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| Brian Oshman ![]() Join Date: Apr 29 2001 Location: High Bridge, NJ Age: 41
Posts: 2,328
Rep Power: 13 ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | Re: Newbie Here: Overwhelmed..What do I do first? UK consumers who close their eyes and hold their breath may be at risk from the unknown effects of inhaling dihydroxyacetone (DHA), a chemical used in spray tans. In the US, the Food and Drug Administration (FDA) has issued warnings to consumers of spray tanning to take precautions, but there are no restrictions on the use or sale of DHA in cosmetic products in Europe. DHA was approved by the FDA in the 1970s, for application as a lotion or cream to external parts of the body, but not to the lips or any body surface covered by a mucous membrane or the area around the eye. DHA is used increasingly as a spray, but the FDA has never tested these sprays. 'We are not aware of any bad systemic effects of inhaling DHA,' said Jude McNally, director of the Arizona Poison & Drug Center, 'but the truth is, the testing has not been done and we just do not know.' DHA is the only skin-tinting ingredient with FDA approval. It works by reacting with amino acids in dead skin cells to produce a dark colour. DHA itself may not be dangerous, but many formulations that include DHA also include lead, arsenic and mercury, none of which are safe to inhale. This month the FDA recommended that commercial facilities specifically protect the area surrounding the eyes, lips, nasal passages and other mucous membranes. The US National Tanning Training Institute recommends the use of an exhaust fan with a filter to remove overspray. But the UK Health & Safety Executive admits there are no specific recommendations regarding using products containing DHA, despite increasing evidence that customers and spray operators are not using the protective equipment provided by manufacturers. The FDA advises that all users of spray tans ask the following questions: Is the entire area of the eyes protected from contact with the spray? Are lips and all mucous membranes, including nasal passages, the mouth and other more intimate areas, protected? Is there protection from inhalation or ingestion? If the answer is no, you should be worried. |
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| | #62 (permalink) |
| Brian Oshman ![]() Join Date: Apr 29 2001 Location: High Bridge, NJ Age: 41
Posts: 2,328
Rep Power: 13 ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | Re: Newbie Here: Overwhelmed..What do I do first? Even the FDA believes spray tans are dangerous -- although you most likely have never heard that. If you go to a spray tanning salon, you are likely to be told that the treatment is completely safe and has the full backing of the U.S. government. In fact, the spray tan solution, DHA, contains lead, mercury and arsenic. In the 1970's the U.S. government approved DHA for bronzers intended to be rubbed on your skin -- but it has not specifically approved its use in spray tan booths. When it is inhaled or sprayed onto the porous mucous membranes of your body, it can enter your bloodstream, leading federal regulators to call the procedure "unsafe". DHA has been known to cause coughing, difficulty breathing, fainting, and dizziness. The greatest danger comes if you undergo the procedure without protecting your eyes, nose and mouth. Sources: CBS3 May 17, 2006 Associated Content September 19, 2008 Dr. Mercola's Comments: As the misguided propaganda against sun exposure took off in the 1980s, alternatives to getting that glowing tanned look started to sprout. First came the self tanners that left you looking like a streaky carrot, followed by any number of lotions, powders, and eventually, spray tanning booths. As is usually the case, consumers tend to believe that if a product is on the market it must be safe. Unfortunately, that assumption often turns out to be wrong. And such may be the case with spray tanning booths as well. Spray tans are generally considered a healthy alternative to baking in the sun, but that quick tan can come at a steep price. Far steeper than tanning in the sun following safe tanning guidelines, and with absolutely none of the health benefits that the sun will provide. Most Significant Reason Why Spray Tans are Harmful They give you the illusion of health by allowing you and others to believe that you have had significant UVB exposure to improve your vitamin D levels, when in fact they don’t increase your vitamin D levels at all. If you have been reading this newsletter for any length of time you understand the enormous benefits of vitamin D. Are you really willing to exchange the cosmetic appeal for true health when it is relatively easy to get sun exposure in the summer, and safe tanning beds in the winter? So What’s in That Spray Tanning Solution? One of the main ingredients in today’s spray tanning solutions is dihydroxyacetone, a color additive that darkens your skin by reacting with amino acids in the surface layer of your skin. This is oftentimes abbreviated as DHA, but please do not confuse that with the healthy DHA omega-3 fat. Modern sunless tanning products contain anywhere between 1 percent to 15 percent DHA. The higher the concentration, the darker your tan gets as it develops over several hours. The industry claims DHA is a simple carbohydrate sugar solution, but some toxicologists disagree. Over four years ago, Dr. Thomas Pierce, a toxicologist who investigated the harmful effects of tanning beds, issued a warning that DHA is not as simple or harmless as it may seem. "It is not an ingestible sugar, and no one should be eating it," he said in a previous interview. Part of the problem is that the U.S. government’s regulations for DHA allow several contaminants, and many spray tan solutions contain lead, arsenic and mercury. Lead in particular is known to affect brain development, and no one knows how large the effect may be on your baby, should you be pregnant while using spray tanning. My advice would be to avoid spray tanning entirely, but especially during pregnancy to avoid unnecessary exposure to these dangerous toxins. These contaminants are allowable because DHA was originally approved by the FDA in the 1970s for topical application only. They never imagined it would be sprayed on in a fine mist that can come in contact with your lips, lungs or other sensitive membranes that can allow it to enter your blood stream. The FDA has never specifically approved the use of DHA in spray tan booths. In addition to DHA and potential lead, mercury and arsenic contaminants, spray tanning solutions can contain as many as 45 different ingredients. And no one really knows whether this chemical cocktail is safe or not. Potentially the harm could be great as chemicals are very easily absorbed through your skin, and the health benefits of spray tanning are nonexistent. What Does the FDA Say About Spray Tanning? According to the FDA: DHA is listed in the regulations as a color additive for use in imparting color to the human body. However, its use in cosmetics--including sunless "tanning" products--is restricted to external application (21 CFR 73.2150). According to the CFR, "externally applied" cosmetics are those "applied only to external parts of the body and not to the lips or any body surface covered by mucous membrane" (21 CFR 70.3v). The industry has not provided safety data to the FDA in order for the agency to consider approving it for use on these exposure routes, including "misting" from tanning booths. Naturally, when spray tanning you expose your entire body, including your eyes, nose, mouth, and potentially your lungs, to a very fine mist of DHA tanning solution. Some of the adverse reactions from spray tanning received by the FDA from consumers include: Rashes Coughing Dizziness Fainting Is Your Spray Tanning Salon Adhering to Safe Practices? Should you decide to use a spray tanning facility, the FDA advises you ask the following questions: Am I protected from exposure in my entire eye area? Am I protected from exposure on my lips and all parts of my body covered by mucous membranes? Am I protected from internal exposure caused by inhaling or ingesting the product? If the answer to any of these questions is "no," then you are not protected from the unapproved use of this color additive, and you should request safety measures to protect your eyes and mucous membranes and prevent inhalation. According to toxicologist Dr. Wade, you should simply walk out if a spray tan establishment does not insist you wear protection. "If the material is applied without protecting the eyes, nose and mouth, it's being applied incorrectly and could be harmful," he said in an interview with CBS. My Personal Advice? Avoid spray tanning booths and lotions entirely. A fake tan does not provide any health benefits whatsoever. Please remember the fact that the surface of your skin gets tanned by chemical means does not mean that your body is making vitamin D – a biochemical process that occurs when your skin is exposed to UVB radiation either from natural sunlight or from a safe tanning bed. Let met state it more simply. Having a tan, after safely exposing yourself to the sun or a safe tanning bed, IS healthy. Saturating your body with potentially toxic chemicals to give it some color is not. For more information about the numerous health benefits of safe sun exposure, please search my site. The value of regular sun exposure has been so ignored and warnings against it so deceptive, I wrote an entire book on this subject, called Dark Deception. What to Do if You Have You Been Harmed by a Cosmetic Product Anyone can report adverse reactions from cosmetic products, including sunless tanners, to the nearest FDA office, listed in the blue section of your telephone book. Or, you can contact the FDA's Center for Food Safety and Applied Nutrition, Adverse Events Reporting System (CAERS) by phone at (301) 436-2405 or by e-mail at CAERS@fda.hhs.gov . By reporting adverse reactions, you can help get unsafe products off the market. Related Links: Lack of Sunshine Causes One Million Deaths a Year Even If You Live in Sub Tropical Environments You Can Be Vitamin D Deficient Sunshine is Nature's Disease Fighter |
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| Brian Oshman ![]() Join Date: Apr 29 2001 Location: High Bridge, NJ Age: 41
Posts: 2,328
Rep Power: 13 ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | Re: Newbie Here: Overwhelmed..What do I do first? Health Risks of Lead Poisoning Lead is a toxin that has the ability to impede the development and function of every organ and system in the body. Once it enters the body, lead travels through the bloodstream. A small portion of the ingested lead remains in the bloodstream, while some is deposited and stored in the kidneys and brain. Most, however, is stored in the bones. This lead moves in and out of the bones as the body absorbs nutrients and grows. Lead stays in the body for a long time. The "half life" of lead in bone, or the time it takes half of the amount of lead stored in bones to leave the body, can be more than twenty years. Therefore, one can be lead poisoned through high exposure to lead during a short period of time (acute), or through low exposure over a long period of time (chronic). Even tiny amounts of lead can be dangerous to a person's health, and its effects on the body can be devastating and irreversible. Health Risks To Children The Center for Disease Control estimates that nearly two million American children under the age of six have at least low-level lead poisoning. The CDC also estimates that 10% of all children suffer from lead poisoning. Even children who appear to be healthy can have high levels of lead in their bodies. Children are usually lead poisoned by ingesting the invisible lead-contaminated dust through normal hand-to-mouth activity. A small child may eat paint chips or soil that contains lead. Children also are likely to place their hands or other objects covered with lead-contaminated dust into their mouths. They can breathe in lead-contaminated dust, especially during renovations that disturb painted surfaces. Lead poses a more serious threat to children than to adults because their growing bodies absorb more lead than adult's bodies, and their brains and nervous systems are more sensitive to the damaging effects of lead. The blood lead level of concern is 10 µg/dl or greater. Blood lead levels in children of 100 to 150 µg/dl are associated with swelling of the brain, resulting in severe brain damage and even death. Lead exposures this high in the United States are relatively rare today; however, these levels are encountered in industrialized countries that are not controlling lead exposures. At low exposures, the effects of childhood lead poisoning can include: impaired growth hearing loss behavior problems* headaches impaired short-term memory * Such as attention deficit hyperactivity disorder (ADHD). Health Risks To Adults Lead poisoning in adults occurs most often to those exposed to lead-contaminated dust in lead related jobs and hobbies. At high levels, the lead can have an adverse effect on various nerves, such as the motor nerves. This damage can result in the inability to maintain the hand or foot in a normal position due to weakness of muscle tone because of nerve damage ("wrist drop" or "foot drop"). According to a recent study published in the April 17, 1996, Journal of the American Medical Association (pp. 1171-1176), long-term exposure to lead is linked to an increased risk of hypertension in men. A second study published in the same issue (pp. 1177-1181) suggests that low-level lead exposure impairs kidney function in middle-aged and older men. Additional effects of prolonged lead exposure in adults can include: respiratory problems nerve disorders reproductive disorders digestive problems memory loss difficulties during pregnancy Health Risks To Pregnancies Approximately 4.4 million, or 9 percent, of U.S. women of childbearing age have elevated blood lead levels. Lead, which is stored in the bones, moves out of the bones with calcium. If a woman was previously exposed to lead, the lead stored in her body may be released at an accelerated rate as calcium moves from her body to the unborn child, especially if her diet is calcium-deficient. The tissues of the unborn baby can absorb lead as the infant develops in the womb. The developing brain is extremely vulnerable to the harmful effects of lead during this time. Due to the fact that lead can pass through the placenta to the fetus, a pregnant woman exposed to lead can place her unborn child at an increased risk of: low birth weight learning disabilities birth defects premature birth miscarriage still birth Health Risks To The Elderly Lead moves in and out of the bones with calcium, an essential nutrient for body cells. When calcium intake is insufficient, due to dietary deficiencies or hormonal changes, bones release the stored lead along with calcium. Osteoporosis intensifies the mobilization of lead stored in the bones, placing the elderly who have previously been exposed to lead at risk of suffering the effects of lead poisoning. |
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| | #66 (permalink) |
| Brian Oshman ![]() Join Date: Apr 29 2001 Location: High Bridge, NJ Age: 41
Posts: 2,328
Rep Power: 13 ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | Re: Newbie Here: Overwhelmed..What do I do first? Toxicology: How Mercury Harms Humans Elemental (metallic) mercury and all of its compounds are toxic, exposure to excessive levels can permanently damage or fatally injure the brain and kidneys. Elemental mercury can also be absorbed through the skin and cause allergic reactions. Ingestion of inorganic mercury compounds can cause severe renal and gastrointestinal damage. Organic compounds of mercury such as methyl mercury are considered the most toxic forms of the element. Exposures to very small amounts of these compounds can result in devastating neurological damage and death. For fetuses, infants and children, the primary health effects of mercury are on neurological development. Even low levels of mercury exposure such as result from mother's consumption methylmercury in dietary sources can adversely affect the brain and nervous system. Impacts on memory, attention, language and other skills have been found in children exposed to moderate levels in the womb. How do people get exposed to mercury? Air borne mercury is highly toxic when inhaled. How does it get in the air? Metallic mercury slowly evaporates when exposed to the air. The air in a room can reach unhealthy levels just from the mercury in a broken thermometer; Mercury may be released into the air when coal, oil, or wood are burned as fuel or when mercury-containing wastes are incinerated. The resulting mercury concentrations in outdoor air are usually low and of little direct concern. However, mercury in the air can fall to the ground with rain and snow, landing on soil or in bodies of water, causing contamination. Lakes and rivers are also contaminated when there is a direct discharge of mercury-laden industrial or municipal waste into the water. When mercury enters bodies of water, biological processes transform it to methylmercury, a highly toxic and bioaccumulative form. Fish can absorb methylmercury from their food and directly from water as it passes over their gills. The cycle of mercury in nature is complex. This illustration summarizes how methylmercury accumulates at the higher levels of the food chain and becomes concentrated in fish and animals that eat fish. Methylmercury in the water and sediment is taken up by tiny animals and plants known as plankton. Minnows and juvenile fish eat large quantities of plankton over time. Larger predatory fish consume many smaller fish, accumulating methylmercury in their tissues. The older and larger the fish, the greater the potential for high mercury levels in their bodies. Fish are caught and eaten by humans and animals, causing methylmercury to accumulate in human tissues. Most people are exposed to mercury by eating fish containing mercury. There is no method of cooking or cleaning them that will reduce the amount of mercury in a meal. From the mid-1950s to the 1970s, several mass poisonings took place in Japan and in Canada involving methylmercury from consumption of fish from contaminated waters. Although instances of poisoning from fish consumption in the U.S. have not been reported, the possibility of such poisoning has been a subject of concern. In the U.S., the number of states that have issued health advisories limiting consumption of fish has risen steadily from 27 states in 1993 to 41 states in 1999. A total of 2,073 advisories were issued.http://www.epa.gov/waterscience/fish/ Currently, concern is focused on the health impacts of chronic exposures to low levels of mercury from dietary sources. Preliminary estimates of mercury levels in hair and blood samples from the 1999 National Health and Nutrition Examination Survey suggest that approximately 10% of women have mercury levels within one tenth of potentially hazardous levels indicating a narrow margin of safety for some women. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.htm. The National Research Council (NRC) issued a report estimating that as many as 60,000 newborns a year in the U.S. are now at risk for adverse neurodevelopmental effects from dietary mercury http://www.nap.edu/books/0309071402/html/. These studies strongly support efforts to reduce methylmercury exposure. Occupational Health Hazards in Biomedical Facilities The most common potential mode of occupational exposure to mercury in biomedical facilities is probably via inhalation of vapors. If not cleaned up properly, spills of even small amounts of elemental mercury, such as may result from breakage of thermometers, can contaminate indoor air above recommended limits and lead to serious health consequences. Some organic mercury compounds such as methylmercury, find limited use in biomedical research procedures such as gel electrophoresis and as a reference in nuclear magnetic spectroscopy. At least two fatal exposures have occurred in laboratories. The most recently reported incident involved a chemistry professor with an interest in the toxicology of heavy metals. During an experiment performed in a fume hood, she accidentally spilled several drops of methylmercury onto a gloved hand. The spill was considered inconsequential and cleaned up without special measures. Approximately two months later, the professor began to develop symptoms of neurotoxicity. She died despite receiving aggressive chelation therapy and medical support |
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| Police Department ![]() | Re: Newbie Here: Overwhelmed..What do I do first? I am only going to say two things to Jamison1 and then I am out of this forum for good. I have been helping you on the side and then.....I just read the additional posts here. So...I am not longer going to offer my advice or assistance to you because of two things. 1. You totally redacted the article that you posted on here.... (More Young Women Get Skin Cancer Sun-Damaged Skin Slideshow Study Shows Increase in Melanoma Among Young Women) ...you know it and I know it because I have the article. You purposefully cut out and eliminated the info that supported UV exposure and tanning beds to make your point. You just lost your credibility with me. 2. You come to us and ask for help and I think we extended that professional courtesy to you. If we were all so "driven" to just promote our business and make money...WHY would we help others like you? Because we are good people, confident business men and women, mentors ...and most have been doing this longer than I have had birthdays so they are wise. If someone helps me to that extent I am forever grateful. I am not sure I would turn around and aim a shot gun at them. You are entitled to your opinion and your beliefs. Others may not agree and that is fine to debate but WHY you are opting to poke people in the chest that you are coming to for help is beyond me. If you wonder why it sparked so much response and outrage...well that is why. Wow! Therefore, even if you have a response to this I won't even take the time to read it because it is not worth my time anymore so if you respond you do it for yourself only. You can't say I did not warn you that people here are very educated on both subjects. A few articles clipped off the internet does not an expert make. Most people that know me know that I very hard to shake and I strive to never be unprofessional. But, in this case I can only say that it is disappointing to say the least to see the direction this took and read the "terms" used in posts to describe people here. In closing, I have NO doubt about the future success of your business. **Sorry to all TT people if I got personal but I invested time in helping this person I thought was genuine. Last edited by CrystalSS; 07-28-2009 at 11:08 PM. |
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| | #68 (permalink) |
| Brian Oshman ![]() Join Date: Apr 29 2001 Location: High Bridge, NJ Age: 41
Posts: 2,328
Rep Power: 13 ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | Re: Newbie Here: Overwhelmed..What do I do first? The Health Hazards of Arsenic: Arsenic is the most notorious of the chemicals contained in CCA. It is legendary as a poison - its use dating back thousands of years. Arsenic was known to Aristotle and Socrates, and used by Nero and other villains throughout history to poison their enemies. "Arsenic and Old Lace", a famous play by John Kesselring, easily comes to mind when one thinks about arsenic. Moreover, arsenic is also an element- it is atomic number 33 in our periodic table- and it is probably the most mysterious and multi-faceted element in the periodic chart. It is a metalloid element, but when refined, arsenic is tasteless, odorless and colorless. Since arsenic is ubiquitous, it is important to differentiate between inorganic arsenic, the type of arsenic found in pesticides and CCA, which is quite toxic, and organic arsenic, which is generally less toxic. In fact, one form of organic arsenic, arsenobetaine, occurs naturally in marine organisms where it is sometimes referred to as "fish arsenic" and is considered "practically nontoxic"(5). Even well-trained toxicologists are known to err on this point, that fish arsenic is not considered toxic, as there have been no reports of long term ill effects from the consumption of seafood. However, its chemical cousins, the inorganic arsenicals, such as the arsenic contained in CCA, are of great concern to all. The health hazards of arsenic are so wide and so varied that they take up hundreds of pages of text in public health service manuals published by the U.S. government (6). In addition, the California Environmental Protection Agency lists both forms of arsenic (arsenic trioxide and arsenic pentoxide) as carcinogens and developmental toxins under Proposition 65. To understand more about the human health hazards posed by arsenic, we shall review them in detail below. Please note that for brevity, hazards to plants, marine life and animals are omitted. 2.1 General and Systemic Effects of Arsenic Exposure: Due to the unfortunate exposure of several population groups around the world to arsenic in their water supplies, the adverse health effects of long term arsenic exposure are well known and well documented. They include the following systemic effects: 2.1.1 Toxicological: As previously mentioned, arsenic is a human poison (toxin). Mild chronic poisoning can occur at doses as low as 0.15 mg daily. According to the Journal of Pesticide Reform, "the lethal dose of arsenic for an adult human is between 1 and 2.5 milligrams per kilogram (mg/kg) of body weight"(7). Thus, for a typical adult male weighing 165 pounds (75 kg), the fatal dose can be as little as 75 milligrams. 2.1.2 Dermatological: Skin cancers in the form of basal cell or squamous cell carcinomas, are one of the most serious long-term dermatological health hazards from continuous exposure to arsenic. Other serious dermatological hazards from chronic arsenic exposure can include pre-cancerous actinic keratosis (AK), darkening of the skin (hyperpigmentation), Mees' lines in the fingernails, or hair loss. Papillomas (warts or corns), as well as hyperkeratosis (lesions) of the palms and soles of the feet and torso have also been evidenced. However, less serious effects from arsenic exposure can be manifested as just a skin irritation or rash. 2.1.3 Cardiovascular, Hepatic and Hematological: Cardiovascular side effects affecting the heart and arteries from chronic arsenic exposure include high blood pressure, irregular heartbeat, premature hardening of the arteries (arteriosclerosis), vascular lesions, diabetes mellitus, abnormal heart function and even myocardia. Hazards to the liver (hepatic effects) include cirrhosis, abnormal liver function, as well as symptoms such as "jaundice or simply an enlarged and tender liver"(8). Long term arsenic exposure can produces serious hematological (blood) problems ranging from anemia to more life-threatening ailments such as assorted forms of cytopenia, aplastic anemia and even acute leukemia in rare instances. Blackfoot's disease, a severe vascular disorder that causes a black discoloration of the feet and can lead to gangrene and limb amputation, is a well known complication of long term arsenic exposure, as seen in studies done in Bangladesh and Taiwan. 2.1.4 Respiratory: Continuous arsenic exposure can cause irritation and damage to the mucous membranes in nasal passages and airways, including pharyngitis and rhinitis, and can also aggravate symptoms of asthma. However, the greatest and most prevalent risk of prolonged arsenic exposure via inhalation is lung cancer. (see Carcinogenic effects below). 2.1.5 Gastrointestinal and Renal: The EPA's "Hazard Summary for Arsenic and its Compounds" states that "inhalation exposure to inorganic arsenic has resulted in gastrointestinal effects (nausea, diarrhea, and abdominal pain)"(9). Irritation of the digestive tract has also been common in the case of oral exposure(10). Other symptoms of oral or inhalational arsenic exposure can include dry mouth, severe nausea and vomiting, abdominal pain and cramps, internal bleeding and diarrhea. "Chronic low-dose arsenic ingestion…may produce a mild esophagitis, gastritis, or colitis with respective upper and lower abdominal discomfort. Anorexia, malabsorption and weight loss may be present."(8) The kidneys are also easily damaged by any oral exposure to arsenic, as they serve to excrete the arsenic and therfore tend to accumulate arsenic. This can result in a range of kidney-related problems, from oliguria to complete renal failure. 2.1.6 Neurological: The two most commonly-reported neurological effects of severe or chronic arsenic exposure are "pins and needles" feeling in the hands and feet, and partial paralysis of the limbs. In severe cases, degeneration of the peripheral nervous system has been noted. Elimination of the source of arsenic exposure has in some cases led to improvement over time of some, but not all, of the neurological symptoms. Some permanent damage is not uncommon. Other noted neurological side effects include hearing loss, memory loss, headaches, depression, anxiety attacks, and muscle and joint pain. 2.1.7 Carcinogenic: Chronic oral, dermal or inhalational arsenic exposure can lead to several kinds of cancer. The most common are skin cancer, bladder cancer, and lung cancer, the latter being most prevalent in cases of inhalational exposure. Skin cancer can result from dermal or oral exposure, and patients with arsenic-related skin cancer are more prone to other internal cancers. "More recent epidemiological studies in Taiwan have reported tumors of the lung, liver, bladder and kidney associated with arsenic-induced skin cancers."(11) Other cancers attributed to arsenic exposure include prostrate cancer, hepatic angiosarcoma, nasal cavity cancer, and colon cancer.(12) Because of the numerous and extensive carcinogenic risks posed by arsenic exposure, the Environmental Protection Agency (EPA) has ranked it as an Group A carcinogen. 2.1.8 Reproductive/Developmental: There are serious concerns with arsenic exposure and its potential to cause birth defects in both laboratory animals and humans. New information now suggests that arsenic is also an endocrine disruptor. Numerous studies have been published since the early 1940s that show that both arsenic and chromium can cause a variety of birth defects in laboratory animals. The few available human studies show similar results. In fact, both arsenic and chromium are listed as known teratogens in the reference manual, "Catalog of Teratogenic Agents, 9th edition" by Thomas Shephard, M.D. In addition, arsenic is listed as a "developmental toxin" by the California Environmental Protection Agency. One comprehensive study article on arsenic’s potential for reproductive toxicity, "The Role of Arsenic as a reproductive toxin with particular attention to neural tube defects", published in 1996, serves as a comprehensive review of many of the available studies and reaches the conclusion that "arsenic should be considered a probable human reproductive toxin"(13). Moreover, it has also been shown that "humans have been found to be more sensitive to arsenic that most laboratory animals"(14), by a factor of as much as 300 times. This heightened human sensitivity to arsenic's toxicity is likely to also be true from a teratogenic standpoint. A review of the published scientific studies indicates that laboratory animals exposed to arsenic produced offspring with many different kinds of malformations, including cleft lip, cleft palate, open eye, limb defects, ear deformities, exencephaly, and protruding organs. This was true for several different species of laboratory animals, and the resultant malformations were dependant on both dosage and timing. Here are some excerpts from those studies: A. In a study entitled "Malformations Induced by Sodium Arsenate" by Ferm and Carpenter, published in 1968 (15), their findings revealed that "administration of intravenous sodium arsenate on day 8 of gestation resulted in exencephaly in fetuses of the golden hamster." [Note: exencephaly is a neural tube disorder in which the brain of the fetus is located outside of the skull. It is generally fatal.] B. Dr. Ronald Hood published several studies on the teratogenic effects of arsenic. One study published in 1972 entitled "The Teratogenic Effects of Sodium Arsenate in Mice" (16), stated that, "administration of a barely sublethal dose of sodium arsenate to pregnant mice on days 6 to 11 of gestation produced a variety of malformations in the surviving fetuses." (The percentage of grossly malformed mice ranged as high as 63%, depending on the day of treatment.) The malformations included exencephaly, trunk and limb defects, protuding internal organs, and cleft palate and cleft lip. C. A second 1972 study by Dr.Hood, entitled "Effects of Sodium Arsenite on Fetal Development"(16), stated that "The most common defects associated with arsenite treatment were exencephaly, micrognathia, and open eye… arsenite exposure was also associated with skeletal anomalies." The study also found that "Arsenite is effective [as a teratogenic agent] at a much lower dose level that is arsenate (10 vs. 45 mg/kg)." In a 1978 study, Dr. Hood was also able to generate similar fetal malformations in mice, including open eye, exencephaly, and cleft palate, by administering oral and injected doses of sodium arsenate (16). D. In a paper published by UCLA’s Center for Environmental Risk Reduction (17), the statement is made that, "In addition to its toxic and carcinogenic effects on the adult population, investigators suspect that arsenic may cause neural tube defects (NTDs) in human embryos exposed in utero; arsenic is a known teratogen in rodents producing NTDs and a variety of other fetal malformations, as well as inducing embryolethality. The few human studies reported have all found associations between high environmental arsenic levels and adverse outcomes of pregnancies." E. A series of studies were published in 1978 and 1979 by Nordstrom, Beckman and Nordenson (18) that documented the reproductive hazards of arsenic by studying women who worked in a copper smelter in Sweden and were exposed to arsenic dust. These studies showed that due to their exposure, "babies born to women exposed to arsenic dust had a higher than expected incidence of congenital malformations", including lower-than-normal birth weights and spontaneous abortions. F. In addition, there have been recent studies that detail the concerns about arsenic as an endocrine disruptor. One new study, published this year in the journal Environmental Health Perspectives (19), details how arsenic affects the glucocortoid receptors within the nucleus of the cell itself. It states that "very low levels of arsenic-equivalent to about 10 parts per billion" can cause effects inside the cell that "alter hormonal function in the glucocortoid system". G. The Florida Center for Solid and Hazardous Waste Management, whose groundbreaking work on how CCA leaches from pressure-treated wood has helped to bring the hazards of CCA-treated lumber to the foreground, is also planning further research testing this year on CCA as a endocrine disruptor using hormonally active chemical assays. The studies listed above are just a sample of some of the many studies published worldwide that detail the reproductive hazards of arsenic exposure both to animals and humans. However, in spite of this wealth of laboratory data, many scientists and doctors remain skeptical that exposure to arsenic can cause birth defects in human populations. There are even a few recent studies (published by Dr. DeSossa of Mitretek Systems) that refute most, if not all ,of the known studies on the teratogenic hazards of inorganic arsenic compounds(20). However, it should also be noted that the sponsor of these studies is ATOFINA Chemicals, Inc., formerly known as Elf Atochem, a manufacturer of arsenic chemical products. So, skeptics need only look to the recent class action lawsuit filed by the citizens of Bryan, Texas, who claimed numerous injuries due to their exposure to arsenic that was allegedly released from the Elf Atochem plant. The plant manufactured arsenic trioxide (a cotton defoliant) and pentavalent arsenic acid, an ingredient used in CCA wood preservative. The lawsuit, Lillian Hayden et. al. vs. Elf Atochem North American, claimed that nearby residents who were exposed to arsenic suffered personal injuries and illnesses, including cancers, central nervous system impairment, and assorted birth defects. A cluster of 13 children, born between 1990 and 1993 to families who lived close to the plant, suffered from arsenic-related birth defects such as anencephaly, microencephaly, holoprosencephaly, spina bifida, micro-phthalmia, anophthalmia, renal agenesis, myelomeningocele and coarctation of the aorta. Several of the children died. Elf Atochem recently settled this lawsuit for $41.4 million. As part of the terms of the settlement, Elf Atochem has agreed "not to produce, use, or handle arsenic or arsenic-containing materials, organophosphates, pesticides, fungicides, herbicides, insecticides and rodenticides at the Bryan Plant, except as necessary for remediation activities" (21). 2.1.9 Mutagenic: The effects of arsenic on the genes, reads like a microcosm of its effects on the entire body as a whole. The deleterious effects noted in studies include "DNA damage and a wide variety of genetic alterations, which can range from simple gene mutations (DNA base pair changes) to grossly visible changes in chromosome structure or number (clastogenesis). Some of these changes may cause genetic damage transmissible to subsequent generations…"(8). Further studies indicate that arsenic may cause genetic damage by interfering with the mechanism by which DNA repairs itself. 3.0 General and Systemic Effects of Chromium Exposure: Arsenic often gets the most attention in any discussion of the hazards of CCA and pressure-treated wood. However, the hazards of chromium, in particular hexavalent chromium, which is known to be present in CCA-treated wood at levels as high as 50% of the total chromium (22), and is proven to leach from CCA-treated wood, have in many cases gone unmentioned. However, hexavalent chromium is as insidious as its partner arsenic. It is also a known teratogen and is classified as a Group A carcinogen by the EPA. (Note: hexavalent chromium and its related compounds are known by many chemical names: chromium VI, Cr(VI), chromium trioxide, chromic acid, sodium dichromate, and potassium dichromate.) Furthermore, there are an equivalent number of laboratory studies that detail the health and reproductive hazards of exposures to hexavalent chromium. As done previously with arsenic, we shall review the details from these studies below. 3.1 General Effects: In the "ToxFaqs for Chromium", the Agency for Toxic Substances and Disease Registry (ATSDR) details the following health hazards related to chromium exposure: Very heavy exposure: damage to the nose, lungs, stomach and intestines, and possible asthma attacks. High/moderate or chronic exposure: damage to the nose, (including nasal septal perforation, nasal ulcers/lesions, nasal bleeding, itching, or a constant runny nose), damage to the lungs, which can increase the risk of non-cancerous lung diseases, skin irritation, (including allergic contact dermatitis leading to severe redness and swelling), skin ulcers, changes in pulmonary function, kidney problems such as renal proteinuria, and asthma attacks, if the individual is allergic to chromium. Very heavy ingestion: stomach upsets, ulcers, convulsions, kidney and liver damage or death. According to the Journal for Pesticide Reform, additional health hazards from heavy chromium exposure include "diarrhea, blood loss into the digestive tract, and cardiovascular shock followed by liver and kidney necrosis"(7). In the EPA's "Toxicological Review of Hexavalent Chromium", it is reported that in a study of 155 Chinese people exposed to hexavalent chromium in well water with an estimated dose rate of 0.57mg/kg-day, (Zhang and Li, 1987), "the reported effects at this dose included oral ulcers, diarrhea, abdominal pain, indigestion, vomiting, leukocytosis, and presence of immature neutrophils… Subjects were observed to have elevated white blood cell counts with respect to controls, as well as a higher per capita rate of cancers, including lung cancer and stomach cancer… The study suggests that gastrointestinal effects may occur in humans following exposures to hexavalent chromium at levels of 20 ppm in drinking water."(23). For hexavalent chromium, the lethal dose is 50 mg/kg of body weight for humans. For a typical adult male weighing 165 pounds (75 kg), the fatal dose would be 3.75 grams. 3.2 Carcinogenic: Exposure to chromium has been known to cause lung cancer since the early 1930s. Numerous epidemiological studies since then have confirmed this fact. Based on extensive research on groups of workers in the chrome plating, tanning and welding industries, it is now known that exposure to hexavalent chromium in the workplace increases the risk of lung cancer in exposed persons by a factor of as much as 1500. As mentioned earlier, the EPA has classified hexavalent chromium as a Group A carcinogen. 3.3 Reproductive/Developmental: There have been numerous studies performed on laboratory animals using both chromium and hexavalent chromium that demonstrate teratogenic effects that parallel those found in tests with arsenic. Here are excerpts from some of those studies: A. A landmark study published in 1978 by Dr. T.F. Gale (24), "The Embryotoxic Effects of Chromium Trioxide in Hamsters", stated that "the present paper demonstrates that intravenously administered hexavalent chromium trioxide is embryolethal and produces some teratogenic effects in surviving hamster fetuses, including cleft palate and skeletal defects." In this study, Dr. Gale was able to produce cleft palates in 85% of the hamster fetuses with a dose of 7.5 mg/kg of chromium trioxide. Other defects were also elicited, including exencephaly, micrognathia, skeletal defects including unossified vertebrae, abnormal limbs, and internal defects, such as enlarged heart. The study continues by stating that, "Chromium… produces general [teratogenic] effects, i.e. edema and retardation, as well as site-specific damage to the developing secondary palate. …The cause may be related to the fact that chromium delays the overall maturation of some fetuses. In conclusion, chromium trioxide has been demostrated to be both embryolethal and teratogenic when administered [intravenously] on the 8th day of gestation in hamsters." [Note: the 8th day of gestation for a hamster equates to days 24-28 of gestation in humans.] B. Dr. Gale also produced other studies(25) on the teratogenic effects of chromium trioxide, including "The effect of time of administration of chromium trioxide on the embryotoxic response in hamsters", published in 1979. In this study, chromium trioxide was injected into pregnant hamsters on days 7,8,9, 10 or 11 of gestation in order to determine the effect of altering the time of treatment on embryotoxicity. The study noted that "cleft palate [was] the major malformation detected…". The study also "suggests a delay in growth as a major factor in chromium-induced cleft palate." C. In a study published in 1979 by the University of Tokyo(26), "Embryotoxic and fetotoxic effects of chromium trioxide in mice", reported that, "In the group [of mice] treated with 20 mg/kg of CrO3 [chromium trioxide] on day 8 of gestation, external malformations were observed at the highest rate (about 30%, which included a high proportion of cleft palate)." The study concluded that "these results imply that CrO3 has some teratogenic and embryocidal actions as well as effects on the growth of the mouse fetus." Newer studies have also shown that oral doses of hexavalent chromium compounds cause malformations in laboratory animals, including rats and mice. D. In a 1989 study by Dr. Trivedi et. al, published in Reproductive Toxicology, mice were given high oral doses of potassium dichromate, (a hexavalent chromium chemical compound), in daily doses of 250 ppm, 500 ppm and 1000 ppm, throughout their entire gestational period. Abnormalities reported by the study included "decreased fetal weight, increased resorptions, and increased abnormalities (tail kinking, delayed ossification of the cranium) in exposed mice… Additional effects included treatment-related increases in abnormalities in the tail, wrist forelimbs and subdermal hemorrhagic patches in the offspring." (27). E. To further explore the teratogenic effects of hexavalent chromium, Dr. Junaid et al., published a study in Toxicology Letters in 1996, which involved exposing female mice during days 6-14 of their gestations (a critical developmental phase in the gestational period) to potassium dichromate in their drinking water in doses of 250, 500, and 750 ppm. The results were disturbing. The study's authors reported teratogenic effects and malformations which included "retarded fetal development and embryo- and fetotoxic effects including reduced fetal weight, reduced number of fetuses (live and dead) per dam, higher incidences of stillbirths and postimplantation loss in the 500 and 750 ppm dosed mothers… significantly reduced ossification in nasal, frontal, parietal, interparietal, caudal, and tarsal bones was observed in the high-dose group…" (28). F. In that same year, (1996), a nearly identical study was conducted by Dr. Kanojia et. al and published in Toxicology Letters. This study, however, tested whether pre-gestational exposure to hexavalent chromium would prove to cause reproductive harm to the offspring of exposed female rats. The rats were exposed to doses of 250, 500 and 750 ppm for 20 days prior to fertilization. Chromium was detected in the blood, placenta, and fetuses of these test animals in proportion to the dosage they were given. Once again, severe malformations and birth defects were noted in the offspring of the test animals, including "a reduced number of implantations, retarded fetal development, and embryo- and fetotoxic effects including reduced number of fetuses (live and dead) per dam, and higher incidences of stillbirths and postimplantation loss in the 500 and 750 ppm dosed mothers. Significantly reduced parietal and interparietal ossification was observed in the high-dose group." (29) So, even exposure to hexavalent chromium compounds before gestation causes birth defects in laboratory animals, probably due to the bioacumulation of chromium in the mother and the fetus. These findings clearly show the cause-and-effect relationship between exposure to hexavalent chromium compounds and birth defects during the time preceeding fertilization and the critical early phases of fetal development. It is important to note that in the Junaid study, exposure to hexavalent chromium during the period of days 6-14 of the mice's gestational period produced extensive fetal malformations. This critical time period correlates to days 18-42 of the human getational period (30). So I guess it is better to directly apply the cancer? ![]() |
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| Brian Oshman ![]() Join Date: Apr 29 2001 Location: High Bridge, NJ Age: 41
Posts: 2,328
Rep Power: 13 ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() ![]() | Re: Newbie Here: Overwhelmed..What do I do first? ^^^You should have left your post. That was interesting too. If we look at every aspect of life with modern advancement we will find things that are not exactly good for us but the real key is moderation no matter what it is. (well except for directly applying cancer and death with a spray gun) Ban That Sticky, Nasty Crap!® |
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