Interphone researchers are conducting the largest-ever study investigating if cellphones cause cancer, examining studies from 6,400 tumors in patients from 13 countries. Final results are expected in early 2009, but the preliminary ones are badbadbad.
Israeli researchers in the study found that regular cellphones users are a whopping 50 percent more likely than non-users to get brain tumors. Another Interphone study looking at the UK and Scandinavia found a 40 percent greater tumor risk in people who've used cellphones for over 10 years, though on the bright side, nothing scary for people who've used them for less than a decade.
People who begin using mobile phones before age 20 are more than five times as likely to develop a malignant brain tumor, according to an international group of scientists who studied the effects of electromagnetic fields and radio frequency radiation on living cells and human health.
The team examined the results of 15 studies from health researchers in six different countries, and reported their findings in the journal Pathophysiology. The scientists also called on nations worldwide to adopt tougher safety standards for mobile phone use and to issue warnings about the potential danger of cell phone radiation, particularly for children.
Nonionizing radiation: Electromagnetic fields and radiofrequency cell phones
The association of exposure to nonionizing radiation, specifically exposures in the radiofrequency range (RF) or electromagnetic fields in the extremely-low-frequency range, and the development of primary BTs remains unresolved. Of particular interest is the questionable correlation between both gliomas and meningiomas and cellular phone use. These exposures are ubiquitous, and recent research focuses principally on mobile phones, because these RF exposures occur near the head and brain. The possible influence of currently acceptable low-level RF exposures on carcinogenesis has been suggested by some studies and warrants further investigation. While Although the relative rarity of primary BTs necessitates a case-control study design, these studies experience severe limitations with exposure assessment because of their reliance on personal recall of cases and controls of their RF exposures (ie, cell phone use). The INTERPHONE study, which was coordinated by the International Agency for Research on Cancer, included investigations from 13 European Union countries using a common protocol for the inclusion of cases and controls and for data collection using the same questionnaire. Between 2000 and 2003, the study recruited 2708 patients with gliomas, 2409 patients with meningiomas, and 1000 patients with acoustic neuroma and their respective population-based controls. Several country-specific results from those studies have been published.[70-74] These results, which overall do not identify increased risks for malignant or nonmalignant tumors in most studies, suggest in some studies a nonsignificant increase in the risk associated with longer duration of use or longer follow-up. Publication of the combined results on cell phone use related to the risk for these tumors, ie, the INTERPHONE study, will be forthcoming. In the same vein as the INTERPHONE study, a study is being established to examine the synergistic effect between chemicals and metals and electromagnetic fields.
ryanrs: An imperceptible amount of heat is not going to damage your body
peppito to ryanrs: When a molecule absorbs non-thermal energy, say a protein absorbing a radio wave, it is possible that it can use that energy to fold or react in the wrong way
ryanrs to peppito: Non-ionizing radiation causes effects beyond thermal heating? I encourage you to cite a source.
peppito: [various jokes, distractions, and general unhelpfulness]
parudox to ryanrs: Microwave radiation can alter protein conformation without bulk heating. Good enough?
ryanrs to parudox: YES!
peppito to parudox: You shouldn't help these people.
"There is more smoke than fire here," said Dr. Michael Thun, vice president emeritus of epidemiology and surveillance research for the American Cancer Society. "The radio frequency that comes from a cell phone is half way between a microwave oven and an FM radio. It's non-ionizing radiation, which doesn't change DNA and lead to cancer, and there has been no increase in brain cancer."
Title Effects of exposure to DAMPS and GSM signals on ornithine decarboxylase (ODC) activity: II. SH-SY5Y human neuroblastoma cells.
Abstract PURPOSE: An increase in Ornithine Decarboxylase (ODC) activity was reported in L929 murine fibroblast cells after exposure to a digital cellular telephone signal. This result was not confirmed by several other studies, including the one reported in a companion paper. As a partner in the Perform-B programme, we extended this study to human neuroblastoma cells (SH-SY5Y), using well-defined waveguide systems to imitate exposure to radiofrequency radiation (RFR): Digital Advanced Mobile Phone System (DAMPS) or Global System for Mobile communications (GSM) signals emitted by mobile phones. MATERIALS AND METHODS: Human neuroblastoma cells (SH-SY5Y) were exposed at various Specific Absorption Rates (SAR) to DAMPS or GSM signals using different set-ups. Cell ODC activities were assayed using 14CO2 generation from 14C-labeled L-ornithine. RESULTS: SH-SY5Y cells were incubated for 20 hours, and were blindly exposed to 50 Hz-modulated DAMPS-835 or 217 Hz-modulated GSM-1800 for 8 or 24 h using Information Technologies in Society (IT'IS) waveguides equipped with fans. After cell lysis, ODC activity was determined using 14C-labeled L-ornithine. ODC activity was estimated by the 14CO2 generated from 14C-labeled L-ornithine, as generated d.p.m. 14CO2/h/mg protein. The results showed that, irrespective of the signal used (835 MHz/DAMPS, or 1800 MHz/GSM) and exposure conditions (duration and SAR), human SH-SY5Y neuroblastoma cells did not exhibit any alteration in ODC enzyme activity. CONCLUSION: This work did not show a significant effect of mobile phone RFR exposure on ODC activity in neuroblastoma cells (SH-SY5Y).
Electrical power and mobile communications deliver enormous benefit to society, but there are concerns whether the electric and magnetic field (EMF) emissions associated with the delivery of this benefit are linked to cancer or other health hazards. This article reviews the strength of the available epidemiological and laboratory evidence and notes that this falls short of what is normally required to establish a causal link. However, because of scientific uncertainty a cautious approach is often advocated, but here, too, there may be a tendency to judge these risks more harshly than those in other areas with similar strength of evidence.
Cell phones and brain tumors: a review including the long-term epidemiologic data.
Khurana VG, Teo C, Kundi M, Hardell L, Carlberg M.
BACKGROUND: The debate regarding the health effects of low-intensity electromagnetic radiation from sources such as power lines, base stations, and cell phones has recently been reignited. In the present review, the authors attempt to address the following question: is there epidemiologic evidence for an association between long-term cell phone usage and the risk of developing a brain tumor? Included with this meta-analysis of the long-term epidemiologic data are a brief overview of cell phone technology and discussion of laboratory data, biological mechanisms, and brain tumor incidence. METHODS: In order to be included in the present meta-analysis, studies were required to have met all of the following criteria: (i) publication in a peer-reviewed journal; (ii) inclusion of participants using cell phones for > or = 10 years (ie, minimum 10-year "latency"); and (iii) incorporation of a "laterality" analysis of long-term users (ie, analysis of the side of the brain tumor relative to the side of the head preferred for cell phone usage). This is a meta-analysis incorporating all 11 long-term epidemiologic studies in this field. RESULTS: The results indicate that using a cell phone for > or = 10 years approximately doubles the risk of being diagnosed with a brain tumor on the same ("ipsilateral") side of the head as that preferred for cell phone use. The data achieve statistical significance for glioma and acoustic neuroma but not for meningioma. CONCLUSION: The authors conclude that there is adequate epidemiologic evidence to suggest a link between prolonged cell phone usage and the development of an ipsilateral brain tumor.
Making the Case
One of the earliest epidemiological investigations of lung cancer was initiated in the late 1940s by Wynder and Graham.21 Their retrospective study included four groups of respondents. The first consisted of 605 male hospitalized patients diagnosed with epidermoid, undifferentiated and unclassified carcinomas. The second group included 100 hospitalized male lung cancer patients and 186 patients diagnosed with a chest disease. The third group involved 1,322 patients, without lung cancer, recruited from St. Louis hospitals. The final group consisted of eighty-three hospitalized patients who were interviewed by physicians in New York, Boston, and Hines, Illinois.
Data were collected using standardized format interviews about smoking behaviors.22 On completion of the interview, when available, the site of lesion, microscopic diagnosis, and Papanicolaou and etiological class were recorded. Respondents were clustered into six [End Page 337] categories: nonsmokers, light smokers (one to nine cigarettes per day for more than twenty years), moderately heavy smokers (ten to fifteen cigarettes per day for more than twenty years), heavy smokers (sixteen to twenty cigarettes per day for more than twenty years), excessive smokers (twenty-one to twenty-four cigarettes per day for more than twenty years), and chain smokers (thirty-five cigarettes or more per day for more than twenty years).
Among the men in the first group, all of whom had been diagnosed with lung cancer, 1.3 percent had no smoking history while 86.4 percent were either heavy (35.2 percent), excessive (30.9 percent), or chain (20.3 percent) smokers. In the second group, all of the lung cancer patients were smokers; 30 percent were excessive smokers, 23 percent were chain smokers.23 In the third group, men without cancer in the general hospital population, the percentage of nonsmokers was 14.6 percent higher than among the first two groups, but 54.7 percent were either heavy (35.6 percent), excessive (11.5 percent) or chain (7.6 percent) smokers. Of the eighty-three patients with lung cancer in group four, 86.4 percent were either heavy, excessive, or chain smokers.
Wynder and Graham believed they had demonstrated a definite association between smoking and the risk of lung cancer, which indicated that age was not as important a variable as smoking. They concluded that excessive and prolonged cigarette smoking seemed to be an important factor in the induction of lung cancer, and that lung cancer in nonsmokers was rare.24
In the late 1940s the New York State Department of Health's Bureau of Cancer Control in Albany and its Roswell Park Memorial Institute in Buffalo collaborated on an investigation of the causes of lung cancer. This study, published in 1950 by Morton L. Levin, Hyman Goldstein, and Paul R. Gerhardt, also supported a link between smokingand cancer. Since 1938, researchers at Roswell Park (a public [End Page 338] hospital specializing in cancer) had routinely recorded the smoking habits of patients admitted to the hospital before their diagnoses were known. The study was based on histories taken of 1,045 male patients with lung, lip, pharynx, esophagus, colon, or rectum cancer and a few patients with cancer at different sites. Levin, et al., chose 605 different male non-cancer patients for comparison because they had signs referable to the same sites, but that later proved not to be cancer. The data showed that 84.8 percent of the cancer patients smoked cigarettes, pipes, or cigars; but 77.8 percent of noncancer patients smoked similarly. When adjusted for age, the investigators found that cigarette smokers who smoked for twenty-five years had twice as many cases of lung cancer than pipe smokers, cigar smokers, or nonsmokers.25 They also showed that lip cancer was increased among pipe smokers and cigar smokers, but not cigarette smokers. Unlike Wynder and Graham, Levin and his colleagues did not report the relationship between amount smoked and the risk of lung cancer. Also, they did not describe how the case histories were taken or whether a standardized form was used. Moreover, Levin admitted that "the reliability of the quantitative aspects of smoking obtained by a history is of course highly variable."26
Contemporaneously, Hill and Doll initiated a study among patients admitted to the hospital for lung, stomach, colon, or rectum cancer. Eligible patients were identified by admitting clerks, house-physicians, the cancer registrar, and staff from radiotherapy departments. Those who were eligible and interested were interviewed using a questionnaire on their smoking habits. In addition, hospital patients without cancer, matched in terms of age and gender, were enrolled as controls. Between April 1948 and October 1949, 2,370 cases were identified and a final sample consisting of 1,732 cases was selected. Data collection involved face-to-face interviews on topics such as life-time smoking habits, ages started or stopped smoking, the amount smoked prior to admission, changes in their smoking history, most intense smoking habit, varying proportions of pipes and cigarettes smoked, and inhalation behavior. To classify as a smoker the subject must have smoked at least one cigarette a day for a year. [End Page 339]
The control group consisted of 709 general medical and surgical patients, matched except that they differed slightly with regard to their residence. Non-smokers were significantly (p<> ACS epidemiologist E. Cuyler Hammond and Surgeon General Leonard Scheele were dismissive of Wynder and Graham's retrospective study.30 Graham recalled that "Hammond told me that if he had anything to do with it, we would not get our grant from the American Cancer Society renewed. He went on to say also that he had no confidence in your results or in the answers to the questionnaire that Miss Croninger [Wynder and Graham's research assistant] was getting." Graham decided that he did not want to have any further dealings with the American Cancer Society. "I think the attitude of Hammond, which was supported by Cameron [Medical and Scientific Director of the ACS], was inexcusable and I feel somewhat sour on the whole [End Page 340] bunch."31 Wynder called Surgeon General Leonard Scheele to find out the reasons for the grant denial and asked him whether he had read Wynder and Graham's JAMA article.32 Wynder reported Scheele's reaction: "This article had not proved [sic] anything. He said the same correlation could be drawn to the intake of milk." Scheele added that "no kind of interviewing could get satisfactory results from patients." Moreover, he concluded: "since nothing had been proved [sic] there exists no reason why experimental work should be conducted along this line."33
Negative reactions to Wynder's data collection methods came from other cancer researchers. For instance, Dr. James W. Ellis, of the Bureau of Disease Control, State of California Department of Public Health, wrote to Graham "that if your conclusions are based upon statistics complied [sic] by Dr. Ernest Wynder, we very [sic] skeptical of their validity." According to Ellis, Wynder's investigations in the Bay Area and in Los Angeles was observed by "the leading men in those areas" and for a few days he was accompanied by one of Ellis's investigators. "The concensus [sic] of opinion," Ellis claimed, "was that Dr. Wynder was extremely biased in his approach, asked leading questions regarding smoking habits, and received directed answers. He was uninterested in other possible factors and ignored them. He impressed us as one who was trying to bolster a theory rather than make an objective survey."34
Despite these concerns, or because of them, other studies were initiated, some by Wynder's and Graham's critics. In order to overcome the methodological problems associated with retrospective studies, Doll and Hill in Britain and Hammond and Horn in the U.S. began conducting prospective studies in the early 1950s. As Doll and Hill wrote: "Further retrospective studies of that same kind would seem to us unlikely to advance our knowledge materially or to throw any new light upon the nature of the association. If, too, [End Page 341] there were any undetected flaw in the evidence that such studies have produced, it would be exposed only by some entirely new approach." Doll suggested that the next "approach we considered should be 'prospective.' It should determine the frequency with which the disease appeared, in the future, among groups of person whose smoking habits were already known."35
In summer and fall of 1951, Hammond and Daniel Horn of the ACS designed a standardized questionnaire to be used in a prospective study. Four pages long, it covered areas such as demographic characteristics and smoking history.36 To conduct the interviews Hammond and Horn recruited and trained approximately 22,000 volunteers from 394 counties in nine states to collect the data. Each trained volunteer received a packet containing eleven questionnaires and was asked to recruit five to ten white men between fifty and sixty-nine years of age whom they could track for several years. Initial enrollment began in January 1952, and the follow-up began on 1 November 1952. Death certificates from the state health departments were checked if a subject could not be reached. If cancer was indicated as a cause of death, efforts were made to gather further details from the physician listed on the death certificate and from the hospital, tumor clinic, or cancer registry records when available. The second follow-up began on 1 November 1953 and included 190,134 men, 4,854 (2.6 percent) of whom had died.37
For purposes of analysis, the sample was divided into three categories: never smoked, occasionally only, and regular smokers. Within [End Page 342] each of the categories, age groups were constructed. The findings showed that regular smokers had a significantly higher mortality rate than men who never smoked across all age groups (p<>The association appeared causative when other evidence was included; for instance the earlier statistical studies by Lombard and Doering (1928), Pearl (1938), and the Massachusetts State Health Department (1945), all of which also found a statistically significant association between smoking and lung cancer. They pointed to trends in cigarette use in the United States. In 1920 the rate of consumption was 630 per person fifteen years of age or older. By 1953 it had risen to 3,500 per person.38 The cumulative meaning of all this evidence, concluded Hammond and Horn, was that the relationship between cigarette smoking and cancer was cause and effect.
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