Many bottled soft drinks and related beverages contain benzene, a well-known carcinogen. The EPA defines a "safe" level of benzene as zero. Yet the Environmental Working Group, a watchdog organization, found levels of benzene in soft drinks at levels between 5 and 138 parts per billion.

A fair amount of benzene is taken in by our bodies by air pollution and drinking water. The U.S. Food and Drug Administration has known for almost 15 years that potassium benzoate and sodium benzoate react with ascorbic acid to form benzenes. Potassium benzoate, sodium benzoate and ascorbic acids are all commonly used to preserve freshness in soft drinks.

The excess of diabetes reported for the Benzene Sub registry occurred in the group aged 10 to 17 years, suggesting it is likely that IDDM is the type of diabetes most prevalent. It has been demonstrated that most IDDM patients have autoantibodies to the pancreas (Lernmark et al., 1981), as well as to other organs Benzene has been shown to stimulate the hypothalamic-pituitary-adrenocortical (HPA) axis of mice (Hsieh et al., 1991), accompanied by increased ACTH/corticosterone release into the blood.

Corticosteroids are associated with the development of diabetes by reducing insulin sensitivity, or possibly by impairing islet function frequently associated with the development of impaired glucose tolerance. The secretion of anti-insulin hormones, such as growth hormones or adrenocorticotrophic hormone (ACTH), are also believed to play an important role in IDDM development (Rodriguez, 1986). Steroid hormones play an important role in determining the severity of beta cell damage in the infected mouse, with androgens and glucocorticoids being particularly critical (Craighead, 1981). Ethanol can enhance the immunosuppressive effects of benzene. In addition, it has been demonstrated that various benzene metabolites depress the production of interferon (Cheung et al., 1988; Popp et al., 1992). IDDM is associated with a variety of hematologic changes (such as anemia) and malignancies (such as lymphocytic leukemia, lymphoma, and multiple myeloma) that might be directly related to or simply coincidental with the diabetes (Bern, 1982). From the literature reported it can be seen that all of these conditions are also associated with exposure to benzene.

Anthropogenic emissions to the air are approximately 34,000 metric tons per year (USEPA, 1989), Absorption of benzene varies with route of exposure. In humans, respiratory uptake has been determined to vary from approximately 47% (Nomiyama and Nomiyama, 1974) to 80% (Srbova et al., 1950), although dermal absorption can range from 0.05% to 0.2% (Franz, 1984). Absorption data for oral exposure in humans is not available; however, in animals, absorption rates following oral exposure to benzene were found to be from 90% to almost 100% (Parke and Williams, Ingestion of contaminated food items has been suggested as a potentially important pathway of human exposure to benzene (Hattemer-Frey et al., 1990 and many foods contain high levels of benzene. Benzene is ubiquitous in the environment, having been measured in air, water, and human biological samples. The major environmental sources include automobile exhaust, automobile refueling, hazardous waste sites, underground storage tanks that leak, waste water from industries that use benzene, chemical spills, chemical manufacturing sites, and petrochemical and petroleum industries (Fishbein, 1992; Edgerton and Shah, 1992).

Recently drinking more than one soft drink daily -- whether it's regular or diet -- may be associated with an increase in the risk factors for heart disease and diabetes, Framingham researchers reported in Circulation: Journal of the American Heart Association. "In those who drink one or more soft drinks daily, there was an association of an increased risk of developing the metabolic syndrome." Metabolic syndrome is a cluster of cardiovascular disease and diabetes risk factors including excess waist circumference, high blood pressure, elevated triglycerides, low levels of high-density lipoprotein (HDL "good" cholesterol) and high fasting glucose levels.

Prior studies linked soft drink consumption to multiple risk factors for heart disease. However, this study showed that the association not only included drinking regular calorie-laden soft drinks, but artificially sweetened diet sodas as well, researchers said. "If you are drinking one or more soft drinks a day, you may be increasing your risk of developing metabolic risk factors for heart disease."

The researchers also observed that compared to participants who drank less than one soft drink daily, those who drank one or more soft drinks a day had a:

* 31 percent greater risk of developing new-onset obesity (defined as a body mass index [BMI] of 30 kilograms/meter2 or more);

* 30 percent increased risk of developing increased waist circumference;

* 25 percent increased risk of developing high blood triglycerides or high fasting blood glucose;

* 32 percent higher risk of having low HDL levels. "It didn't matter whether it was a diet or regular soft drink".

"Results also don't appear to be driven by the dietary pattern of soft drink users, i.e, by other food items that are typically consumed along with soft drinks," Vasan, the study author, said. So perhaps what we have blamed for so long, the high fructose corn syrups, the empty calories, the aspartame in soft drinks, is not the only thing causing an increase in these diabetic risk factors. In combination with benzenes, it is highly likely that we have found yet another toxic substance that adds to our inability to avoid diabetes.

"Diabetes may in fact be a major side effect of antibiotics and other common pharmaceuticals." - Dr. Lisa Landymore-Lim, Independent scientist for Atomic Health Limited

Doctors are on notice that many drugs have toxic effects that can participate in destroying insulin creation and cell receptivity to it. In her 1994 book, Poisonous Prescriptions, Landymore-Lim says that diabetes may in fact be a major side effect of pharmaceutical drugs. The book provides evidence from studies and hospital records. Diabetes, usually thought to be largely a genetic disorder, may actually have increased so much in the last 50 years due in large part to the proliferation in the use, and over-use, of medicines. In 2004 the American Diabetes Association, the American Psychiatric Association, the North American Association for the Study of Obesity, and the American Association of Clinical Endocrinologists made a similar announcement warning people to be careful to watch for signs they are developing diabetes, obesity or high cholesterol if they are taking Abilify, Clozaril, Geodon, Risperdal, Seroquel or Zyprexa. What medicines, food and water have increasingly in common are the chemical poisons they contain.

Researchers at the University of Liverpool recently released their studies that examined the toxic effects on nerve cells in the laboratory of using a combination of four common food additives -- aspartame, monosodium glutamate (MSG) and the artificial colourings brilliant blue and quinoline yellow. The findings of their two-year study were published at the end of 2005 in the journal Toxicological Sciences. The Liverpool team reported that when mouse nerve cells were exposed to MSG and brilliant blue or aspartame and quinoline yellow in laboratory conditions, combined in concentrations that theoretically reflect the compound that enters the bloodstream after a typical children's snack and drink, the additives stopped the growing of nerve cells and interfered with proper signaling systems. The mixtures of the additives had a much more potent effect on nerve cells than each additive on its own.

The study reported that the effect on cells could be up to four times greater when brilliant blue and MSG were combined and up to seven times greater when quinoline yellow and aspartame were combined, than when the additives were applied on their own. What we can begin to conclude is that future research is going to show how all the toxic chemicals in the food, air, water and medicines we consume are combining to destroy our health. Any one poison discussed here in sufficient quantity can destroy cell physiology, the pancreas beta cells, and diminish cell receptivity to insulin.

We are depending more and more on processed foods, and with each year, the FDA approves more and more chemicals for use in foods. With each year, the food industry is using more and more chemicals in their products. These chemicals increase shelf life, kill bacteria, improve taste, replace fats, replace carbohydrates, and cause chronic diseases that eventually kill people. Junk food is really a cover up image for something quite a bit nastier than the image that junk congers. Junk foods are actually slow-acting poisons because they come to us loaded with highly toxic chemicals. We can only imagine the worst when we think about FDA approval processes for in reality the FDA is poisoning the public. The FDA is the wellhead of most iatrogenic diseases and death. There is no excuse for an agency charged with protecting public health to have allowed the massive poisoning of the public via food, drugs and public water supplies.

Bisphenol A Exposure May Lead to Obesity

Bisphenol A (BPA) exposure may lead to obesity, altered glucose metabolism, insulin resistance and Diabetes. Not only are chemicals used in foods, affecting the rates of diabetes, but chemicals used in everyday plastics are contributing to the rise in obesity and insulin resistance.

Debate over BPA is one of the most contentious environmental health issues faced by government and industry. Traces are found in the bodies of nearly all Americans tested, and low levels -- similar to amounts that can leach from infant and water bottles –- mimic estrogen.

Extensive scientific literature reports adverse health effects from bisphenol A at very low doses. Studies show that bisphenol A can alter the expression of several hundred genes with effects varying among special tissues and depending upon the timing of exposure. More than 150 laboratory animal studies suggest that bisphenol A exposure at very low doses is linked to a staggering number of health problems, including prostate and breast cancer, obesity, hyperactivity, diabetes, altered immune system, lowered sperm count, and early puberty.

A study by Dr. Beverly Rubin and her colleagues at Tufts University Medical School showed that bisphenol A makes rodents grow larger after they are exposed in the womb, confirming similar findings from previous studies (17). When rats were fed 100 µg/kg/day of bisphenol A during pregnancy through lactation, their offspring were notably heavier after birth and into adulthood. Significantly, in the female offspring, the lower of the two bisphenol A doses used in the study produced a larger and more persistent effect on body weight relative to the higher dose. In addition, the fact that the effect persisted long after exposure for the female offspring suggests that bisphenol A may increase the number of fat cells in the rats and predispose them to heavier weight throughout life.

In 2002, a team of researchers at the Ehime College of Health Science in Japan discovered that bisphenol A can increase the conversion of embryonic cells into fat cells (18). In the body, this effect could result in larger numbers of fat cells developing. In addition to converting to fat cells, treated cells increased their fat content by 150 percent over 11 days. Combined with insulin, bisphenol A increased the fat content of cells by 1300 percent. In other words, this experiment documented that bisphenol A could trigger and promote the two main processes in developing obesity. In 2004, another study confirmed these findings, showing that bisphenol A alone and with insulin increased the uptake of sugar into fat cells (19).

A recent study by Dr. Paloma Alonso-Magdalena and her colleagues showed that low-level, chronic exposure of adult mice to 10 µg/kg/day of bisphenol A caused insulin resistance, the precursor to Type II diabetes in people as well as hypertension and cardiovascular disease (20). Dr. Alonso-Magdalena's study showed that even a single dose of bisphenol A at levels currently found in humans can result in altered levels of blood glucose and insulin, and twice daily exposure for just four days results in insulin resistance.

Several studies show an increased rate of postnatal growth in both males and females as a result of maternal doses between 2.4 and 500 µg/kg/day (21). Accelerated postnatal growth is associated not just with obesity but with insulin resistant diabetes, hypertension, and heart disease as well.

Is it any wonder that we are seeing the rising rate of diabetes in our children and adolescents? The use of bisphenol A and the products containing them have increased through the years as our use of glass and safer non plastic containers has decreased. Its hard to even find non-plastic onctainers for everyday use. And what is especially disturbing is news coming to light that bisphenol A is being used in baby bottles for the feeding of our infants at a very early age.

The number of children in the U.S. that are overweight have doubled in the last 30 years (National Institutes of Health). Currently about 20% of children, or one child in five is overweight. The increase is true for children and adolescents of all age groups and races and for boys and girls.

Rising Obesity Trend in Adolescents

Bisphenol A is a polycarbonate plastic. Bisphenol A-based polycarbonate is used as a plastic coating for children's teeth to prevent cavities, as a coating in metal cans to prevent the metal from contact with food contents, as the plastic in food containers, refrigerator shelving, baby bottles, water bottles, sport drink bottles, returnable containers for juice, milk and water, micro-wave ovenware and eating utensils. In a small prospective study, researchers in Japan report that bisphenol A levels are higher in women with a history of repeated spontaneous miscarriages. This research was based on proof that BPA causes meiotic aneuploidy in mice. Meiotic aneuploidy is the commonest cause of miscarriage in people.

The effects of this chemical on our chromosomes will reach into generations yet to come affecting not only ourselves, but our children and our grandchildren. Researchers have found that the effects of continual low dose exposures may not show up for years. Growing children are particularly at risk to toxic chemicals in their environment because they are physiologically more susceptible to them.

The Lancet analysed the prevalence of Type 2 diabetes in Ontario, Canada between 1995 and 2005. It found an increase of 69 per cent over the 10 years compared with the World Health Organisation's prediction of a 39 per cent increase between 2000 and 2030. Dr. Lorraine Lipscombe, of the Institute for Clinical Evaluation Science, Toronto, said that it also saw a higher rise in the rate of cases in younger people under 50 than in older people. "A 27 per cent increase has taken place after only five years," she said. "Rising rates of obesity could be the cause of this striking growth and effective public health interventions to manage and prevent obesity are sorely needed."

The CDC says that diabetes is disabling, deadly and on the rise. The incidence of diabetes is skyrocketing not only in adults but in the juvenile population as well. Healthcare experts have called the alarming rise in diabetes and its related complications "an epidemic" that threatens to spiral out of control.

In 1997, 15.7 millions adults in the United States were reported to have diabetes. By the year 2002, this number had already swelled to 18.0 million or 8.7% of all adults. Diabetes and its complications now claim hundreds of thousands of lives in the U.S. each year, incurring total expenses of over $130 billion in direct and indirect costs to the healthcare system. Worldwide, the number of people with adult-onset diabetes is predicted to explode in the next 10 years, doubling to an estimated 221 million people. By contrast only 43,171 people in the United States were diagnosed with AIDS and only 18,017 died.

Scientists have discovered a variant gene that leads to a sizable extra risk of Type 2 diabetes -- 38 percent of Americans who have inherited a single copy of the gene have a 45 percent greater risk of Type 2, the estimated 7 percent who carry two copies are 141 percent more likely to develop the disease. What scientists are saying is that if all the variant genes in the population were erased, so would be 21 percent of diabetes cases. Another way of expressing variations in genetic makeup is constitution. Some people are gifted with stronger constitutions (genes) than others and are more able to stand up to massive chemical assaults on their bodies. Genetic causes do not in anyway explain the explosive increases in diabetes but increasing concentrations of environmental poisons penetrating our bodies via our air, water, food and medicines can evoke breakdowns in genetic function.

Women who reported mixing and applying agricultural pesticides during early pregnancy have a two times higher risk of developing gestational diabetes during the pregnancy. The strong association between first trimester pesticide exposure and gestational diabetes mellitus suggests that pesticide exposures may affect glucose metabolism and insulin resistance. Specifically, four herbicides (2,4,5-T; 2,4,5-TP; atrazine; or butylate) and three insecticides (diazinon, phorate, or carbofuran) were associated with reporting gestational diabetes. Women who reported agricultural pesticide exposure (mixing or applying pesticides to crops or repairing pesticide application equipment) during pregnancy were more than twice as likely to report GDM as compared to women reporting no pesticide use in pregnancy.

Exposure to dioxins by any route is known to cause various systemic effects in exposed animals. The general population is exposed to small amounts of dioxins, as exemplified by the fact that dioxins have been found in virtually all samples of adipose tissue and blood (serum lipids) from individuals with no known previous exposure. It is primarily the dioxins with chlorine atoms in the 2, 3, 7 and 8 positions that are retained in animals and humans and which selectively concentrate in body fat and lipids. A recent study on the health status of Vietnam veterans who participated in Operation Ranch Hand did not find any signs of liver disease, but did report increased levels of triglycerides and cholesterol in the blood (a second report does not support these increases). In addition, an increase in body fat, diabetes, and blood pressure were also noted. These effects were strongly associated with TCDD levels in the serum.

Ranch Hand veterans also had changes in blood (increased white blood cells, platelet, IgA, and sedimentation rates) which suggest a chronic inflammatory response. It has take two decades of litigation for the U.S. Government to finally recognize the devastating effects of dioxin exposure that have disabled our veterans with cancers and diabetes. The average time it takes to remove one half of the TCDD from the body is around 7 years. The half-lives of other dioxins in the body are not known. About 98% of the daily intake of dioxins for the general population comes from ingesting food and milk. Inhalation exposure to dioxins for the general population constitutes a minor portion of daily intake. Average intake of TCDD for adults has been calculated to be about 25 picograms (pg) per day or 0.35 pg per kilogram (kg) of body weight per day. If all dioxins and furans are included and TEFs are used, the total average daily intake of TCDD equivalents for adults is about 90 pg/day or 1.3 pg/kg body wt/day.

There are numerous other sources that contribute to dioxins in the environment. Dioxins are known to form concurrently with furans during combustion processes such as: incineration of municipal solid waste and industrial waste, and are associated with ash generated in the incineration process. Emissions from these sources vary greatly and depend on management practices and the applied technologies. Combustion of many chlorine-containing materials (such as plastic material like polyvinyl chloride, paper, wood treated with pentachlorophenols, pesticide-treated waste, and PCBs) can produce dioxins and furans. Dioxins and furans have also been detected in emissions from coal-fired power plants, home-heating systems, exhaust from cars running on leaded gasoline, and cigarette smoke.

Phthalates are a group of man-made chemicals that are structurally related to the organic acid, phthalic acid. The most important use of phthalates is in plastics, especially PVC where they act as plasticisers. Phthalates are also present in a wide range of industrial, household and consumer products, including personal care products. such as nail polish, hair sprays, soaps, shampoos, perfumes, moisturizers. They are found in pipes, vinyl wall and floor coverings, roofing materials, safety glass, car parts, lubricating oils, detergents, food packaging, adhesives, paints, inks, medical tubing, blood bags, pharmaceuticals, footwear, electrical cables, stationery, and (until recently) in toys.

More than 75% of the U.S. population carries detectable levels of several phthalate metabolites. Studies have found associations between some phthalate metabolites and antiandrogenic effects in humans, including both infant and adult males. Recently a study published in Environmental Health Perspectives showed that exposure to phthalates correlated with two metabolic abnormalities in men: abdominal obesity and insulin resistance. Four phthalate metabolites were significantly associated with greater waist circumference and three with increased insulin resistance, PCP (organic chemical Pentachlorophenol) was used in the timber industry for years as a cheap treatment for sapstain, a fungal infection commonly found in softwoods such as pine. It is an organic chemical produced by reacting chlorine gas with phenol. The process creates a number of toxic impurities such as tetrachlorophenol, hexachlorobenzene and several types of dioxins and dibenzofurans. The main route of absorption is through the skin. Some of the more chronic health effects, including cancer and diabetes, do not appear until long after exposure. The sawmill workers were constantly exposed to PCP as they mixed chemicals and handled wet, treated timber.

According to the World Health Organization DIAMOND Project Group on Epidemics, a major difficulty in the area of IDDM research -- despite strong epidemiologic evidence that environmental agents are potent causes of IDDM (Diabetes Epidemiology Research International, 1987) -- is that the identification of such agents has been elusive. It is noteworthy that several recent epidemiologic studies have reported that the incidence of IDDM is increasing, suggesting that long-term changes in the environment are altering the probability of eventual diabetes.

Among the most pernicious substances ever created is a group of chemicals known as POPs or Persistent Organic Pollutants. Among them: DDT, dioxins, PCBs and Chlordane. And even though twelve POPs -- the so-called "dirty dozen" -- were restricted or banned by international convention in 2003, they continue to pose a threat to people and wildlife because POPs accumulate in the food we eat. Virtually every person on the planet has POPs in their body and the chemicals have been linked to cancers, birth defects and disabilities. Now a group of researchers in Korea have found strong evidence linking POPs and diabetes.

Dr. David Carpenter, Professor of Environmental Health and Toxicology at the State University of New York at Albany, reviewed the Korean study and said, "Well, one considers individual pollutants the magnitude was between three and five fold increased risk but the most striking observation was when they considered the sum of all six pollutants that they monitored and they selected pollutants that we all have in our bodies so that very few individuals had levels below the level of detection. Under those circumstances they were getting increased risk of the order of thirty-eight fold which is absolutely enormous."

"The amount of persistent organic pollutants in each person's body is a reflection of their diet, where they live, what the concentration of these substances is in the air they breathe, and probably related to how rapidly they metabolize these compounds." - Dr. David Carpenter

Dr. Carpenter continued saying, "The most interesting observation in this paper is that there was no relationship between being obese and developing diabetes in those persons that did not have high levels of these organic pollutants in their bodies. It may well be that people that are obese eat much more animal fat than people that are not obese and these persistent organic pollutants are all found in animal fats. So the question really is whether it is the obesity that leads to the diabetes or rather the presence of these persistent organic pollutants. It may well be that it's the pollutants that cause the diabetes, not the obesity."

"In the human body these compounds last about ten years before you get rid of half of them. In the environment they're even more persistent." - Dr. David Carpenter

Food is not considered junk just because of high fat or sugar content, there is a long list of poisonous chemicals used by the food industry that are striking people down. And there are many serious nutritional deficiencies in today's food that diminish the bodies capacity to deal safely with these chemicals and heavy metals -- with magnesium and selenium deficiencies at the top of the list.

Magnesium deficiency is a predictor of diabetes; diabetics both need more magnesium and lose more magnesium than most people. In two new studies, in both men and women, those who consumed the most magnesium in their diet were least likely to develop type 2 diabetes, according to a report in the January 2006 issue of the journal Diabetes Care.

The human race is facing an abyss, a massive breakdown in body chemistry. All indications suggest that the medical industrial complex will not squarely face the facts and the research and will not work in earnest to reduce the chemical exposures the masses are facing. Too much money is involved in manufacturing hundreds of millions of tons of chemicals each year and huge fortunes are made by the economic elite in the sale of toxins that are dragging large segments of the population to their sick beds and early graves. Our civilization is poisoning itself and the medical and dental communities participate with passion.

References:

Yoon, JW et al. Effects of environmental factors on the development of insulin-dependent diabetes mellitus. Department of Microbiology and Infectious Diseases, Julia McFarlane Diabetes Research Unit, University of Calgary, Alberta, Canada. Clin Invest Med. 1987 Sep;10(5):457-69

Toxicity of Fluoride to Diabetic Rats. C.A.Y. Banu Priya et al; International Society for Fluoride Research; FLUORIDE 30 (1)1997, pp 51 - 58 (http://www.fluoride-journal.com/97-...)

Professor I.M. Trakhtenberg. Trakhtenberg, I.M. From Russian translation. Chronic Effects of Mercury on Organisms. In Place of a Conclusion Thiol poisons, especially mercury and its compounds, reacting with SH groups of proteins lead to the lowered activity of various enzymes containing sulfhydryl groups. This produces a series of disruptions in the functional activity of many organs and tissues of the organism.

Timoshina IV, Liubchenko PN, Khzardzhian VG. Ter Arkh. 1985;57(2):91-5. [Article in Russian] Examination of the exocrine function of the pancreas in 52 workers exposed to lead, including 36 with the symptoms of intoxication (mild in 33 and marked in 3) revealed the primarily hyposecretory response of acinar cells stimulated with pancreozymin and secretin, while the hyposecretory and dyspancreatic responses were recorded less frequently. The endocrine function of the pancreas was revealed to be also lowered, which was confirmed by the decreased blood fasting insulin content and low blood insulin content after glucose intake as well. The changes in pancreatic function are among the pathogenetic mechanisms of the abdominal syndrome observable during lead intoxication.

Shirng-Wern Tsaih et al. Lead, Diabetes, Hypertension, and Renal Function: The Normative Aging Study. Harvard Medical School, Boston, Massachusetts. Environmental Health Perspectives Volume 112, Number 11, August 2004

Cadmium sources: Tap water, fungicides, marijuana, processed meat, rubber, seafood (cod, haddock, oyster, tuna), sewage, tobacco, colas (especially from vending machines), tools, welding material, evaporated milk, airborne industrial contaminants, batteries, instant coffee, incineration of tires/rubber/plastic, refined grains, soft water, galvanized pipes, dental alloys, candy, ceramics. Increasing rates of type 2 diabetes worldwide suggest that diabetes may be caused by environmental toxins. Cadmium is a widespread environmental pollutant that accumulates in the pancreas and exerts diabetogenic effects in animals. To test the hypothesis that exposure to cadmium is associated with impaired fasting glucose and type 2 diabetes, we examined the associations between urinary cadmium and the prevalence of impaired fasting glucose (prediabetes) and diabetes in the Third National Health and Nutrition Examination Survey (NHANES III). In this large cross-sectional study, urinary cadmium levels are significantly and dose-dependently associated with both impaired fasting glucose and diabetes. These findings, which require confirmation in prospective studies, suggest that cadmium may cause prediabetes and diabetes in humans. Urinary cadmium, impaired fasting glucose, and diabetes in the NHANES III Pathophysiology/Complications - National Health and Nutrition Examination Survey Diabetes Care, Feb, 2003

Vandiver J, "Chicken Feed," Daily Times (Salisbury, Md.), January 4, 2004

Tseng CH, Tseng CP, Chiou HY, Hsueh YM, Chong CK, Chen CJ. Epidemiologic evidence of diabetogenic effect of arsenic. Toxicol Lett. 2002 Jul 7;133(1):69-76.

Tseng CH, Tseng CP, Chiou HY, Hsueh YM, Chong CK, Chen CJ. Epidemiologic evidence of diabetogenic effect of arsenic. Toxicol Lett. 2002 Jul 7;133(1):69-76.

Mahfuzar Rahman et al. Division of Occupational and Environmental Medicine, Department of Health and Environment, Faculty of Health Science Linkoping University Sweden. Department of Occupational and Environmental Health(DOEH), National Institute of Preventive and Social Medicine (NIPSOM), Mohakhali, Dhaka-1212 Bangladesh. American Journal of Epidemiology 1998; Vol. 148, No.2: 198-203 The crude prevalence ratio for diabetes mellitus among keratotic subjects exposed to arsenic was 4.4 (95% confidence interval 2.5-7.7) and increased to 5.2 (95% confidence interval 2.5-10.5) after adjustment for age, sex, and body mass index (http://www.ehponline.org/docs/2003/...) .

Lasky T, Sun W, Kadry A, Hoffman MK. Mean total arsenic concentrations in chicken 1989-2000 and estimated exposures for consumers of chicken. Office of Public Health and Science, Food Safety and Inspection Service, U.S. Department of Agriculture, Washington, DC, USA.

Tseng CH, Tseng CP, Chiou HY, Hsueh YM, Chong CK, Chen CJ. Epidemiologic evidence of diabetogenic effect of arsenic. Toxicol Lett. 2002 Jul 7;133(1):69-76.

A solution of alloxan at 2% diluted in saline at 0.9% was administered to the animals in a single dose corresponding to 40 mg of alloxan per kg of animal weight injected into their penial vein. Alloxan induces irreversible diabetes mellitus after 24 hours following its administration and the condition proves to be chronic by laboratory tests after seven days. Experimental Model of Induction of Diabetes Mellitus in Rats; Acta Cir. Bras. vol.18 no.spe S o Paulo 2003 (www.scielo.br/scielo.php?pid=S0102-...)

Researchers who are studying diabetes commonly use the chemical to induce the disorder in lab animals. Unfortunately, most consumers are unaware of alloxan and its potentially fatal link to diabetes because these facts are not well publicized, are hidden by FDA approval, and certainly doctors and the food industry are not informing parents that they and their children are being poisoned by white flour containing alloxan. Diabetes and Chemical Poisoning. (http://imva.info/)

Consumer Reports (Feb. 2006): (http://www.curezone.com/foods/aspar...)

(http://www.elpais.es/articulo/elpsa...)

Genetically Engineered Food Biotech, Biotechnology, GMO, Genetically Modified (http://www.organicconsumers.org/gel...)

Health Hazards of Genetically Manipulated Foods; (http://www.soyinfo.com/haz/gehaz.shtml)

Dr. Irina Ermakova added flour from a GM soya bean -- produced by Monsanto to be resistant to its pesticide, Roundup -- to the food of female rats, starting two weeks before they conceived, continuing through pregnancy, birth and nursing. Others were given non-GM soya and a third group was given no soya at all. She found that 36 per cent of the young of the rats fed the modified soya were severely underweight, compared to 6 per cent of the offspring of the other groups. More alarmingly, a staggering 55.6 per cent of those born to mothers on the GM diet perished within three weeks of birth, compared to 9 per cent of the offspring of those fed normal soya, and 6.8 per cent of the young of those given no soya at all. (http://www.organicconsumers.org/ge/...)

Malatesta M, Caporaloni C, Rossi L, Battistelli S, Rocchi MBL, Tonucci F, Gazzanelli G (2002) Ultrastructural analysis of pancreatic acinar cells from mice fed on genetically modified soybean. Journal of Anatomy 201:409-415

Agency for Toxic Substance and Dissease Registry (http://www.atsdr.cdc.gov/NER/BENZEN...) Foods Containing Benzene (level is ug/kg, where available)

Vegetables

* Dry red beans

* Leek

* Mushroom

* Onion, roasted

* Parsley

* Potato, cooked peel

* Soybean milk

* Trassi, cooked

Beverages

* Cocoa

* Coffee

* Jamaican rum (120)

* Tea

* Whiskey

Fruits

* Apple

* Citrus fruit

* Cranberry and bilberry

* Black currants

* Guava

* Cayenne pineapple

* Strawberry (trace)

* Tomato, hothouse

Dairy products

* Butter (0.5)

* Blue cheese

* Cheddar cheese

* Other cheese

Meat, Fish, and Poultry

* Cooked beef (2-19)

* Irradiated beef (19)

* Cooked chicken (<10)

* Egg, hard-boiled (500-1900)

* Egg, uncooked (2100)

* Haddock fillet (100 to 200)

* Lamb, heated (<10)

* Mutton, heated (<10)

* Veal, heated (<10)

* Codfish

Nuts

* Filbert, roasted

* Peanut, roasted

* Macadamia nut

Soft Drinks, Diet And Regular, Linked To Increase In Risk Factors For Heart Disease; 26 Jul 2007 (http://www.medicalnewstoday.com/art...)

Journal Diabetes Care. February 2004

Lau K, McLean WG, Williams DP, Howard CV. Synergistic Interactions Between Commonly Used Food Additives in a Developmental Neurotoxicity Test. Toxicol Sci. 2005 Dec 13; (http://www.ncbi.nlm.nih.gov/entrez/...)

U.S. Environmental Protection Agency's Current Safety Threshold for Bisphenol A. The current safety threshold established by the U.S. EPA -- called the reference dose (i.e., safe dose) -- was set based on animal experiments conducted prior to 1988 showing that 50 milligrams per kilogram of body weight caused weight loss in rodents. U.S. EPA declared 50 mg/kg/day the lowest observed adverse effect level, or LOAEL. To arrive at the current reference dose, U.S. EPA assumed without further study that a dose 1000 times lower than the LOAEL (i.e., 50 micrograms per kilogram per day, or 50 µg/kg/day) would be an acceptable reference dose. As over 40 studies now illustrate, the official reference dose of 50 µg/kg/day is well above the levels at which adverse affects have been found in numerous animal studies over the past decade. For example, Dr. Kembra Howdeshell and her colleagues found that the female offspring of pregnant mice fed bisphenol A at the low dose of 2.4 micrograms per kilogram per day experienced the early onset of puberty. If U.S. EPA were to use 2.4 µg/kg/day as a LOAEL and apply the same logic used to establish the current standard, thereference dose would be 2.4 nanograms per kilogram per day (ng/kg/day). A reference dose of 2.4 ng/kg/day would eliminate commercial uses of bisphenol A in food and beverage containers and products that babies are likely to put in their mouths. (http://www.telegraph.co.uk/news/mai...)

American Diabetes Association: Diabetes Facts and Figures [factsheet online] 1997 [cited August 1999][16 screens].

CDC. (http://www.cdc.gov/diabetes/pubs/pd...)

Brancati FL, Wang NY, Mead LA, Liang KY, Klag MJ. Body weight patterns from 20 to 49 years of age and subsequent risk for diabetes melli-tus. Arch Intern Med 1999;159:957-963.

Kopelman PG, Hitman GA. Exploding type II [correspondence]. Lancet 1998;352:SIV5.

HIV/AIDS Surveillance Report 2003;15. The finding is being reported in the journal Nature Genetics by researchers at Decode Genetics, a company in Reykjavik, Iceland, that specializes in finding the genetic roots of human diseases. January 16, 2006

Saldana TM, O Basso, JA Hoppin, DD Baird, C Knott, A Blair, MC Alavanja and DP Sandler. 2007. Pesticide exposure and self-reported gestational diabetes mellitus in the Agricultural Health Study. Diabetes Care. 30(3):529-34. (http://www.environmentalhealthnews....)

GreenFacts Digest on Phthalates - Phthalates and Metabolism: Exposure Correlates with Obesity and Diabetes in Men; Melissa Lee Phillips; Environ Health Perspect. 2007 June; 115(6): A312.