1. Magnetic Bracelets Cut Osteoarthritis Pain - Study
British researchers have discovered that Magnetic bracelets can help to ease the pain of osteoarthritis of the hip and knee, said.In a study of nearly 200 sufferers of the joint disease, patients who wore a standard-strength magnetic bracelet reported having less pain than those who wore weaker or non-magnetic bracelets for 12 weeks. "We found evidence of a beneficial effect of magnetic wrist bracelets on the pain of osteoarthritis of the hip and knee," Professor Edzard Ernst, of the Peninsula Medical School in Plymouth, southern England, said in a report in the British Medical Journal.Although the results are consistent with previous studies that analysed magnetic therapy, the scientists said they did not know whether the reported improvement was due to the bracelet, the placebo effect, a believed benefit from a treatment that has no effect, or both. "Whatever the mechanism, the benefit from magnetic bracelets seems clinically useful," Ernst and his colleagues added.The patients wearing the higher strength magnetic bracelets reported the biggest improvement, which the scientists said suggested the magnetic strength is important. The benefits were in addition to improvements from standard treatments for the illness. Osteoarthritis is the most common form of arthritis, which is a leading cause of disability. It can affect any joint in the body but is common in the knees and hips. Pain in a joint after inactivity, swelling and stiffness are symptoms. There is no cure but treatments can reduce pain and maintain movement.
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2. What is NSF rating?
NSF International (NSF) is a private, independent, none-profit organization. They develop and maintain voluntary standards, which are dedicated to helping solve public health and environmental safety problems, NSF ratings are recognized around the world. They comply fully with federal guidelines, Under the certification program, they evaluate, test and inspect products, as well as conduct unannounced audits at the manufacturing facilities of water filters to assure that they continue to meet the requirements of the program. Only companies with NSF certified products under and ANSI accredited program may use the accreditation marks in combination with the NSF mark.
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3. Chlorine in Water
Disinfection of drinking water through processes including filtration and chlorination was one of the major achievements of public health, beginning in the late 1800s and the early 1900s. Chloroform and other chlorination disinfection by-products (CBPs) in drinking water were first reported in 1974. Chloroform and several other CBPs are known to cause cancer in experimental animals, and there is growing epidemiologic evidence of a causal role for CBPs in human cancer, particularly for bladder cancer. It has been estimated that 14-16% of bladder cancers in Ontario may be attributable to drinking water containing relatively high levels of CBPs; the US Environmental Protection Agency has estimated the attributable risk to be 2-17%. These estimates are based on the assumption that the associations observed between bladder cancer and CBP exposure reflects a cause-effect relation. An expert working group (see Workshop Report in this issue http://www.phac-aspc.gc.ca/publicat/cdic-mcc/19-3/b_e.html) concluded that it was possible (60% of the group) to probable (40% of the group) that CBPs pose a significant cancer risk, particularly of bladder cancer. The group concluded that the risk of bladder and possibly other types of cancer is a moderately important public health problem. There is an urgent need to resolve this and to consider actions based on the body of evidence, which, at a minimum, suggests that lowering of CBP levels would prevent a significant fraction of bladder cancers. In fact, given the widespread and prolonged exposure to CBPs and the epidemiologic evidence of associations with several cancer sites, future research may establish CBPs as the most important environmental carcinogens in terms of the number of attributable cancers per year.
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4. Disinfection of Drinking Water: Historical Perspective
In the 19th century, major outbreaks of waterborne diseases were common in Canada, the United States and other developed nations. Beginning in the early years of the 20th century, the provision of chlorinated drinking water virtually eliminated typhoid fever, cholera and other waterborne diseases, representing one of the great achievements of public health. Chlorine was discovered in 1774 by the Swedish chemist Karl Wilhelm Scheele and confirmed to be an element in 1810 by Sir Humphrey Davy.
Use of chlorine as a disinfectant was first introduced by Semmelweis on the maternity ward of the Vienna General Hospital in 1846 to clean the hands of medical staff and prevent puerperal fever. In 1881 Koch showed that pure cultures of bacteria were destroyed by hypochlorites.
The first continuous usage of chlorination in the US began in 1908 for the water supply to Jersey City, New Jersey, and at a site that served the Chicago Stockyards to control sickness in livestock caused by sewage-contaminated water. In Canada, the earliest use of chlorination found by this author was in Peterborough, Ontario, in 1916.
Chlorination has been the main method of disinfecting drinking water in Canada, the United States and many other countries for several decades and has proven effective against most waterborne pathogens.
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5. Health Effects of Chlorination Disinfection By-products
Chlorine's potent oxidizing power causes it to react with naturally occurring organic material in raw water to produce hundreds of chlorinated organic compounds, referred to generically as chlorination disinfection by-products (CBPs). One of the most commonly occurring groups of CBPs, the trihalomethanes (THMs), was first identified at higher concentrations in chlorinated drinking water than in natural raw water by Rook and by Bellar et al.
Raw drinking water supplies were found to have low background levels of mutagenic activity with relatively large increases in mutagenicity after chlorination. The mutagenic activity of chlorinated water is caused mainly by reactions of chlorine with natural humic substances released by the breakdown of vegetation in the source waters. Recently, the chlorinated hydroxyfuranones (e.g. MX) have been shown to be responsible for a major part of the mutagenic activity. Other CBPs, including brominated THMs and haloacetic acids, are also mutagenic. The concentration of THMs correlates strongly with the amount of organic precursors in raw water and, although imperfect, it can be a useful indicator of the level of total CBPs in treated water.
Although numerous CBPs have been identified in chlorinated drinking water, very few have been subjected to carcinogenicity bioassays. Chloroform induced significant increases in kidney tumours in male rats when administered in high concentrations in drinking water. Chloroform also produced kidney tumours in male rats and liver tumours in male and female mice when administered by gavage in corn oil. Unlike the brominated THMs, chloroform appears not to be carcinogenic through a direct DNA reactive mechanism, acting instead through regenerative cell proliferation, possibly with an exposure threshold. In studies of the three other THMs, bromoform administered by corn oil gavage induced intestinal tumours in male and female rats; chlorodibromomethane by corn oil gavage produced liver tumours in both sexes of mice; and bromodichloromethane by corn oil gavage induced intestinal and kidney tumours in male and female rats, kidney tumours in male mice and liver tumours in female mice.
After the THMs, the most commonly occurring group of CBPs in drinking water is the haloacetic acids (HAAs). Comparing published results from the two most studied HAAs, dichloroacetate in drinking water induced hepatic tumours in both rats and mice, but trichloroacetate induced hepatic tumours only in mice. Both compounds appear to act as tumour promoters, but likely via different mechanisms: trichloroacetate has been shown to be a peroxisome proliferator, whereas dichloroacetate affects cell cycle kinetics. While none of the brominated HAAs have been tested in carcinogenicity bioassays, preliminary screening tests have indicated a potential for the induction of liver tumours by bromochloroacetate, dibromoacetate and bromodichloroacetate; lung tumours by bromodichloroacetate; and colonic tumours by dibromoacetate.
MX (3-chloro-4- (dichloromethyl)-5- hydroxy-2 (5H)-furanone) is a CBP and is one of the most potent known mutagens as determined by the Ames assay. MX is reported to occur at much lower concentrations than the THMs or HAAs, yet it appears to account for about one third of the mutagenicity of chlorinated drinking water. DeMarini et al. found that MX produced 50-70% hotspot 2-base deletions and 30-50% complex frameshifts; no other compound or mixture is known to induce such high frequencies of complex frameshifts. MX caused several types of cancer or benign tumours in rats, including thyroid, liver, adrenal gland, lung, pancreas, breast, lymphomas and leukemias.
As noted in the following report, results of the epidemiologic studies of cancer have been most consistent in showing an association between exposure to THMs and bladder cancer. Conflicting results have been observed with respect to cancers of the colon and rectum. In 1996, King and Marrett reported the results of a large population-based case-control study of bladder cancer conducted in Ontario. Persons exposed to chlorinated surface water for 35 or more years had an increased risk of bladder cancer compared with those exposed for less than 10 years (odds ratio = 1.41, confidence interval [CI] = 1.10-1.81)). Persons exposed to THM levels of at least 50 µg/L for 35 or more years had 1.63 times the risk of those exposed for less than 10 years (CI = 1.08-2.46). The authors concluded that the risk of bladder cancer increases with both duration and concentration of exposure to chlorination by-products, with population-attributable risks of about 14-16% for Ontario. Approximately 1150 persons in Ontario will be diagnosed with bladder cancer in 1998. If CBPs do cause bladder cancer, then roughly 160-185 cases of bladder cancer per year in Ontario are attributable to such exposure.
There have been about 20 case-control and cohort epidemiologic studies of CBPs and cancer risk since 1978. The US Environmental Protection Agency (EPA) reviewed these studies and identified 5 case-control studies (including the King and Marrett study) that met the criteria of being population-based, well designed and having adequate exposure assessment. The EPA concluded that, based on the entire cancer epidemiology database, bladder cancer studies provide better evidence than other types of cancer for an association between exposure to chlorinated surface water and cancer.
The EPA recognized that a causal relationship between chlorinated surface water and bladder cancer has not yet been demonstrated conclusively by epidemiologic studies, but concluded that the /assumption/ of a potential causal relationship is supported by the weight of evidence from toxicology and epidemiology. Based on this assumption, the EPA estimated that the attributable risk of bladder cancer due to exposure to chlorinated water in the US is in the range of 2-17%; the annual number of bladder cancer cases attributable to such exposure was estimated to be in the 1100-9300 ranges. The EPA also stated that it believes that the overall evidence from available epidemiologic and toxicological studies on chlorinated surface water continues to support a hazard concern and a prudent public health protective approach for regulation.
The expert working group convened by the Laboratory Centre for Disease Control (see Workshop Report in this issue) observed that the few available epidemiologic studies of CBP exposure and pregnancy outcome indicated associations between exposure to THMs and spontaneous abortion, growth retardation and birth defects. However, these studies were weak in exposure assessment and control of potential confounders. When tested in rats, rabbits and mice, chloroform was not teratogenic, but both bromodichloromethane and chlorodibromomethane have shown evidence of fetotoxicity. Other CBPs have produced adverse effects on the testes and on sperm production in male rats and congenital heart defects in rats exposed in utero.
Recently, a prospective study that included concurrent trihalomethane sampling data showed that women who drank at least five glasses per day of cold tap water containing at least 75 µg/L total THMs had an adjusted odds ratio of 1.8 for spontaneous abortion (CI = 1.1-3.0). Of the four individual THMs, only high bromodichloromethane exposure (consumption of at least five glasses per day of cold tap water containing at least 18 µg/L of bromodichloromethane) was associated with spontaneous abortion, both alone (adjusted OR = 2.0, CI = 1.2-3.5) and after adjustment for the other trihalomethanes (adjusted OR = 3.0, CI = 1.4-6.6).
The expert group concluded that it was possible (60% of the group) to probable (40% of the group) that CBPs pose a significant cancer risk, particularly of bladder cancer. The group concluded that the risk of bladder and possibly other types of cancer is a moderately important public health problem. They also determined that there was insufficient evidence to establish a causal relationship between CBPs and adverse reproductive outcomes in humans, but that confirmation of the available limited data could establish CBPs as an important health problem. Finally, the group concluded that there were not enough data available to conduct a quantitative risk/benefit/cost evaluation and recommended that developing health risk data be monitored to determine when such an evaluation would be possible.
To the extent that epidemiologic studies randomly misclassify individual exposures to CBPs, the resulting risk estimates may be lower than the true risks. It is likely that many of the epidemiologic studies published to date have misclassified individual exposures to chlorinated water or CBPs. To lessen the impacts of this type of misclassification, Lynch et al. recommended that future epidemiologic studies of this type should quantify exposures more extensively.
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