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Ranitidine, sold under the name of Zantac, is a medication that decreases stomach acid production. Zantac has recently been found to contain nitroso-dimethylamine (NDMA), a well-known carcinogen. The fact that NDMA causes cancer has been known since the 1950s, and its presence in Zantac is alarming. Nitrosamines in general were thought to increase the risk of cancer based on several animal studies. Early on, the International Agency for Research on Cancer (IARC) classified nitrosamines as probable human carcinogens, as has the EPA. NDMA is found at low concentrations in some foods such as cured meats, tobacco, and in some household products. The US FDA has suggested a limited daily exposure to NDMA of 96 nanograms (a nanogram is one billionth of a gram). One study reported an NDMA content in Zantac in excess of 2 million nanograms per tablet, while another study using simulated stomach acid containing Zantac reported an NDMA content of 300,000 nanograms per Zantac tablet which is still 3000 times the FDA's recommended daily intake limit.

There is some evidence that the active ingredient in Zantac, ranitidine, imported from India and China, included NDMA as a contaminant. There are still other reports that ranitidine, the major component of Zantac, may breakdown forming NDMA on its own. One study reported a significant concentration of NDMA in urine after ingesting ranitidine. Both sources of NDMA may be appropriate to consider, but its presence in such high levels in Zantac tablets puts the users of this medication at high risk of developing cancer.

Exposure of workers to nitrosamines have resulted in increased incidences of cancers at various sites in man. These workers are reported to have increased mortality from cancers of the esophagus, oral cavity, colorectal, uterus, pharynx, liver, prostate, and brain. Other studies suggest an increased risk of kidney, stomach, colon, bladder, and pancreatic cancers. NDMA is a known human carcinogen. Its presence in Zantac exposes man to increased risk of various cancers.

Known Health Risks

After a review of the world's literature on the health effects of vaping on adolescents and adults, it is difficult not to conclude that there is insufficient data available to provide any significant evidence as to the long-term health effects of vaping since no long-term human epidemiological studies have been reported. Further complicating the situation is the fact that there are numerous products being used with many different flavorants, and the quality control of these products is virtually non-existent. There are, however, many red flags.

While E-cigarettes are made to deliver habit-forming nicotine to the user, there are a number of other components to the E-liquid that goes into the device including propylene glycol and glycerol which when volatilized produce the smoke that emanates from the smoker's lungs. Other components of the smoke include ethylene glycol, diethylene glycol, methylglyoxal, acetyl propionyl, and acetoin. When vaporized in the E-cigarette apparatus, these materials have been shown to decompose forming formaldehyde, acetaldehyde, acrolein, butyraldehyde, and diacetyl, the latter being the cause of "popcorn lung" among flavoring workers. Beyond that, exposure to formaldehyde is known to result in respiratory sensitization and can also result in cross-sensitization to other aldehydes, including those found in perfumes. Formaldehyde is found also in some building products and adhesives, leaving the smoker susceptible to many potential sources capable of exacerbating a respiratory asthma-type attack. Acrolein is another aldehyde that attacks and destroys respiratory tissue.

One of the other problems that results in inhaled contaminants is the finding of heavy metals in the inhaled smoke. Within the E-device, there are metal coils made up of nickel-chromium alloys as well as chromium-aluminum alloys. There are reports that show traces of other metals including copper, silver, zinc, and tin that can leach into the e-liquid, resulting in the device emitting nanoparticles of heavy metals in the smoke. The FDA has labeled both nickel and chromium as respiratory toxicants and carcinogens.

The world's literature contains no chronic long-term studies of the effects of using E-cigarettes. There are some reports of short-term studies which report effects on pulmonary function but no chronic studies and little or no quality control of the products being marketed. E-vaping appears to be popular among the younger generation, and as adolescents' lungs are developing, they are the most susceptible to permanent damage by serious respiratory toxicants present in the E-smoke.

Although long-term epidemiology studies on E-cigarettes have not been reported, there are studies on the components of the inhaled vapor emanating from them. E-cigarettes produce vapors containing some very potent respiratory toxins including acrolein and formaldehyde. While acrolein is capable of destroying lung tissue which can lead to pulmonary edema and other pulmonary deficits, formaldehyde inhalation can result in an allergic asthma-like condition including cross-sensitization to other aldehydes such as those used in perfume. Of course, there is the added problem that inhalation of nicotine, a main component of the vaping process, is highly addictive providing a gateway to tobacco smoking. Further, nicotine inhalation increases the risk of emphysema, cardiovascular problems, and nervous system effects. Vaping carries an increased risk for heart disease and pulmonary deficits such as COPD and asthma-like syndromes. There is enough information on some of the components of E-cigarettes to support the opinion that the chronic use of E-cigarettes will result in lung damage and cardiopulmonary damage, particularly for young smokers.


Coal tar creosote is used extensively to preserve crossties on the railroad. Railroad workers have to handle these heavy wooden ties that are freshly coated with creosote. Typically, the railroad workers get creosote all over their hands and arms. The components of creosote are lipophilic in that they are soluble in fatty tissue and are stored in fatty tissue. They easily penetrate the skin and enter into general circulation in the body and are carried to critical organs resulting in organ specific mutations and increased risk of cancer.

Coal tar creosote contains over 200 components many of which are polynuclear aromatic hydrocarbons (PAHs). Several of these compounds are also present in cigarette smoke and are carcinogenic to man. One of the most studied multi-organ carcinogens in coal tar creosote is benzo(a)pyrene which has been known to increase the risk of cancer in man based on animal studies dating back to the 1970s. Although most of the components of coal tar creosote are not particularly volatile, benzene is also present in coal tar creosote and is readily inhaled during contact with creosote. Benzene is known to cause various blood dyscrasias including acute mylegenous leukemia.

Long-term exposure to coal tar creosote by contact with the skin greatly increases the risks of developing cancer in man. Workers handling railroad ties by hand should be protected from skin contact with the creosote and from inhalation of the volatiles in coal tar creosote.


Formaldehyde is ubiquitous. If you are allergic to it, it will cause you to suffer asthma-like pulmonary function deficits that will not only be triggered by formaldehyde itself, but also by other aldehydes commonly found in perfumes and other odorants. It also is capable of causing allergic reactions on skin in sensitized individuals. Formaldehyde is typically present in most homes from numerous sources including particle board which may be used in various cabinets, flooring, urea-formaldehyde insulation, tobacco smoke, fumes from gas stoves, cooking processes, and various consumer products including cosmetics and crease-resistant new clothing. Particle board is made up of wood chips held together with a phenol-formaldehyde resin which can off-gas formaldehyde. If you think that you are allergic to formaldehyde, you can go to your allergist and be patch tested; but this test is only meaningful if the results are positive. A negative test does not mean that you are not allergic to formaldehyde. Patch tests for formaldehyde have been shown to be unreliable in many cases. Formaldehyde is also a known animal carcinogen producing nasal tumors in rats, and a suspect human carcinogen linked to lymphatic and hematopoietic cancers including lymphoma, multiple myeloma, and leukemia; but the association is not strong. Formaldehyde also has been shown to result in mutagenicity and to produce chromosomal aberrations.


The contamination of drinking water in Flint, Michigan, is a disaster of massive proportions. Considering the fact that children have been exposed from the time that they were conceived in the womb to their birth and development represents a template for numerous neurological and developmental problems. Exposure from drinking water consumed by the mother while the child is still in the womb coupled with direct exposure of the neonate via drinking water and foods cooked in contaminated water results in exposure during the most critical period of a child's development.

The first three years of life is a period of incredible growth in the neonate. By age 3, the brain has grown dramatically producing billions of cells and hundreds of trillions of connections, or synapses, between these cells. Many of these developmental processes can be altered by the presence of lead in brain tissue.

Thus, children are the most susceptible to the toxic effects of lead. Lead is passed from mother to fetus and neonate via transplacental transfer and mother's milk. From fetus to neonate to young child, lead is accumulated faster in children than in adults, resulting in serious neurobehavioral problems, delayed developmental effects, and mental retardation. Lead is distributed to the brain, liver, kidney, and bones. Lead also disrupts hemoglobin formation causing anemia. Currently, no safe level of lead in a child's blood has been identified, but a level of 5 /dl is considered a good guideline for maximum lead levels in children; however, there are scientific studies showing adverse effects at blood levels of less than 5 /dl. In assessing the potential causal relationship in lead cases, we must be certain of the source. In the case of contaminated drinking water in Flint, Michigan, there is no question of the source.

National Institutes of Health Update:

For additional information see a March 2002 Centers for Disease Control and Prevention publication entitled "Managing Elevated Blood Lead Levels Among Young Children" [] and


The Animas River Is Dead - Heavy Metals
A strong statement, but not so far fetched when you consider that the River is contaminated with cadmium (probably responsible for its yellow color), lead, arsenic, beryllium, copper, aluminum, and mercury at concentrations that exceed the EPAs own safe maximum contamination levels.

The Animas River is Dead - Health Effects
Still a strong statement but note that the levels being measured in the water at this time present an immediate health problem for those using the water source for drinking and irrigating crops. Animals will also be affected. Most effects of heavy metals are not immediately experienced, but many of them result from the accumulation of heavy metals in the body which may produce chronic effects including kidney damage, central nervous system damage particularly in young people and newborns, and, indeed, cancer, among other effects. In essence, the Animas River is dead to those who seek to use it to survive.

The Animas River is Dead - No Practical Solution
While the river may be cleansed as some of the soluble metal salts are washed downstream into New Mexico and Utah, it is truly what is left behind that guarantees that the Animas is dead. When the EPA breached the dam holding back the 3 million gallons of contamination from the gold mine, the release obviously contained both soluble salts of heavy metals (measured by the EPA on August 5th and 6th,) but also the more long lasting "insoluble" salts and heavy metals. These insoluble salts will settle to the bottom of the River mixing with silt and other organic matter. There is no practical manner to remove these sediments, unless the entire Animas River is dredged. Even then, the disruption of the silt bed will send more heavy metal sludge further downstream.

The Animas River is Dead - Heavy Metal Mobility
Since dredging is impractical, the only apparent alternative is to let the heavy metals sink into the silt. Insoluble heavy metals can be chelated or otherwise taken up by bacteria and other organisms in the silt and become mobile. A good example of this is the formation of methyl mercury from the insoluble heavy metal in the presence of such organisms. As the mercury is taken up in this way it works its way up the food chain and ends up in a larger organism such as the fish. This accumulation does not occur overnight, but it takes years. Fish become uneatable with associated health risks if consumed. Animals who drink the water and eat the fish also become contaminated. The Animas dies a slow death in this way with no practical way to stop it.

The Animas River is Dead - Misconceptions
Even though news programs show an official drinking the water, fish swimming actively in the water, and they speak of the Animas River cleansing itself, the Animas River is dead. These exhibitions are meant to calm the fears of local residents, but the Animas River is dead for years to come, if not forever.


Recently, I returned from a two-week business trip in Hong Kong. During that time, I provided five days of court testimony for the defense of a shampoo product containing trace amounts of 1,4-dioxane. What qualifies me to testify on such a topic? I am a board certified consulting toxicologist and a recognized expert witness in the field of toxicology. I have over 30 years of experience as a consultant in toxicology providing expert testimony in toxicology for both plaintiff and defense. In preparation for this case, I expended over 100 hours studying the issue of 1,4-dioxane in shampoo and other consumer products. Further, I have personally used 1,4-dioxane regularly as a solvent while doing research in the field of synthetic organic chemistry for over 10 years.

I became involved in this matter because a libel suit was brought against a magazine who claimed that the use of a particular shampoo would increase the risk of cancer. 1,4-dioxane has been shown to produce cancer in animals treated at doses that are 40,000 times or more greater than the doses that man would encounter in using shampoo. Animal studies showed an increase in cancer incidences that most probably resulted from cytotoxicity followed by cell proliferation and endogenous mutations leaving the tissue subject to promotion by 1,4-dioxane or other factors. A key piece of information is that 1,4-dioxane is not genotoxic. This fact makes it clear that there is a threshold for liver cancer in animal studies which has been demonstrated repeatedly. There is also a threshold in man, and I can clearly state, as others have, that there is no risk of cancer in man as a result of using shampoo containing as much as 30 ppm, or more. Similarly, other consumer products containing 30 ppm of 1,4-dioxane are safe to use without an increased risk of cancer.

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