which potassium retention is present.

In patients with diminished renal function, administration of solutions containing potassium ions may result in potassium retention.

WARNING: THIS PRODUCT CONTAINS ALUMINUM THAT MAY BE TOXIC Aluminum may reach toxic levels with prolonged parenteral administration if kidney function is impaired. Premature neonates are particularly at risk because their kidneys are immature, and they require large amounts of calcium and phosphate solutions, which contain aluminum.

Research indicates that patients with impaired kidney function, including premature neonates, who receive parenteral levels of aluminum at greater than 4 to 5 mcg/kg/day accumulate aluminum at levels associated with central nervous system and bone toxicity. Tissue loading may occur at even lower rates of administration.

ADVERSE REACTIONS: involve the possibility of combined potassium and phosphorus intoxication from over dosage. The signs and symptoms of potassium intoxication include paresthesia of the extremities, flaccid paralysis, listlessness, mental confusion, weakness and heaviness of the legs, hypotension, cardiac arrhythmias, heart block, electrocardiographic abnormalities such as disappearance of P waves, spreading and slurring of the QRS complex with development of a biphasic curve and cardiac arrest. Phosphorus intoxication results in a reduction of serum calcium and the symptoms are those of hypocalcemic tetany.

In the event of over dosage, discontinue infusions containing potassium phosphate immediately and institute corrective therapy to restore depressed serum calcium and to reduce elevated serum potassium levels.




IDENTIFICATION AND USE: a food additive that is used as a flavor enhancer primarily in Asian cooking although it is commonly found in many processed foods. MSG comes from glutamic acid that is naturally found in mushrooms, fermented soy products such as soy sauce and parmesan cheese. Glutamic acid is part of a large category of glutamates which ultimately make up the fifth taste category of umami.

HUMAN EXPOSURE AND TOXICITY: glutamate is absorbed from the gut by an active transport system specific for amino acids. This process is saturable, can be competitively inhibited, and is dependent on sodium ion concentration. During intestinal absorption, a large proportion of glutamic acid is transaminated and consequently alanine levels in portal blood are elevated. If large amounts of glutamate are ingested, portal glutamate levels increase. This elevation results in increased hepatic metabolism of glutamate, leading to release of glucose, lactate, glutamine, and other amino acids, into systemic circulation. The pharmacokinetics of glutamate depend on whether it is free or incorporated into protein, and on the presence of other food components.

Digestion of protein in the intestinal lumen and at the brush border produces a mixture of small peptides and amino acids; di-and tri-peptides may enter the absorptive cells where intracellular hydrolysis may occur, liberating further amino acids. Defects are known in both amino acid and peptide transport. Glutamic acid in dietary protein, together with endogenous protein secreted into the gut, is digested to free amino acids and small peptides, both of which are absorbed into mucosal cells where peptides are hydrolyzed to free amino acids and some of the glutamate is metabolized.

Excess glutamate and other amino acids appear in portal blood. As a consequence of the rapid metabolism of glutamate in intestinal mucosal cells and in the liver, systemic plasma levels are low, even after ingestion of large amounts of dietary protein.

ANIMAL STUDIES: according to Dr. Russell Blaylock, who wrote a book on the subject called Excitotoxins: The Taste That Kills, sensitivity to MSG builds up in our bodies until we reach what he calls our “threshold of sensitivity.” That’s because MSG overstimulates our nervous system — exciting our nerves and causing an inflammatory response. With time, these repetitive inflammatory responses cause our nerves to start producing more and more nerve cells that are sensitive to this kind of stimulation.

The more overly-sensitive nerve cells we have, the stronger our immediate response to MSG will be. Way back in 1957, a team researchers decided to see if glutamate could help repair a diseased retina. Remember, glutamate is a common and necessary amino acid in our diet (arguably the most common neurotransmitter in the brain), so this presupposition isn’t so far-fetched.

The researchers fed rats MSG and were shocked by their results. Rather than repairing the disease, the MSG destroyed the retinal cells that allow vision! A decade later, the neuroscientist Dr. John Olney used their method of destroying retinal cells so that he could study visual pathways to the brain. He found that MSG not only destroyed retinal vision cells, but also parts of the brain. This brain damage was done as neurons became over excited, virtually exciting themselves to death. He called this “excitotoxicity,” and that has led subsequent researchers to describe MSG as an “excitotoxin.” While the naturally occurring glutamates in food aren’t dangerous, processed free glutamic acids like MSG are. Not only do they cause brain damage and lead to nervous disorders, but they also cause radical hormone fluctuations. Mice injected with MSG become rapidly obese, inactive, and have other hormonal issues.

ADVERSE REACTIONS: can involve symptoms such as numbness, burning sensation, tingling, facial pressure or tightness, chest pain, headache, nausea, rapid heartbeat, drowsiness, and weakness. Asthmatics may experience these symptoms as well as difficulty in breathing.




IDENTIFICATION AND USE: Mueller Hinton Agar is based on the formula recommended by Mueller and Hinton2 for the primary isolation of Neisseria species. Mueller and Hinton selected pea meal extract agar as a simple transparent medium containing heat stable ingredients.3 During their modification, starch replaced the growth-promoting properties of pea extract, acting as a “protective colloid” against toxic substances.

Bauer, Kirby, Sherris and Tuck4 recommended Mueller Hinton Agar for performing antibiotic susceptibility tests using a single disk of high concentration. This unsupplemented medium has been selected by the Clinical and Laboratory Standard Institute (CLSI)1 for several reasons. This medium is low in sulfonamide, trimethoprim and tetracycline inhibitors, and provides satisfactory growth of most non-fastidious pathogens along with demonstrating batch-to-batch reproducibility.

Mueller Hinton Agar is often abbreviated as M-H Agar, and complies with requirements of the World Health Organization. Mueller Hinton Agar is specified in FDA Bacteriological Analytical Manual for food testing, and procedures commonly performed on aerobic and facultatively anaerobic bacteria.7 A variety of supplementscan be added to Mueller Hinton Agar, including 5% defibrinated sheep or horse blood, 1% growth supplement and 2% sodium chloride.

PRINCIPLES OF THE PROCEDURE: Beef Extract and Acid Hydrolysate of Casein provide nitrogen, vitamins, carbon, and amino acids in Mueller Hinton Agar. Starch is added to absorb any toxic metabolites produced. Agar is the solidifying agent.

A suitable medium is essential for testing the susceptibility of microorganisms to sulfonamides and trimethoprim. Antagonism to sulfonamide activity is demonstrated by para-aminobenzoic acid (PABA) and its analogs. Reduced activity of trimethoprim, resulting in smaller growth inhibition zones and inner zonal growth, is demonstrated on medium possessing high levels of thymide. The PABA and thymine/thymidine content of Mueller Hinton Agar are reduced to a minimum, reducing the inactivation of sulfonamides and trimethoprim.




IDENTIFICATION AND USE: Neomycin is used for reducing bacteria in the intestines. It may also be used for other conditions as determined by your doctor. Neomycin is an aminoglycoside antibiotic. It kills sensitive bacteria by stopping the production of essential proteins needed by the bacteria to survive.


  • you are allergic to any ingredient in neomycin or to any other aminoglycosides (eg, gentamicin)
  • you are taking fludarabine, nondepolarizing muscle relaxants (eg, vecuronium), or penicillin
  • you have intestinal obstruction, ulcers of the bowel, or inflammatory bowel or stomach disease

HUMAN EXPOSURE AND TOXICITY: Neomycin may cause permanent hearing loss, nerve damage, and severe kidney damage. Hearing loss can occur even after the drug is stopped. If you already have kidney problems or hearing difficulty, tell your doctor. Notify your doctor immediately if any of the following occur: ringing in your ears, hearing loss, unusual tingling, muscle twitching, seizures. Neomycin may be stopped if you develop kidney or hearing problems. Your doctor will monitor your progress to minimize the possibility of these effects occurring and may run certain tests (eg, hearing and/or kidney tests). Do not use neomycin with other medicines that can cause nerve, kidney, or hearing problems. Other factors that increase the risk of these side effects occurring include advanced age or dehydration (unusual thirst).

Neomycin may also cause severe muscle relaxation progressing to paralysis and breathing problems. This possibility increases if you are also taking anesthetics, neuromuscular-blocking agents (eg, succinylcholine), or if you are receiving massive transfusions of citrate anticoagulated blood. Use with other aminoglycosides (eg, paromomycin) or other nephrotoxic/neurotoxic medicines (eg, bacitracin), advanced age, and dehydration all increase the risk of side effects. Potent diuretics (eg, ethacrynic acid, furosemide) should also be avoided because they can cause hearing loss.

ADVERSE EFFECTS: some neomycin side effects may not need any medical attention. As your body gets used to the medicine these side effects may disappear.

MINOR SIDE EFFECTS: irritation or soreness of the mouth/rectal area, nausea or vomiting.

MAJOR SIDE EFFECTS: any loss of hearing, clumsiness, diarrhea, difficulty in breathing, dizziness, drowsiness, greatly decreased frequency of urination or amount of urine, increased amount of gas, increased thirst, light-colored, frothy, fatty-appearing stools, ringing or buzzing or a feeling of fullness in the ears, skin rash, unsteadiness, weakness.

RENAL SIDE EFFECTS: The major renal side effect of oral neomycin is nephrotoxicity, which has occurred even at recommended doses and in patients with normal renal function.

Early signs of nephropathy include mild proteinuria, sloughing of renal tubular epithelial cells, formation of cellular casts, and decreases in creatinine clearance. Often there is a high output renal failure where daily urine volume may appear unchanged until significant increases in serum creatinine and BUN levels occur.

Neomycin damages renal tubules by causing tubular epithelial cell necrosis. It is considered the most nephrotoxic aminoglycoside.

NERVOUS SYSTEM SIDE EFFECTS: early symptoms of neomycin-induced auditory toxicity may manifest as high tone hearing loss, tinnitus, or a feeling of fullness in the ear, or its onset may be asymptomatic. If ototoxicity occurs, the onset of hearing loss is between several days to 6 weeks after therapy begins; however, it may not occur for months or years after neomycin has been discontinued. Symptoms of vestibulotoxicity may include tinnitus, vertigo and ataxia.

Neomycin is considered more ototoxic than vestibulotoxic. It progressively accumulates in the inner ear and which leads to sensory hair cell loss in the in the cochlea and damage to the stria vascularis. In an animal study, neomycin was found to be more ototoxic than gentamicin, kanamycin and dihydrostreptomycin.

One case report series describes 5 cases of hearing impairment associated with long-term oral neomycin therapy for hepatic encephalopathy. Doses ranged from 2 to 12 g/day and were administered for 8 to 28 months; in 2 cases paromomycin was also administered. Renal failure did not occur.

Nervous system side effects associated with oral neomycin therapy have included neuromuscular blockade, respiratory paralysis, and eighth cranial nerve damage with hearing loss, even at recommended doses and in patients with normal renal function. Symptoms of neurotoxicity include numbness, tingling, muscle twitching, and convulsions.[Ref]

OTHER SIDE EFFECTS: oral neomycin therapy may result in overgrowth of nonsusceptible organisms, especially fungi. A case of fatal Candida albicans pyelonephritis and septicemia following preoperative bowel preparation with oral neomycin and bacitracin has been reported.

GASTROINTESTINAL SIDE EFFECTS: most commonly include nausea, vomiting and diarrhea. Clostridium difficile colitis has also been reported with oral neomycin therapy.




IDENTIFICATION AND USE: to reduce the development of drug-resistant bacteria and maintain the effectiveness of Neomycin Sulfate tablets and other antibacterial drugs, Neomycin Sulfate tablets should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.

Neomycin Sulfate has been shown to be effective adjunctive therapy in hepatic coma by reduction of the ammonia-forming bacteria in the intestinal tract. The subsequent reduction in blood ammonia has resulted in neurologic improvement.

HUMAN EXPOSURE AND TOXICITY: Neomycin Sulfate is poorly absorbed from the normal gastrointestinal tract. The small absorbed fraction is rapidly distributed in the tissues and is excreted by the kidney in keeping with the degree of kidney function. The unabsorbed portion of the drug (approximately 97%) is eliminated unchanged in the feces.

Growth of most intestinal bacteria is rapidly suppressed following oral administration of Neomycin Sulfate, with the suppression persisting for 48 to 72 hours. Nonpathogenic yeasts and occasionally resistant strains of Enterobacter aerogenes (formerly Aerobacter aerogenes) replace the intestinal bacteria.

As with other aminoglycosides, the amount of systemically absorbed neomycin transferred to the tissues increases cumulatively with each repeated dose administered until a steady state is achieved. The kidney functions as the primary excretory path as well as the tissue binding site, with the highest concentration found in the renal cortex. With repeated dosings, progressive accumulation also occurs in the inner ear. Release of tissue-bound neomycin occurs slowly over a period of several weeks after dosing has been discontinued.

Protein binding studies have shown that the degree of aminoglycoside protein binding is low and, depending upon the methods used for testing, this may be between 0% and 30%.

MICROBIOLOGY: in vitro tests have demonstrated that neomycin is bactericidal and acts by inhibiting the synthesis of protein in susceptible bacterial cells. It is effective primarily against gram-negative bacilli but does have some activity against gram-positive organisms. Neomycin is active in vitro against Escherichia coli and the Klebsiella-Enterobacter group. Neomycin is not active against anaerobic bowel flora.

If susceptibility testing is needed, using a 30 mcg disc, organisms producing zones of 16 mm or greater are considered susceptible. Resistant organisms produce zones of 13 mm or less. Zones greater than 13 mm and less than 16 mm indicate intermediate susceptibility.

ADVERSE EFFECTS: the risk of hearing loss continues after drug withdrawal. Aminoglycosides can cause fetal harm when administered to a pregnant woman.

Aminoglycoside antibiotics cross the placenta and there have been several reports of total irreversible bilateral congenital deafness in children whose mothers received streptomycin during pregnancy. Although serious side effects to fetus or newborn have not been reported in the treatment of pregnant women with other aminoglycosides, the potential for harm exists. Animal reproduction studies of neomycin have not been conducted. If neomycin is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.

NURSING MOTHERS: it is not known whether neomycin is excreted in human milk, but it has been shown to be excreted in cow milk following a single intramuscular injection. Other aminoglycosides have been shown to be excreted in human milk. Because of the potential for serious adverse reactions from the aminoglycosides in nursing infants, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

PEDIATRIC USE: the safety and efficacy of oral Neomycin Sulfate in patients less than 18 years of age have not been established. If treatment of a patient less than 18 years of age is necessary, neomycin should be used with caution and the period of treatment should not exceed two weeks because of absorption from the gastrointestinal tract.

The most common adverse reactions to oral Neomycin Sulfate are nausea, vomiting and diarrhea. The “Malabsorption Syndrome” characterized by increased fecal fat, decreased serum carotene and fall in xylose absorption has been reported with prolonged therapy. Nephrotoxicity, ototoxicity and neuromuscular blockage have been reported




IDENTIFICATION AND USE: NADH stands for “nicotinamide adenine dinucleotide (NAD) + hydrogen (H).” This chemical occurs naturally in the body and plays a role in the chemical process that generates energy. People use NADH supplements as medicine.

NADH is used for improving mental clarity, alertness, concentration, and memory; as well as for treating Alzheimer’s disease. Because of its role in energy production, NADH is also used for improving athletic endurance and treating chronic fatigue syndrome (CFS).

Some people use NADH for treating high blood pressure, high cholesterol, jet lag, depression, and Parkinson’s disease; boosting the immune system; opposing alcohol’s effects on the liver and the hormone testosterone; reducing signs of aging; and protecting against the side effects of an AIDS drug called zidovudine (AZT).

Healthcare providers sometimes give NADH by intramuscular (IM) or intravenous (IV) injection for Parkinson’s disease and depression.

HUMAN EXPOSURE AND TOXICITY: NADH produced by our bodies is involved in making energy in the body. While there is some evidence that suggests NADH supplements might reduce blood pressure, lower cholesterol, help chronic fatigue syndrome by providing energy, and increase nerve signals for people with Parkinson’s disease, there isn’t enough information to know for sure how or if these supplements work.

ADVERSE EFFECTS: NADH seems safe for most people when used appropriately and short-term, up to 12 weeks. Most people do not experience any side effects when taking the recommended amount each day, which is 10 mg.

SPECIAL PRECAUTIONS AND WARNINGS: not enough is known about the use of NADH during pregnancy and breast-feeding. Stay on the safe side and avoid use.




IDENTIFICATION AND USE: nonylphenol ethoxylates (NPEs) are surfactants that have been in commerce for over 50 years. Products containing NPEs are used in many sectors, including textile processing, pulp and paper processing, paints, resins and protective coatings, oil and gas recovery, steel manufacturing, pest control products and power generation. A variety of cleaning products, degreasers and detergents are also available for institutional and domestic use. These products have numerous applications, including controlling deposits on machinery, cleaning equipment, and scouring fibres; as wetting and de-wetting agents; in dyeing and machine felt cleaning and conditioning; and in product finishing. NPEs have also been used in a wide range of consumer products, including cosmetics, cleaners, and paints.

HUMAN EXPOSURE AND TOXICITY: nonylphenol ethoxylates are thought to interfere with hormones in animals and may therefore interfere with the development and reproductive system in animals. They are listed as endocrine disrupting chemicals on the EU List. NPE is very toxic to fish and other water-dwelling organisms and is considered a hormone disrupting substance, mimicking estrogen. It degrades relatively readily in the environment to form the even more harmful nonylphenol (NP).

Nonylphenol is not readily biodegradable and take months or even longer to degrade in surface waters or in soils and sediments (where it tends to be immobilized). Non-biological degradation is negligible.

Bioconcentration and bioaccumulation is significant in water-dwelling organisms and birds, where it has been found in internal organs at between 10 and 1000 times greater than the surrounding environment. Nonylphenols are not broken down effectively in sewage treatment plants.

ADVERSE EFFECTS: there is little evidence for any significant effects of exposure to nonylphenol ethoxylates on human health. However, exposure to high levels of nonylphenol ethoxylates may cause irritation of the lungs, digestive system, skin and eyes.

Nonylphenol ethoxylates are thought to interfere with hormones in animals and may therefore interfere with the development and reproductive system in animals. They are listed as endocrine disrupting chemicals on the EU List.

The International Agency for Research on Cancer has not designated nonylphenol ethoxylates in terms of their carcinogenicity.




IDENTIFICATION AND USE: Octylphenol ethoxylates (OPEs) are a group of related chemicals. They are chemically very similar to Nonylphenol ethoxylates (NPEs). Under normal conditions, OPEs are thick liquids or waxy solids, varying in colour from clear to light orange. OPEs are stable. The degree to which they are soluble in water varies, but most are readily soluble in organic (carbon-containing) solvents.

Releases of OPEs may occur during their manufacture or during the many uses and disposal of products containing them. There are not thought to be any natural sources of OPEs to the environment.

ENVIROMENTAL EXPOSURE: OPEs are known to be very toxic to wildlife, particularly aquatic organisms. There is also concern that they mimic the behaviour of animal hormones, that they are an “endocrine disruptor”. OPEs break down relatively easily into Octylphenols (OPs), which are more harmful and can be very persistent in the environment. This persistence means that they can be transported far from the point of original release of OPEs. OPs are accumulated and concentrated by aquatic organisms and birds. It is therefore possible that the presence of OPEs and hence OPs in the environment poses a long-term threat to wildlife on both a local and global scale.

HUMAN EXPOSURE AND TOXICITY: Octylphenol ethoxylates can enter the body either by inhalation of air containing octylphenol ethoxylates, ingestion of contaminated food or water, or by dermal contact with octylphenol ethoxylates or products containing octylphenol ethoxylates.

ADVERSE EFFECTS: there is little evidence available for the full effects of exposure to octylphenol ethoxylates on human health. However, exposure to high levels of octylphenol ethoxylates may cause irritation of the lungs, digestive system, skin and eyes. Octylphenol ethoxylates are thought to interfere with hormones in animals and may therefore interfere with the development and reproductive system in animals. Octylphenol ethoxylates readily degrade in the environment to the more toxic, octylphenol. The International Agency for Research on Cancer has not designated octylphenol ethoxylates in terms of their carcinogenicity. However, exposure to octylphenol ethoxylates at normal background levels is unlikely to have any adverse effect on human health.




IDENTIFICATION AND USE: Ovalbumin is a glycoprotein that comprises 54% of the total proteins obtained from the white of eggs. It is a member of the serpin superfamily.

Ovalbumin and albumin were some of the very first proteins to be studied. Ovalbumin was first crystallized in 1890 by Hofmeister. In 1938, Neuberger reported that the carbohydrate moiety contained two moles of hexosamine, four moles of mannose, and some unidentified nitrogeneous material.




IDENTIFICATION AND USE: Phenol, is a toxic, colorless crystalline solid with a sweet tarry odor that resembles a hospital smell. It is commonly used as an antiseptic and disinfectant. It is active against a wide range of micro-organisms including some fungi and viruses, but is only slowly effective against spores.

  • The primary use of phenol is in the production of phenolic resins, which are used in the plywood, construction, automotive, and appliance industries.
  • Phenol is also used in the production of caprolactam and bisphenol A, which are intermediates in the manufacture of nylon and epoxy resins, respectively.
  • Other uses of phenol include as a slimicide, as a disinfectant, and in medicinal products such as ear and nose drops, throat lozenges, and mouthwashes.

HUMAN EXPOSURE AND TOXICITY: individuals may be exposed to phenol through breathing contaminated air or through skin contact in the workplace.

Other exposures to phenol may occur through the use of phenol-containing medicinal products (including mouthwashes, toothache drops, throat lozenges, analgesic rubs, and antiseptic lotions) or smoking tobacco.

Phenol can be detected in urine; this test can be used to determine whether a person has recently been exposed to phenol or to substances that are changed to phenol in the body. However, no test will tell whether a person has been exposed only to phenol, because many substances are changed to phenol in the body.

ACUTE EFFECTS: inhalation and dermal exposure to phenol is highly irritating to the skin, eyes, and mucous membranes in humans.

CHRONIC EFFECTS (NONCANCER): anorexia, progressive weight loss, diarrhea, vertigo, salivation, and a dark coloration of the urine have been reported in chronically exposed humans. Gastrointestinal irritation and blood and liver effects have also been reported. In one study, muscle pain, weakness, enlarged liver and elevated levels of liver enzymes were found in an individual after inhalation and dermal exposure to phenol and a few other chemicals.

Application of phenol to the skin results in dermal inflammation and necrosis. Cardiac arrhythmias have also been reported in humans exposed to high concentrations of phenol.

Chronic inhalation exposure of animals to phenol has shown central nervous systems (CNS), kidney, liver, respiratory, and cardiovascular effects.

REPRODUCTIVE/ DEVELOPMENTAL EFFECTS: no studies were located concerning the developmental or reproductive effects of phenol in humans. Animal studies have reported reduced fetal body weights, growth retardation, and abnormal development in the offspring of animals exposed to phenol by the oral route. Decreased maternal weight gain and increased maternal mortality were also observed.

CANCER RISK: small, non-significant excesses in certain types of cancers were reported in occupationally exposed workers; however, these effects were not clearly related to phenol exposure.

Animal studies have not seen tumors resulting from oral exposure to phenol, while dermal studies have reported that phenol applied to the skin may be a tumor promotor and/or a weak skin carcinogen in mice.

EPA has classified phenol as a Group D, not classifiable as to human carcinogenicity, based on a lack of data concerning carcinogenic effects in humans and animals.




IDENTIFICATION AND USE: In the body, almost all phosphorus is combined with oxygen, forming phosphate. Bone contains about 85% of the body’s phosphate. The rest is located primarily inside cells, where it is involved in energy production. Phosphate is necessary for the formation of bone and teeth. Phosphate is also used as a building block for several important substances, including those used by the cell for energy, cell membranes, and DNA (deoxyribonucleic acid). The body obtains phosphate from foods and excretes it in urine and stool.




IDENTIFICATION AND USE: Gomori buffers, the most commonly used phosphate buffers, consist of a mixture of monobasic dihydrogen phosphate and dibasic monohydrogen phosphate. By varying the amount of each salt, a range of buffers can be prepared that buffer well between pH 5.8 and pH 8.0.

Phosphates have a very high buffering capacity and are highly soluble in water. However, they have a number of potential disadvantages: Phosphates inhibit many enzymatic reactions and procedures that are the foundation of molecular cloning, including cleavage of DNA by many restriction enzymes, ligation of DNA, and bacterial transformation. Because phosphates precipitate in ethanol, it is not possible to precipitate DNA and RNA from buffers that contain significant quantities of phosphate ions.




IDENTIFICATION AND USE: Polymyxin B sulfate is a drug of choice in the treatment of infections of the urinary tract, meninges, and bloodstream caused by susceptible strains of Ps. aeruginosa. It may also be used topically and subconjunctivally in the treatment of infections of the eye caused by susceptible strains of Ps. aeruginosa.

HUMAN EXPOSURE: Clostridium difficile associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including Polymyxin B for Injection, and may range in severity from mild diarrhea to fatal colitis. Treatment with antibacterial agents alters the normal flora of the colon leading to overgrowth of C. difficile.

C. difficile produces toxins A and B which contribute to the development of CDAD. Hypertoxin producing strains of C. difficile cause increased morbidity and mortality, as these infections can be refractory to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea following antibiotic use. Careful medical history is necessary since CDAD has been reported to occur over two months after the administration of antibacterial agents.

If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued. Appropriate fluid and electrolyte management, protein supplementation, antibiotic treatment of C. difficile, and surgical evaluation should be instituted as clinically indicated.

NEPHROTOXIC REACTIONS: Albuminuria, cylinduria, azotemia, and rising blood levels without any increase in dosage.

NEUROTOXIC REACTIONS: Facial flushing, dizziness progressing to ataxia, drowsiness, peripheral paresthesias (circumoral and stocking glove), apnea due to concurrent use of curariform muscle relaxants, other neurotoxic drugs or inadvertent overdosage, and signs of meningeal irritation with intrathecal administration, e.g., fever, headache, stiff neck and increased cell count and protein cerebrospinal fluid.

OTHER REACTIONS OCCASIONALLY REPORTED: Drug fever, urticarial rash, pain (severe) at intramuscular injection sites, and thrombophlebitis at intravenous injection sites.




IDENTIFICATION AND USE: Polysorbate 80 is a common excipient and solubilizing agent used in the pharmaceutical industry. Polysorbate 80 (also known as polyoxyethylene-sorbitan-20 mono-oleate, or Tween 80) is used in the pharmaceutical and cosmetic industry in lotions, medical preparations (e.g., vitamin oils, vaccines, and intravenous preparations) and as an excipient in tablets.

A solubilizing agent acts as a surfactant and increases the solubility of one agent in another. A substance that would not normally dissolve in a particular solution is able to dissolve with the use of a solubilizing agent.

Polysorbate 80 is used as a solubilizing agent in IV formulations of the antiarrhythmic drug amiodarone. Rare case reports of liver toxicity have been published suggesting polysorbate 80 may contribute to liver toxicity with the IV formulation of amiodarone. The package labeling of amiodarone warns that polysorbate 80 is also known to leach DEHP (dioctyl phthalate) from PVC and dosing recommendations should be followed closely.

ANIMAL EXPOSURE/TOXICITY: Polyoxyethylene (20) sorbitan monooleate (polysorbate 80, Tween 80), a surfactant, has been widely used as a solvent for pharmacological experiments. In the present study, polysorbate 80 was found to have toxicity of a low order in both the mice and rats when given by i.p. and p.o. routes.

It produced mild to moderate depression of the central nervous system with a marked reduction in locomotor activity and rectal temperature, exhibited ataxia and paralytic activity and potentiated the pentobarbital sleeping time. On intravenous administration in dogs, it had a dose-dependent hypotensive effect. Polysorbate 80 did not have a direct stimulant or relaxant effect on either guinea pig ileum or rat uterus, however, it antagonised the contractions induced by acetylcholine, histamine, barium, 5-hydroxytryptamine and carbachol in a dose-dependent manner. A direct relaxant effect was observed on rabbit jejunum.

A dose-dependent myocardial depressant effect was observed on guinea pig and rabbit paired atrial preparations. On the electrically-driven guinea pig left atrial preparation, polysorbate 80 exhibited a dose-dependent negative inotropic action. Polysorbate 80 did not induce diuresis in rats upto a dose of 2.5 ml/kg.

The results of the present study indicate that polysorbate 80 can neither be used as a solvent for isolated tissue experiments nor when considered for intravenous administration. However, polysorbate 80 can be employed safely as a vehicle for neuropsychopharmacological experiments in doses not exceeding 1 ml/kg.

HUMAN EXPOSURE/TOXICITY: Certain drugs such as dalargin, loperamide or tubocurarine are not transported across the blood-brain barrier (BBB) and therefore exhibit no effects on the central nervous system. However, effects on the central nervous system can be observed when these drugs are loaded onto polybutylcyanoacrylate (PBCA)-nanoparticles and coated with polysorbate 80.

The mechanism by which these complexed nanoparticles cross the BBB and exhibit their effects has not been elucidated. Cultured microvessel brain endothelial cells of human and bovine origin were used as an in vitro model for the BBB to gain further insight into the mechanism of uptake of nanoparticles. With cells from these species we were able to show that polysorbate 80-coated nanoparticles were taken up by brain endothelial cells much more rapidly and in significantly higher amounts (20-fold) than uncoated nanoparticles.

The process of uptake was followed by fluorescence and confocal laser scanning microscopy. The results demonstrate that the nanoparticles are taken up by cells and that this uptake occurs via an endocytotic mechanism.

ADVERSE EFFECTS: side effects include abdominal or stomach pain, accumulation of pus, arm, back, or jaw pain, blurred vision, breathing problems (irregular, noisy, or trouble when resting), chest pain, discomfort, tightness, or heaviness, chills, confusion, cough producing mucus, decrease in the amount of urine, diarrhea, dilated neck veins, dizziness, fainting, or lightheadedness, dry mouth, fast, slow, or irregular heartbeat, fatigue or tiredness (extreme or unusual), fever, headache, nausea, pain, tenderness, swelling, or warmth over injection site, pounding in the ears, rapid breathing, rapid or pounding pulse, shortness of breath, skin discoloration at the injection site, sunken eyes, sweating, swelling of the ankles, face, fingers, feet, hands, or lower legs, thirst, trouble with breathing, unconsciousness, vomiting, weight gain, wheezing, wrinkled skin, anxiety, convulsions, difficulty with speaking (slow speech or unable to speak), double vision, trouble with thinking, trouble with walking, unable to move the arms, legs, or face muscles (including numbness and tingling), fever and sore throat, hives, itching, pale skin, skin rash, unusual tiredness or weakness, constipation, general feeling of discomfort or illness, lack or loss of strength, loss of appetite, muscle aches, pains, or stiffness, pain in the joints, runny nose, shivering, sneezing, trouble with sleeping.

Clinical studies have shown darbepoetin alfa (albumin) to increase the risk of serious side effects (eg, blood clots, stroke, heart attack, heart failure) and death in some cases. It has also been shown to increase the risk of tumor growth in patients with advanced cancer.




IDENTIFICATION AND USE: Porcine circoviruses are small, icosahedral viruses that were discovered in 1974 as contaminants of a porcine kidney cell line. They were later called circoviruses when their genome was found to be a circular, single-stranded DNA molecule. Upon entry into cells, the viral ssDNA genome enters the nucleus where it is made double-stranded by host enzymes. It is then transcribed by host RNA polymerase II to form mRNAs that are translated into viral proteins. There is some evidence that circoviruses might have evolved from a plant virus that switched hosts and then recombined with a picorna-like virus.

Porcine circoviruses are classified in the Circoviridae family, which contains two genera, Circovirus and Gyrovirus. There are two porcine circoviruses, PCV-1 and PCV-2; only the latter causes disease in pigs. Infection probably occurs via oral and respiratory routes, and leads to various diseases including postweaning multisystemic wasting syndrome, and porcine dermatitis and nephropathy syndrome. Virions are shed in respiratory and oral secretions, urine, and feces of infected pigs. Other circoviruses may cause diseases of birds, including psittacine beak and feather disease, and chicken infectious anemia, the latter caused by the sole member of the Gyrovirus genus. There are also circoviruses that infect canaries, ducks, finches, geese, gulls, pigeons, starlings, and swans.

HUMAN EXPOSURE: we have no good evidence that porcine or avian circoviruses can infect humans. In the United States, porcine circovirus sequences can be detected in human feces. These most likely originate from consumption of pork products, most of which also contain porcine circoviruses. Circovirus sequences have also been found in commonly eaten animals such as cows, goats, sheep, camels, and chickens. Outside of the United States, the circoviruses found in human stools do not appear to be derived by meat consumption and might cause enteric infections.

Recently both PCV-1 and PCV-2 sequences were detected in Rotarix and RotaTeq, vaccines for the prevention of rotavirus disease in infants. The source of the contaminant was trypsin, an enzyme purified from porcine pancreas, which is used in the production of cell cultures used for vaccine production.

Several human cell lines have been infected with PCV1 and PCV2 to investigate whether PCV can infect and replicate in human cells. PCV1 persisted in most cell lines without causing any visible changes, while PCV2-transfected cells show cytopathogenic alterations. Expression of viral proteins and replication of viral DNA was observed, but the infection was not to be passed on to fresh cells, indicating that PCV-infection of human cells is non-productive.

ADVERSE EFFECTS: difficulty breathing, vomiting and ear infection, followed by bloody stool.

Then the intestines get blocked and twisted (known as intussusception) which can be deadly and requires surgery on the intestines.




IDENTIFICATION AND USE: Aluminum is established as a neurotoxin, although the basis for its toxicity is unknown. It recently has been shown to alter the function of the blood-brain barrier, which regulates exchanges between the central nervous system and peripheral circulation. The blood-brain barrier owes its unique properties to the integrity of cell membranes that comprise it. Aluminum affects some of the membrane like functions of the blood-brain barrier. It increases the rate of transmembrane diffusion and selectively changes saturable transport systems without disrupting the integrity of the membranes or altering CNS hemodynamics. Such alterations in the access to the brain of nutrients, hormones, toxins, and drugs could be the basis of CNS dysfunction. Aluminum is capable of altering membrane function at the blood-brain barrier; many of its effects on the CNS a well a peripheral tissues can be explained by its actions as a membrane toxin.


  • Adsorbents and absorbents
  • Finishing agents
  • Photosensitive chemicals
  • Processing aids, not otherwise listed


  • Agricultural Products (non-pesticidal)
  • Arts, Crafts, and Hobby Materials
  • Personal Care Products
  • Water Treatment Products

ANIMAL EXPOSURE/TOXICITY: Excessive dietary aluminum has been proposed to be a factor contributing to several neurological disorders in humans. Six 8 week old female Swiss Webster mice were fed for 10 weeks purified diets containing 100 (control, 100 aluminum, 500 (500 aluminum) or 1000 (1000 aluminum) ug aluminum/g diet.

Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances in brain and liver homogenates in the presence or absence of 50 mM ferrous iron. 2-Thiobarbituric acid reactive substances production in the absence of iron in brain homogenates from mice fed the 1000 aluminum diet was higher (30%) than that in the 100 aluminum control group (3.1 versus 2.4 nmol 2-thiobarbituric acid reactive substances/mg protein).

The additional of ferrous iron increased 2-thiobarbituric acid reactive substances production in-brain homogenates from all 3 dietary group. The iron induced 2-thiobarbituric acid reactive substances production was 26% higher in the 1000 aluminum brain homogenates than in the 100 aluminum group (4.9 vs. 3.9 nmol 2-thiobarbituric acid reactive subtances/mg protein). Brain 2-Thiobarbituric acid reactive substances production in the presence and absence of iron was similar between the 100 and 500 aluminum groups. 2-Thiobarbituric acid reactive substances production in liver homogenates measured either with or without iron was similar for the 3 groups.

These results show that, in mice, dietary aluminum intoxication leads to increased brain 2-thiobarbituric acid reactive substance production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue aluminum.

HUMAN EXPOSURE/TOXICITY: evidence is presented indicating that dementias are associated with a relative insufficiency of magnesium in the brain. Such insufficiency may be attributable to low intake or retention of magnesium; high intake of a neurotoxic metal, such a aluminum, which inhibits activity of magnesium requiring enzymes; or impaired transport of magnesium and/or enhanced transport of the neurotoxic metal into brain tissue.

It is proposed that Alzheimer’s disease involves a defective transport process, characterized by both an abnormally high incorporation of aluminum and an abnormally low incorporation that an altered serum protein contributes to the progression of Alzheimer’s disease by having a greater affinity for aluminum than for magnesium, in contrast to the normal protein, which binds magnesium better than aluminum.

The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate aluminum uptake and impede magnesium uptake. Evidence suggests that albumin is the serum protein that is altered.

A new case study from Keele University in the UK1 unequivocally shows high levels of aluminum in the brain of an individual exposed to aluminum at work, who later died from Alzheimer’s disease. While aluminum exposure has been implicated in Alzheimer’s and a number of other neurological diseases, this case claims to be “the first direct link” between Alzheimer’s disease and elevated brain aluminum following occupational exposure. Vaccines present a particularly problematic source of toxic metal exposure.

Aluminum is the most commonly used vaccine adjuvant and is considered “safe” even though research shows it may induce serious immunological disorders and neurological complications in humans. In the video above, Dr. David Ayoub discusses how the aluminum in vaccines may be even more dangerous than mercury. The number of aluminum-containing vaccines children receive today has quadrupled over the past 30 years. In the 1970s, children got only four aluminum-containing vaccines in their first 18 months of life, but now they typically receive 17.

As children’s aluminum burden has increased, so has the prevalence of childhood neurological disorders. In one school, 90 percent of the children developed ADHD during the course of a single school year, and their toxicity profiles all revealed massive amounts of aluminum. Aluminum is also in vaccines and is used as an adjuvant. If you go by the aluminum content on vaccine labels, the amount kids are getting is excessive, but if you add in the aluminum NOT listed on the labels—”accidental exposure” due to contamination—it’s a much more serious problem.

Dr. Ayoub cites one study that found five to six times more aluminum in vaccines than what was actually listed on the labels. When you review the signs and symptoms of aluminum toxicity, they are shockingly similar to the symptoms of autism, ADHD, Alzheimer’s, Parkinson’s, and other neurological diseases. Vaccine adjuvants can cause serious chronic brain inflammation.

ADVERSE EFFECTS: aluminum targets your cerebellum and autonomic nervous system—the part responsible for biological processes over which you have no conscious control (breathing, blood pressure, balance, coordination, etc.). When you look at the MSDS sheet for aluminum, you will see symptoms strikingly similar to those in common neurological diseases, including memory problems, speech impairments and aphasia, dementia, depression, muscle weakness, motor disturbances, and other neurological difficulties.




IDENTIFICATION AND USE: Potassium is a mineral that is found in many foods and is needed for several functions of your body, especially the beating of your heart.

Potassium chloride is used to prevent or to treat low blood levels of potassium (hypokalemia). Potassium levels can be low as a result of a disease or from taking certain medicines, or after a prolonged illness with diarrhea or vomiting.

HUMAN EXPOSURE/TOXICITY: you should not use potassium chloride if you are allergic to it, or if you have certain conditions. Be sure your doctor knows if you have:

  • high levels of potassium in your blood (hyperkalemia)
  • kidney failure
  • Addison’s disease (an adrenal gland disorder)
  • a large tissue injury such as a severe burn
  • severely dehydrated
  • taking a “potassium-sparing” diuretic (water pill) such as amiloride (Midamor, Moduretic), spironolactone (Aldactone, Aldactazide), triamterene (Dyrenium, Dyazide, Maxzide)

To make sure you can safely take potassium chloride, tell your doctor if you have any of these other conditions:

  • kidney disease
  • heart disease or high blood pressure
  • a blockage in your stomach or intestines
  • chronic diarrhea (such as ulcerative colitis, Crohn’s disease)

It is not known whether potassium chloride will harm an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant while using this medication. It is not known whether potassium chloride passes into breast milk or if it could harm a nursing baby. Do not use this medication without telling your doctor if you are breast-feeding a baby.

ADVERSE EFFECTS: uneven heartbeat, muscle weakness or limp feeling, severe stomach pain, and numbness or tingling in your hands, feet, or mouth.

COMMON SIDE EFFECTS: diarrhea, gas, nausea, stomach discomfort, and vomiting.

SEVERE SIDE EFFECTS: severe allergic reactions (rash, hives, itching, difficulty breathing, tightness in the chest, swelling of the mouth, face, lips, or tongue), black, tarry stools, chest pain, irregular heartbeat, listlessness, numbness or tingling in your skin, lips, hands, or feet, severe nausea or vomiting, stomach pain or swelling, unusual confusion or anxiety, unusual muscle weakness or paralysis, vomit that looks like coffee grounds, weak or heavy legs.




IDENTIFICATION AND USE: Genetically engineered human albumin derived from yeast. Currently, only the MMR vaccine contains genetically engineered human protein, which is produced under the brand name recombumin and referred to as “recombinant human albumin” in the package insert.

HUMAN EXPOSURE/TOXICITY: Albumin (human) is used for treating a variety of conditions, including shock due to blood loss in the body, burns, low protein levels due to surgery or liver failure, and as an additional medicine in bypass surgery. Albumin (human) is a concentrate of plasma proteins from human blood. It works by increasing plasma volume or serum albumin levels.

ADVERSE EFFECTS: anaphylactoid reactions, fever, chills, rash, nausea, vomiting, tachycardia.

DERMATOLOGIC SIDE EFFECTS: urticaria, skin rash, pruritus, edema, and erythema.

NERVOUS SYSTEM SIDE EFFECTS: headache, chills, and febrile reactions.


GASTROINTESTINAL SIDE EFFECTS: nausea, vomiting and increased salivation.





IDENTIFICATION AND USE: Sodium bicarbonate reduces stomach acid. It is used as an antacid to treat heartburn, indigestion, and upset stomach. Sodium bicarbonate is a very quick-acting antacid. It should be used only for temporary relief. It works by neutralizing excess acid in the blood. It may also replace bicarbonate when there are excess losses from the body. Sodium bicarbonate is the active ingredient in baking soda.

This medication may be used to make the urine less acidic. This effect helps the kidneys get rid of uric acid, thereby helping to prevent gout and kidney stones. It can make some medications (e.g., sulfonamides) work better or can help your body get rid of too much medication (e.g., phenobarbital). This medication can also prevent and treat certain metabolic problems (acidosis) caused by kidney disease.

HUMAN EXPOSURE/TOXICITY: if you have abnormal levels of sodium, potassium, calcium, or chlorine, your doctor may advise you not to take sodium bicarbonate, or to least monitor levels of your electrolytes closely.

Before taking sodium bicarbonate, tell your doctor if you are on a low-sodium diet or if you have a rare kidney disorder known as Bartter syndrome, because it causes potassium, sodium, and chloride levels to be out of balance.

If your body’s pH is higher than normal (known as alkalosis), you should not take sodium bicarbonate.

People taking sodium bicarbonate should try not to consume large amounts of high calcium-containing foods (such as milk, cheese, or yogurt) and should not take calcium supplements.

Sodium bicarbonate falls under the FDA’s Pregnancy Category C, which means that it should be avoided because we don’t know if it will harm to an unborn baby or fetus.

Experimentally, the administration of intravenous hypertonic sodium bicarbonate has been associated with increased serum osmolality, decreased ionized serum calcium (which is associated with decreased myocardial contractility), and peripheral vasodilation.

Some experts recommend invasive hemodynamic monitoring in acidotic patients before the administration of bicarbonate.

ADVERSE EFFECTS: frequent urge to urinate, headache (continuing), loss of appetite (continuing), mood or mental changes, muscle pain or twitching, nausea or vomiting, nervousness or restlessness, slow breathing, swelling of feet or lower legs, unpleasant taste, unusual tiredness or weakness.

GASTROINTESTINAL SIDE EFFECTS: gastric rupture. As an antacid, sodium bicarbonate, especially after excess food or liquid, can cause excess gas release (when combined with gastric acid). The mortality associated with gastric rupture is as high as 65%. Urinary alkalinization from bicarbonate can cause a falsely positive colorimetric assay for protein.

RENAL SIDE EFFECTS: “False” proteinuria – an excess of serum proteins in the urine, such as in renal disease, after strenuous exercise, or in dehydration.

RESPIRATORY SIDE EFFECTS: suppressed respiratory drive. Rapid infusion of hyperosmolar sodium bicarbonate has been associated with intraventricular hemorrhage in the pediatric literature. Irritability and tetany have been associated with sodium bicarbonate-induced alkalosis or hypernatremia. Due to greater permeability of the blood-brain barrier to hydrogen than to bicarbonate, the pH of cerebrospinal fluid may significantly decrease during sodium bicarbonate administration, which can cause mental stupor or coma.

NERVOUS SYSTEM SIDE EFFECTS: irritability, tetany, mental stupor, coma, and intraventricular hemorrhage.

LOCAL SIDE EFFECTS: IV site pain, venous irritation, and extravasation. Cellulitis, tissue necrosis, ulceration, or skin sloughing have possibly been the result of extravasation. A slow rate of administration of a properly diluted solution into a large bore needle and vein is recommended if IV administration is necessary.

CARDIOVASCULAR SIDE EFFECTS: decreased cardiac contractility possibly resulting from infusion of sodium bicarbonate in patients with severe acidosis.




IDENTIFICATION AND USE: also known as (sodium borate decahydrate; sodium pyroborate; birax; sodium tetraborate decahydrate; sodium biborate) is a natural mineral compound (Na2B4O7 • 10H2O). It was discovered over 4000 years ago.

Borax is usually found deep within the ground, although it has been mined near the surface in Death Valley, California since the 1800s. Although it has numerous industrial uses, in the home borax is used as a natural laundry booster, multipurpose cleaner, fungicide, preservative, insecticide, herbicide, disinfectant, dessicant, and ingredient in making ‘slime’.

Borax crystals are odorless, whitish (can have various color impurities), and alkaline. Borax is not flammable and is not reactive. It can be mixed with most other cleaning agents, including chlorine bleach. Borax may also be used as an insecticide to kill roaches, ants, and fleas. In fact, it is also toxic to people.

HUMAN EXPOSURE/TOXICITY: repeated exposure of a hair preparation containing 3.2% sodium borate and a cleansing cream containing 1.7% sodium borate on the skin of 12 and 14 subjects, respectively. The test material was applied under an occlusive patch to the backs of subjects daily for 21 consecutive days. Sites were scored one hour after patch removal. Applications 4 to 21 of the hair preparation produced erythema and papules in most subjects; the total cumulative irritancy score was 571 (maximum =630). The cleansing cream caused slight erythema in two subjects only, resulting in a total irritancy score of 6.4. The investigators concluded that, under the condition of the study, the hair preparation was a “mild to moderate” cumulative irritant, whereas the cleansing cream was practically nonirritating.

The Kligman maximization procedure was used to study the sensitizing potential of a hair preparation containing 3.2% sodium borate in 25 subjects. The material was initially applied under a 48 hr patch to each subject to determine whether sodium lauryl sulfate (SLS) pretreatment was required. The test material was found to be irritating; it was determined that SLS treatment was unnecessary. The undiluted hair preparation was applied under occlusion to one arm of each subject for 48 hr. This procedure was repeated every other day for 10 days (5 application). 10 days after removal of the fifth induction patch, a 48 hr occlusive challenge patch was applied to a fresh site. Sites were scored at 48 and 72 hr. The hair preparation containing 3.2% sodium borate induced no irritation during challenge phases of the test; this product was determined to be nonsensitizing when applied to human skin.

Two cleansing creams, each containing 1.7% sodium borate, were assayed in panel tests. In each study, panelists were given the product and asked to use it daily for 2 weeks. In a group of 100 subjects, one cream produced no irritation. In the other panel, which included 90 subjects, there was one report of irritation; a subject accidentally instilled some of the cream into her eyes. A stinging sensation was experienced; however, the irritation subsided following eye rinse.

CASE REPORTS: Seven patients with brain tumors who were receiving neutron-capture therapy were administered iv 18.6 to 27.3 g of sodium borate (a range of 32-50 mg/kg/of boron). In this procedure the boron served as the capture element. A consistent hypoxic type of ECG abnormality was observed immediately after the injection. When the boron was rapidly excreted or when the dose of boron was <50 mg/kg, the ECG returned to normal within 24-48 hr. The researchers suggested that the entrance of boron into myocardial cells in appreciable concentrations produced injury resulting in cell hypoxia.

A case-series report of seven infants (aged 6-16 weeks) who used pacifiers coated with a borax and honey mixture for 4-10 weeks concluded that exposures ranged from 12 to 90 g, with a very crudely estimated average daily ingestion of 18-56 mg of boron per kg of body weight. Toxicity was manifested by generalized or alternating focal seizure disorders, irritability, and gastrointestinal disturbances. Although infants appear to be more sensitive than adults to boron compounds, lethal doses are not well documented in the literature.

Ten patients receiving neutron-capture therapy were administered iv doses of sodium borate up to 20 g (2.12 g boron). The median dose was 25 mg/kg boron and the maximum dose was 46 mg/kg boron. The patients received 1-4 doses at intervals of 2 weeks to 3 months. The immediate symptoms were: intense gastrointestinal stimulation leading to nausea, vomiting, urgent defecation and diarrhea, “mild peripheral vascular collapse”, mild mental confusion, and a flushed skin on the face. Later symptoms were: drowsiness, lethargy, and continued gastroirritability. These effects ceased by days 3-5 and no deaths occurred. Toxic effects were not enhanced by up to 4 successive iv administrations.

ADVERSE EFFECTS: chronic eczema. Long-term exposure to borax dust may lead to inflammations of the mucous membranes of the airways (bronchitis, laryngitis) and to conjunctivitis. Ingestion of 5 to 10 g by young children can cause severe vomiting, diarrhea, shock and death. Effects from ingestion include: abdominal pain, diarrhea, headache, nausea, vomiting, weakness, convulsions. Acute oral ingestion of 2 to 20 grams or more of boric acid can result in symptoms that include nausea, vomiting, abdominal pain, diarrhea, depression of the central nervous sytem, and convulsions. Subacute or chronic doses of boric acid may result in signs and symptoms including dermatitis, loss of appetite, nausea, and vomiting. In the occupational setting, exposures to airborne boric acid and borax dusts have been shown to be irritating to the respiratory tract and the eyes of workers. These symptoms for both acute and chronic exposures, include eye irritation; dryness of mouth, nose, or throat; sore throat; and productive cough.

Peripheral blood cultures were exposed to various doses (5 to 500 mg/L) of boron compounds. Sister-chromatid exchange, micronucleus and chromosomal aberration tests were applied to estimate the DNA damage, and biochemical parameters (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, total glutathione, malondialdehyde and total antioxidant capacity) were examined to determine oxidative stress. According to /these/ findings, various boron compounds at low doses were useful in supporting antioxidant enzyme activities in human blood cultures. It was found that the boron compounds do not have genotoxic effects even in the highest concentrations, though in increasing doses they constitute oxidative stress. It is concluded that the tested boron compounds can be used safely, but it is necessary to consider the tissue damages which are likely to appear depending on the oxidative stress.

The effect of borax on human chromosomes was analyzed in this study. Venous blood from 30 male students at Thammasat University, Thailand (age 18-25 years) was collected for lymphocyte cell cultures. This experiment was divided into two groups: the first group was the control group and the second group was the experimental group. The lymphocyte cells in the control group were cultured without borax. The experimental group was divided into four subgroups. The lymphocyte cells in each experimental subgroup were cultured with different concentrations of borax (0.1 mg/mL, 0.15 mg/mL, 0.2 mg/mL and 0.3 mg/mL). Human chromosomes were studied for abnormalities through Giemsa-staining and G-banding. The results show that the numbers of metaphase plates (the metaphase plate which contained 46 chromosomes; 46, XY) and metaphase chromosomes were reduced when lymphocyte cells were cultured with 0.15 mg/mL (57.2%), 0.2 mg/mL (50.8%) and 0.3 mg/mL (42.3%) concentrations of borax. There was a statistically significant difference between the control and experimental subgroups (p < 0.05). Sister chromatid separation was found in the 0.3 mg/ml borax concentration experimental subgroup. This shows that borax (at 0.15, 0.2 and 0.3 mg/mL concentrations) affects the cell and human chromosomes (both numerical and structural abnormalities). Borax may cause human chromosome abnormalities and lead to genetic defects.

OTHER TOXICITY INFORMATION: autopsies have revealed hepatitis, nephrosis and cerebral edema. In some cases autopsies have revealed, necrotic changes in intestines, plethora of internal organs, brain tissue stasis and pulmonary edema. Fatal doses for humans are variously estimated to be 5 to 6 g for children and 10 to 25 g for adults. Borax and boric acid used in powders and ointments have resulted in serious poisonings and death.




IDENTIFICATION AND USE: Sodium citrate/citric acid is used to make urine less acidic and therefore prevent formation of kidney stones. Sodium citrate/citric acid also is useful as a buffer and neutralizing agent for gastric acid. Sodium citrate is broken down to sodium bicarbonate which decreases the acidity of urine, increasing the excretion of substances that cause kidney stones.

HUMAN EXPOSURE/TOXICITY: should not be used in patients with kidney failure. It is not known whether sodium citrate/citric acid entersbreast milk; therefore, it is best to be cautious before using it in nursing mothers. You should not use this medication if you have kidney failure, severe heart damage (such as from a prior heart attack), Addison’s disease (an adrenal gland disorder), high levels of potassium in your blood (hyperkalemia), or if you are severely dehydrated or have heat cramps. Avoid using antacids without your doctor’s advice, including household baking soda (sodium bicarbonate). Antacids that contain aluminum or sodium can interact with citric acid and sodium citrate, causing a serious electrolyte imbalance or aluminum toxicity.

ADVERSE EFFECTS: common side effects of sodium citrate/citric acid are nausea, vomiting, diarrhea, stomach pain, and water retention. Serious side effects of citric acid and sodium citrate include muscle twitching or cramps, swelling or weight gain, weakness, mood changes, rapid and shallow breathing, fast heart rate, restless feeling, black or bloody stools, severe diarrhea, or seizure (convulsions).




IDENTIFICATION AND USE: bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent.
This detergent also is used to supplement cell culture media and to prevent nonspecific binding in affinity chromatography. Sodium Deoxycholate is used to regenerate immobilized polymixin B (Detoxi-Gel D™ Endotoxin Removing Gel, ProductNo. 20339).
Immobilized polymixin B is an effective tool for removing endotoxins (lipopolysaccharide or LPS) from biological samples. Sodium Deoxycholate is the most effective reagent for removing LPS from immobilized polymixin B, allowing reuse of this ligand for additional endotoxin removal.” (128) “Bile acids are often refluxed into the lower oesophagus and are candidate carcinogens in the development of oesophageal adenocarcinoma
HUMAN EXPOSURE/TOXICITY: deoxycholic acid (DCA), is the only one of the commonly refluxed bile acids tested here, to show genotoxicity, in terms of chromosome damage and mutation induction in the human p53 gene. This genotoxicity was apparent at both neutral and acidic pH, whilst there was a considerable increase in bile-induced toxicity at acidic pH. The higher levels of cell death and low cell survival rates at acidic pH may imply that acid bile exposure is toxic rather than carcinogenic, as dead cells do not seed cancer development. We also show that DCA (at neutral and acid pH) induced the release of reactive oxygen species (ROS) within the cytoplasm of exposed cells. The genotoxicity of DCA is ROS mediated, as micronucleus induction was significantly reduced when cells were treated with DCA + the anti-oxidant vitamin C. In conclusion DCA, is an effective genotoxin at both neutral and acidic pH. As bile acids like DCA can induce DNA damage at neutral pH, suppressing the acidity of the refluxate will not completely remove its carcinogenic potential. The genotoxicity of DCA is however, ROS dependent, hence anti-oxidant supplementation, in addition to acid suppression may block DCA driven carcinogenesis in Barrett’s patients. Disruption of the blood-brain barrier (BBB) is a characteristic finding in common neurological disorders. Human data suggest BBB disruption may underlie cerebral dysfunction.
ANIMAL EXPOSURE/TOXICITY: experiments show the development of epileptiform activity following BBB breakdown. In the present study we investigated the neurophysiological, structural and functional consequences of BBB disruption. Adult rats underwent focal BBB disruption in the rat sensory-motor cortex using the bile salt sodium deoxycholate (DOC). Magnetic resonance imaging in-vivo showed an early BBB disruption with delayed reduction in cortical volume. This was associated with a reduced number of neurons and an increased number of astrocytes. In-vitro experiments showed that the threshold for spreading depression and the propagation velocity of the evoked epileptic potentials were increased 1 month after treatment. Furthermore, animals’ motor functions deteriorated during the first few weeks following BBB disruption. Treatment with serum albumin resulted in a similar cell loss confirming that the effect of DOC was due to opening of the BBB. Our findings suggest that delayed neurodegeneration and functional impairment occur following the development of the epileptic focus in the BBB-permeable cerebral cortex
ADVERSE EFFECTS: It is unclear what the side effects of Sodium Deoxycholate are, and it is not reviewed by the CIR or EWG. However, according to its MSDS, Sodium Deoxycholate is hazardous in case of eye contact (irritant), of ingestion, of inhalation. Slightly hazardous in case of skin contact (irritant). There was no information available on its potential carcinogenic or mutagenic effects.



IDENTIFICATION AND USE: Sodium phosphate monobasic dihydrate is a reagent with very high buffering capacity widely used in molecular biology, biochemistry and chromatography. Sodium phosphate dibasic is highly hygroscopic and water soluble. Useful in conjunction with Sodium Phosphate, Dibasic in the preparation of biological buffers. Used in many applications including the purification of antibodies.

ADVERSE EFFECTS lethargy, hyperpyrexia, diarrhea, carpal spasms, coma, renal acute failure, mucosal lesions, aphthous lesions.




IDENTIFICATION AND USE: At room temperature, sodium hydroxide is a white crystalline odorless solid that absorbs moisture from the air. It is a manufactured substance. When dissolved in water or neutralized with acid it liberates substantial heat, which may be sufficient to ignite combustible materials. Sodium hydroxide is very corrosive. It is generally used as a solid or a 50% solution.

Other common names include caustic soda and lye. Sodium hydroxide is used to manufacture soaps, rayon, paper, explosives, dyestuffs, and petroleum products. It is also used in processing cotton fabric, laundering and bleaching, metal cleaning and processing, oxide coating, electroplating, and electrolytic extracting. It is commonly present in commercial drain and oven cleaners.

ADVERSE EFFECTS: Breathing difficulty (from inhalation), lung inflammation, sneezing, throat swelling (which may also cause breathing difficulty), blood in the stool, burns of the esophagus (food pipe) and stomach, diarrhea, severe abdominal pain, vomiting, possibly bloody, drooling, severe pain in the throat, severe pain or burning in the nose, eyes, ears, lips, or tongue, vision loss, collapse, low blood pressure (develops rapidly), severe change in pH (too much or too little acid in the blood), and shock.




IDENTIFICATION AND USE: Sodium phosphate dibasic and sodium phosphate monobasic combination is used to clean or empty your bowels before an imaging procedure called colonoscopy. This medicine works by cleaning your colon and causing you to have diarrhea.

HUMAN EXPOSURE/TOXICITY: the FDA said it has become aware of reports of severe dehydration and changes in serum electrolyte levels from taking more than the recommended dose of OTC sodium phosphate products, resulting in serious adverse effects on organs, such as the kidneys and heart, and in some cases resulting in death.

“The predominant electrolyte disturbances were hyperphosphatemia, hypocalcemia, and hypernatremia,” the FDA said.

The problem surfaced in a review of the agency’s Adverse Event Reporting System database and the medical literature, which turned up 54 cases in 25 adults and 29 children of serious adverse events associated with the oral or rectal use of OTC sodium phosphate drug products used to treat constipation, the FDA said.

“According to the reports, most cases of serious harm occurred with a single dose of sodium phosphate that was larger than recommended or with more than 1 dose in a day,” the FDA said.

USE WITH CAUTION: individuals who may be at higher risk for potential adverse events when the recommended dose of OTC sodium phosphate is exceeded include young children; individuals older than 55 years; patients who are dehydrated; patients with kidney disease, bowel obstruction, or inflammation of the bowel; and patients who are using medications that may affect kidney function.

ADVERSE EFFECTS: allergic reaction: itching or hives, swelling in your face or hands, swelling or tingling in your mouth or throat, chest tightness, trouble breathing, blood in your urine, lower back pain, side pain, or sharp back pain just below your ribs, confusion, weakness, and muscle twitching, decrease in how much or how often you urinate, dizziness or fainting, dry mouth, increased thirst, muscle cramps, nausea or vomiting, fast, pounding, or uneven heartbeat, red or black stools, seizures, severe stomach pain, nausea, vomiting, or bloating.




IDENTIFICATION AND USE: a polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications.

ADVERSE EFFECTS: abdominal cramps, abdominal pain, diarrhea. May cause respiratory tract irritation. May cause skin irritation. May cause eye irritation. The substance may cause effects on the gastrointestinal tract. Finely dispersed particles form explosive mixtures in air.




IDENTIFICATION AND USE: this peptone is obtained by papaic digestion of soya flour. In addition to its nitrogen constituents, this peptone has a high carbohydrate content and is suitable for many purposes. It is widely used in culture media and is often used for the cultivation of many fastidious organisms and where rapid, luxuriant growth is required. However, due to this high content of sugar it is not recommendable for fermentation assays.

HUMAN EXPOSURE/TOXICITY: soybeans contain phytoestrogens, which mimic the body’s natural estrogen hormones. For men, this can lead to a testosterone imbalance, infertility, low sperm count, and increased risk of cancers.

For women, it can cause estrogen dominance, which has been linked to infertility, menstrual troubles and cancer. These phytoestrogens are so strong that a baby consuming only soy formula is consuming the equivalent hormones of 4 birth control pills a day. The high levels of phytic acid in soy inhibit the body’s ability to absorb important minerals, including zinc, calcium, copper, iron and magnesium (which many people are dangerously deficient in already).

Soy also contains protease inhibitors, which can block the enzymes that are necessary for the digestion of certain proteins. The goitrogens in soy are potent anti-thyroid compounds that can lead to endocrine disruption and thyroid disorders. Infants on soy formula have a much higher risk of autoimmune thyroid disease. (note: cruciferous vegetables like broccoli, cauliflower and cabbage have these properties as well, though they are lessened greatly by cooking.

Cooking does not remove these compounds from soy based foods!) Soy is often promoted as an alternative food for celiac and gluten intolerant people, but its lectins can be harmful to the intestines and prevent healing even when gluten is removed.

Soy is POSSIBLY UNSAFE when used as an alternative to cow’s milk in children who are allergic to cow’s milk. Although soy protein-based infant formulas are often promoted for children with milk allergy, these children are often allergic to soy as well.

Don’t give children soy in amounts larger than what is found in food or formula. Researchers don’t know whether soy is safe for children at higher doses.

Pregnancy and breast-feeding: soy protein is LIKELY SAFE to be used during pregnancy and breast-feeding when consumed in amounts normally found in food. However, soy may be POSSIBLY UNSAFE when used during pregnancy in medicinal amounts. Higher doses during pregnancy might harm development of the baby. Not enough is known about the safety of higher doses during breast-feeding. Stay on the safe side and avoid larger doses.

Children: soy is LIKELY SAFE for children when used in amounts commonly found in food or infant formula. Using soy formula does not seem to cause health or reproductive problems later in life. However, soymilk that is not designed for infants should not be used as a substitute for infant formula. Regular soymilk could lead to nutrient deficiencies.

ADVERSE EFFECTS: Cystic Fibrosis: Soymilk can interfere with the way children with cystic fibrosis process protein. Don’t give these children soy products.

Breast cancer: The effects of soy in people with breast cancer are unclear. Some research finds that soy might “feed” certain breast cancers because it can act like estrogen. Other studies have found that soy seems to protect against breast cancer. The difference in effects might have something to do with the amount taken. Because there isn’t enough reliable information about the effects of soy in women with breast cancer, a history of breast cancer, or a family history of breast cancer, it’s best to avoid using soy until more is known.

Endometrial cancer: Long-term use of concentrated soy isoflavone tablets might increase the occurrence of precancerous changes in the tissue lining the uterus. Don’t take concentrated soy isoflavone supplements if you have endometrial cancer.

Kidney failure: Soy contains a chemical called phytoestrogens. Very high levels of phytoestrogens can be toxic. People with kidney failure who use soy products might be at risk for blood levels of phytoestrogens becoming too high. If you have kidney failure, avoid taking large amounts of soy.

Kidney stones: There is some concern that soy products might increase the risk of kidney stones because they contain large amounts of a group of chemicals called oxalates. Oxalates are the main ingredient in kidney stones. Another concern is that people with serious kidney disease aren’t able to process some of the chemicals in soy. This could lead to dangerously high levels of these chemicals. If you have a history of kidney stones, avoid taking large amounts of soy.

Milk allergy: Children who are very allergic to cow’s milk might also be sensitive to soy products. Use soy products with caution.

Urinary bladder cancer: Soy products might increase the chance of getting bladder cancer. Avoid soy foods if you have bladder cancer or a high risk of getting it (family history of bladder cancer).

Under-active thyroid (hypothyroidism): There is a concern that taking soy might make this condition worse.

Asthma: People with asthma are more likely to be allergic to soy hulls. Avoid using soy products.

Hay fever (allergic rhinitis): People with hay fever are more likely to be allergic to soy hulls.

Diabetes: Soy might increase the risk of blood sugar levels becoming too low in people with diabetes who are taking medication to control blood sugar.




IDENTIFICATION AND USE: streptomycin is an antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis. Streptomycin is an Aminoglycoside Antibacterial and Antimycobacterial. The chemical classification of streptomycin is Aminoglycosides.

Streptomycin is a broad-spectrum aminoglycoside antibiotic typically used for treatment of active tuberculosis, always in combination with other antituberculosis agents. Streptomycin is usually used in combination with agents that are known to be hepatotoxic and the role of streptomycin in liver injury has been difficult to assess, but most information suggests that streptomycin is not hepatotoxic.

HUMAN EXPOSURE/TOXICITY: intravenous and intramuscular therapy with streptomycin has been linked to mild and asymptomatic elevations in serum alkaline phosphatase, but therapy rarely affects aminotransferase levels or bilirubin and changes typically resolve rapidly once streptomycin is stopped.

Only isolated case reports of acute liver injury with jaundice have been associated with streptomycin therapy and always in combination with other antituberculosis medications which are more clearly hepatotoxic, such as isoniazid, pyrazinamide and rifampin. Streptomycin and the aminoglycosides are not mentioned in large case series of drug induced liver disease and acute liver failure; thus, hepatic injury is exceedingly rare, if it occurs at all.

Nephrotoxic and ototoxic potential. Nephrotoxicity is caused by accumulation of the drug in proximal renal tubular cells, which results in cellular damage. Tubular cells may regenerate despite continued exposure and nephrotoxicity is usually mild and reversible. Streptomycin is the least nephrotoxic of the aminoglycosides owing to the small number of cationic amino groups in its structure. Otoxocity occurs via drug accumulation in the endolymph and perilymph of the inner ear. Accumulation causes irreversible damage to hair cells of the cochlea or summit of the ampullar cristae of the vestibular complex. High frequency hearing loss precedes low frequency hearing loss. Further toxicity may result in retrograde degeneration of the auditory nerve. Vestibular toxicity may result in vertigo, nausea and vomiting, dizziness and loss of balance. LD50=430 mg/kg (Orally in rats with Streptomycin Sulfate); Side effects include nausea, vomiting, and vertigo, paresthesia of face, rash, fever, urticaria, angioneurotic edema, and eosinophilia.

ADVERSE EFFECTS: common side effects include black, tarry stools, burning, crawling, itching, numbness, prickling, “pins and needles”, or tingling feelings, chest pain, chills, clumsiness, cough, dizziness or lightheadedness, feeling of constant movement of self or surroundings, fever, large, hive-like swelling on the face, eyelids, lips, tongue, throat, hands, legs, feet, or sex organs, nausea, painful or difficult urination, sensation of spinning, shortness of breath, sore throat, sores, ulcers, or white spots on the lips or in the mouth, swollen glands, unsteadiness, unusual bleeding or bruising, unusual tiredness or weakness, vomiting.

Less common side effects include back, leg, or stomach pains, bleeding gums, bloody or cloudy urine, blurred vision, change in vision, dark urine, deafness, difficulty with breathing, difficulty with swallowing, dry mouth, fast heartbeat, general body swelling, headache, hives, impaired vision, itching, loss of appetite, muscle weakness, nosebleeds, pain in lower back or side, pale skin, pinpoint red spots on the skin, puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue, skin rash, thirst, tightness in the chest, wheezing, yellowing of the eyes or skin.

Rare side effects include change in the frequency of urination or amount of urine, drowsiness, increased thirst, swelling of the feet or lower legs, and weakness. Severe toxic nerve reactions are possible for patients with kidney problems who use this medication. Kidney function and complete blood counts should be closely monitored by a health care provider while taking this medication. Appropriate medical equipment should be available for patients taking this medication.




IDENTIFICATION AND USE: a buffer that keeps the pH of a solution constant by taking up protons that are released during reactions, or by releasing protons when they are consumed by reactions. The observation that partially neutralized solutions of weak acids or bases are resistant to changes in pH when small amounts of strong acids or bases are added led to the concept of the ‘buffer’. Succinate buffer is prepared by dissolving succinic acid in distilled water. The pH of the buffer is adjusted with 0.2N sodium hydroxide.




IDENTIFICATION AND USE: Thiomersal (INN), or thimerosal (USP), is an organomercury compound. This compound is a well-established antiseptic and antifungal agent.

The pharmaceutical corporation Eli Lilly and Company gave thiomersal the trade name Merthiolate. It has been used as a preservative in vaccines, immunoglobulin preparations, skin test antigens, antivenins, ophthalmic and nasal products, and tattoo inks.

ANIMAL EXPOSURE/TOXICITY: researchers assigned 41 newborn monkeys to one of three exposure groups. Seventeen of the monkeys were injected with vaccines spiked with thimerosal for a total mercury dose of 20 micrograms per kilogram (μg/kg) at ages 0, 7, 14, and 21 days, mimicking the typical schedule of vaccines for human infants. At the same ages, another 17 monkeys received 20 μg/kg methylmercury by stomach tube to mimic typical methylmercury exposure. A third group of 7 monkeys served as unexposed controls.

The researchers drew blood from all monkeys prior to any exposure and at other points prior to sacrifice, which occurred 2, 4, 7, or 28 days after the last dosing on day 21. Total mercury concentrations were measured in blood samples, and total and inorganic mercury concentrations were measured in brain samples. Organic mercury concentrations were calculated from those values.

The initial absorption rate and tissue distribution of mercury was similar in both exposed groups. However, total mercury progressively accumulated in the blood of methylmercury-exposed monkeys and remained detectable 28 days after the last dose. Among thimerosal-exposed monkeys, total mercury in blood declined rapidly between doses, and the researchers estimated clearance to be 5.4-fold higher than in the methylmercury group. In the thimerosal group, the half-life of total mercury in blood was 6.9 days, compared to 19.1 days for the methylmercury group.

Brain concentrations of total mercury were approximately 3–4 times lower in the thimerosal group than in the methylmercury group, and total mercury cleared more rapidly in the thimerosal group (with a half-life of 24.2 days versus 59.5 days). However, the proportion of inorganic mercury in the brain was much higher in the thimerosal group (21–86% of total mercury) compared to the methylmercury group (6–10%). Brain concentrations of inorganic mercury were approximately twice as high in the thimerosal group compared to the methylmercury group. Inorganic mercury remains in the brain much longer than organic mercury, with an estimated half-life of more than a year. It’s not currently known whether inorganic mercury presents any risk to the developing brain.

Given these findings, the researchers caution that risk assessments for thimerosal based on studies using blood mercury measurements may not be valid, depending on the design of the study. Further, the observed differences in distribution and breakdown of mercury compounds between exposed groups indicate that methylmercury is not a suitable model for thimerosal toxicity.

The researchers emphasize, however, that the risks associated with low-level exposures to inorganic mercury in the developing brain are unknown, and they describe other research linking persistent inorganic mercury exposure with increased activation of microglia in the brain, an effect recently reported in children with autism. They recommend further research focused specifically on the biotransformation of thimerosal and its neurotoxic potential.

HUMAN EXPOSURE/TOXCITY: delayed-type hypersensitivity reactions from thimerosal exposure are well-recognized. Identified acute toxicity from inadvertent high-dose exposure to thimerosal includes neurotoxicity and nephrotoxicity. Limited data on toxicity from low-dose exposures to ethylmercury are available, but toxicity may be similar to that of methylmercury. Chronic, low-dose methylmercury exposure may cause subtle neurologic abnormalities.

Depending on the immunization schedule, vaccine formulation, and infant weight, cumulative exposure of infants to mercury from thimerosal during the first 6 months of life may exceed EPA guidelines. Dr. Hooker, a PhD scientist, worked with two members of Congress to craft the letter to the CDC that recently resulted in his obtaining long-awaited data from the CDC, the significance of which is historic. According to Hooker, the data on over 400,000 infants born between 1991 and 1997, which was analyzed by CDC epidemiologist Thomas Verstraeten, MD, “proves unequivocally that in 2000, CDC officials were informed internally of the very high risk of autism, non-organic sleep disorder and speech disorder associated with Thimerosal exposure.

Mercury has no positive role in the human body; in fact a safe level of mercury exposure is very difficult to determine. It can be present in the environment in several different forms, and while all forms of mercury are toxic to humans, the pattern of toxicity varies with its chemical form, the route of exposure, the amount, the duration and timing of exposure, and the vulnerability of the person exposed. For example, pure elemental mercury (also known as quicksil-ver or Hg) is liquid at room temperature.

If ingested, quick-silver has very low toxicity because it is not absorbed by the gastrointestinal tract and is eliminated completely in the stool. If quicksilver is agitated or heated, however, the liquid mercury becomes a vapor which is readily absorbed by inhalation and is highly toxic to the lungs and central nervous system. The nervous system is the primary target of mercury toxicity, but, depending upon the specific exposure, the kidneys, liver and lungs are also important targets.

High doses of mercury can be fatal to humans, but even relatively low doses of mercury containing compounds can have serious adverse impacts on the developing nervous system, and have recently been linked with possible harmful effects on the cardiovascular, immune and reproductive systems. Mercury and its compounds affect the central nervous system, kidneys, and liver and can disturb immune processes; cause tremors, impaired vision and hearing, paralysis, insomnia and emotional instability.

During pregnancy, mercury compounds cross the placental barrier and can interfere with the development of the fetus, and cause attention deficit and developmental delays during childhood. Fetuses and young children are actively developing and therefore most at risk from health effects including neurological damage, resulting in behavioral problems and learning disabilities.

ADVERSE EFFECTS: neurological effects: Low doses of methyl mercury in pregnant women have been shown to have impacts on the fetus. In a major review of mercury health studies the US National Academy of Sciences stated: ‘Chronic, low-dose prenatal methylmercury exposure from maternal consumption of fish has been associated with …poor performance on neurobehavioral tests, particularly on tests of attention, fine-motor function, language, visual-spatial abilities (e.g. drawing) and verbal memory.

Cardiovascular effects: Two recent epidemiological studies found associations between exposure to low levels of methylmercury and adverse cardiovascular effects. The US National Academy of Sciences concludes that additional studies are needed to better characterize the effect of methyl mercury exposure on blood pressure and cardiovascular function at various stages of life. The European Commission also notes recent evidence suggesting that mercury from fish and seafood may promote or predispose the development of heart disease.




IDENTIFICATION AND USE: xanthan gum is a sugar-like compound made by mixing aged (fermented) sugars with a certain kind of bacteria. It is used to make medicine. Xanthan gum is used for lowering blood sugar and total cholesterol in people with diabetes. It is also used as a laxative.

Xanthan gum is sometimes used as a saliva substitute in people with dry mouth (Sjogren’s syndrome). In manufacturing, xanthan gum is used as a thickening and stabilizing agent in foods, toothpastes, and medicines. Xanthan gum is also an ingredient in some sustained-release pills.

Xanthan gum swells in the intestine, which stimulates the digestive tract to push stool through. It also might slow the absorption of sugar from the digestive tract and work like saliva to lubricate and wet the mouth in people who don’t produce enough saliva.

HUMAN EXPOSURE/TOXCITY: a 7-day control period, 5 male volunteers consumed, on each of 23 consecutive days, a weight of xanthan gum equal to 15 times the current acceptable daily intake (10 mg/kg b.w.) approved by the EEC and by the Joint FAO/WHO Expert Committee on Food Additives; thus, the lightest and heaviest of the volunteers consumed 10.4 g and 12.9 g respectively of xanthan daily.

Measurements before and at the end of the test period showed that the ingestion of xanthan, as a pre-hydrated gel, acted as a bulking agent in terms of its effects on faecal wet and dry weight and intestinal transit time but had no significant effect on plasma biochemistry, haematological indices, urinalysis parameters, glucose tolerance and insulin tests, serum immunoglobulins, triglycerides, phospholipids and HDL cholesterol, breath hydrogen and breath methane concentrations.

There was a moderate (10%) reduction in serum cholesterol and a significant increase in fecal bile acid concentrations. The data indicate that the ingestion of xanthan caused no adverse dietary nor physiological effects in any of the subjects. In particular, all of the enzymatic and other parameters that act as sensitive indicators of adverse toxicological effects remained unchanged.

ADVERSE EFFECTS: xanthan gum is safe when up to 15 grams per day are taken. It can cause some side effects such as intestinal gas (flatulence) and bloating. People who are exposed to xanthan gum powder might experience flu-like symptoms, nose and throat irritation, and lung problems.

Pregnancy and breast-feeding: Not enough is known about the use of xanthan gum during pregnancy and breast-feeding. Stay on the safe side and avoid using amounts larger than those normally found in foods.

Nausea, vomiting, appendicitis, hard stools that are difficult to expel (fecal impaction), narrowing or blockage of the intestine, or undiagnosed stomach pain: Do not use xanthan gum if you have any of these conditions. It is a bulk-forming laxative that could be harmful in these situations.

Surgery: Xanthan gum might lower blood sugar levels. There is a concern that it might interfere with blood sugar control during and after surgery. Stop using xanthan gum at least 2 weeks before a scheduled surgery.




IDENTIFICATION AND USE: proteins in yeast is a common alternative to prokaryotic and higher eukaryotic expression. Yeast cells offer many of the advantages of producing proteins in microbes (growth speed, easy genetic manipulation, low cost media) while offering some of the attributes of higher eukaryotic systems (post translational modifications, secretory expression).

Several yeast protein expression systems exist in organisms from the genera Saccharomyces, Pichia,Kluyveromyces, Hansenula and Yarrowia.

HUMAN EXPOSURE/TOXCITY: study indicates that a significant factor in causing them may be the common bakers or brewer’s yeast, Saccharomyces cerevisiae used in many vaccinations, including HepB, which is given to nearly all newborn babies in the United States before they’re a day old. The specific part of S. cerevisiae that’s of concern is mannan, which is found in the cell walls of yeasts and also in mammalian glycoproteins. These glycoproteins are found in cell walls, connective tissues like collagen, gastrointestinal mucous secretions, and blood plasma. They perform many functions. Obviously, if the immune system goes on the attack against mannan, it can be devastating. Yet, that appears to be happening in many autoimmune diseases. These diseases happen when the body’s own defense system turns on itself, resulting in life-eroding conditions like rheumatoid arthritis, Crohn’s disease, inflammatory bowel disease, systemic lupus erythematosus, anti-phospholipid syndrome, multiple sclerosis, diabetes mellitus type 1, and even heart disease.

The Centers for Disease Control (CDC) has no doubt about the increase in autoimmune diseases and the National Institutes of Health (NIH) has produced a nice document outlining their approach to dealing with it. The “Autoimmune Diseases Research Plan” discusses their approach to dealing with the issue, including the type of research they’re supporting. Nowhere is there any indication that vaccinations are being considered as a potential cause.

Yeast is, of course, used to make bread rise and create the alcohol in beer. So how can it suddenly turn into an enemy? The answer is in how it enters the body, and what enters with it. The purpose of a vaccine is to create a localized storm in the immune system so that it will respond to a co-injected substance, which may be a weakened microbe or a small bit of a microbe, by creating antibodies to it. An irritant, called an adjuvant, is what causes the immune system storm, and the microbe is called an antigen. The catch is that other substances injected with the antigen and adjuvant may also be seen as antigens.

If one of those substances is similar to something that naturally exists in the body, then the immune system may create antibodies to part of its own body, creating an autoimmune disease. Parts of the mannan in yeast are similar or identical to parts of the human body. So S. cerevisiae—yeast—used in vaccines has the potential of causing autoimmune disorders. In fact, S. cerevisiaeis used in a variety of ways in vaccines. It is, when used whole, a potent adjuvant. On top of that, genetic manipulation is now being used on it to create artificial antibodies, so S. cerevisiae is becoming more common in vaccines. The researchers who focused on autoimmune aspects of S. cerevisiae (yeast) found significant correlations between yeast’s mannan and known autoimmune antigens in several autoimmune diseases.

ADVERSE EFFECTS: they found close and, in some instances, exact matches of the genetic sequences. For example, in the case of rheumatoid arthritis, the percent found to match were:


  • Rheumatoid factor: 60%
  • Bip/GRP78: 71%
  • gp130-RAPS: 80%
  • EIF4G1: 88%
  • Anti-citrullinated collagen type 2: 100%

Not only were there significant sequence matches with four known rheumatoid arthritis auto-antigens, there was a perfect match with one. In other conditions, they found:


  • SmN: 53%
  • SSA (Ro): 60%
  • snRNP-SmD3: 64%
  • SSB (La): 69%
  • U2 snRNP B”: 83%


  • P-selectin (protein on surface of blood vessels & platelets): 80%
  • Myosin (involved with muscle contraction): 88%
  • Intercellular adhesion molecule-1 (inflammatory response molecules): 100%


  • β2-Glycoprotein-1 precursor: 56%
  • Annexin A5: 63%
  • Anti-CL/β-2GPI Ig light chain variable region: 73%


  • Thyroglubulin: 52%
  • GAD65: 57%
  • Zinc transporter 8: 57%
  • Transglutaminase: 60%
  • Thyroid peroxidase: 71%
  • Soluble liver/pancreas antigen: 80%
  • Calprotectin (protein S100-A8): 100%


  • Major centromere autoantigen B: 57%
  • RNA polymerase III: 67%
  • U3-snRNP fibrillarin: 75%
  • U3-snRNP MPP10: 75%
  • hU3-55kDA: 86%
  • Nucleophosmin B23: 88%

A perfect match with a molecule may not be necessary to result in an autoimmune response, so percentages of less than 100% may not indicate lack of an autoimmune response. However, the closer the match between a molecule and an antigen, the more likely it is that an autoimmune response will occur.

Although you may not generally think of heart disease as an autoimmune disorder, certain forms of it, such as rheumatic heart disease, are known to be—and as this study seems to indicate, others may be, too.