Unknown authors · 2005
The Bernal Lecture 2004 explored scientific challenges regarding low-frequency electromagnetic fields as a health hazard. The lecture drew on experiences of the EMF Biological Research Trust which funds basic research on ELF-EMF biological effects. The lecture found no compelling experimental evidence that environmental ELF-EMFs induce biological responses.
Unknown authors · 2005
The report describes scientific research on health effects from household appliances, regulations, magnetic field strengths near devices, and resulting exposures. Exposure to electric and magnetic fields from most household appliances is below EU recommended levels. No short-term health effects are expected for those appliances. Outdated literature suggests some older equipment still in use may exceed EU levels, but newer appliances meeting European standards are less likely to exceed them. EU exposure levels are based on effects occurring during or shortly after exposure, and research does not point to a link between cancer and household appliance use.
Unknown authors · 2005
Researchers exposed two clones of MCF-7 breast cancer cells to 50Hz electromagnetic fields and calculated IC(50) values from tamoxifen dose-response curves. The dose-response curves shifted to higher tamoxifen concentrations in an intensity-dependent manner, with a maximal response at 1.2muT. The authors hypothesized that electromagnetic field exposure could contribute to tamoxifen resistance observed in breast cancer after long-term treatment.
Unknown authors · 2005
Researchers exposed rats bearing human breast cancer xenografts to increasing intensities of white fluorescent light during the dark phase and collected blood from premenopausal women at daytime, nighttime, or after 90 minutes of bright light at night. Tumors perfused with nocturnal melatonin-rich blood showed markedly suppressed proliferative activity and linoleic acid uptake compared with tumors perfused with daytime melatonin-deficient blood. Tumors perfused with blood collected after ocular light-at-night exposure exhibited the daytime pattern of high tumor proliferative activity, and the tumor growth response to light during darkness was intensity dependent.
Whitehead TD et al. · 2005
The study aimed to confirm a previous report that CDMA and FDMA radiation increased Fos levels as cells entered plateau phase. Fos mRNA levels were not significantly different from sham exposure at either SAR level for any signal modulation. Therefore, the earlier results could not be confirmed.
Wang J et al. · 2005
Researchers exposed mouse C3H10T1/2 cells to 2450 MHz HFEMF at SARs of 5 to 200 W/kg for 2 hours, with or without methylcholanthrene (MC) and the tumor promoter TPA. Transformed foci of Type II and Type III were counted as the endpoint. No significant differences were observed in malignant transformation frequency between controls and HFEMF with or without TPA. Transformation frequency increased for HFEMF at SAR above 100 W/kg when combined with MC or MC plus TPA, while heat exposure did not increase transformation.
Shirai T et al. · 2005
A 1.439 GHz TDMA signal was used for exposure of the rat head starting from 5 weeks of age, 90 min a day, 5 days a week, for 104 weeks. Brain tumorigenesis was initiated by an intrauterine exposure to N-ethylnitrosourea (ENU) on gestational day 18. No increase in the incidences or numbers per group of brain and/or spinal cord tumors, either in the males or females, was detected in the EMF exposed groups. There were no inter-group differences in body weights, food consumption, and survival rates.
Schoemaker MJ et al. · 2005
Researchers conducted six population-based case-control studies in four Nordic countries and the UK to assess acoustic neuroma risk in relation to mobile phone use. Data were collected by personal interview from 678 cases of acoustic neuroma and 3553 controls. The risk of acoustic neuroma in relation to regular mobile phone use was not raised (OR=0.9, 95% CI 0.7-1.1). Risk of a tumour on the same side of the head as reported phone use was raised for use for 10 years or longer (OR=1.8, 95% CI 1.1-3.1).
Lonn S, Ahlbom A, Hall P, Feychting M. · 2005
Laszlo et al. · 2005
Researchers measured heat-shock factor DNA-binding activity in hamster, mouse, and human cells after exposure to FDMA- or CDMA-modulated microwaves at low or high SARs. The assay could detect a 10% increase in HSF activation from a 1°C temperature rise. No increase in HSF DNA-binding ability was detected from any exposure tested. The results do not support activation of the stress response by mobile communication microwaves.
Huang TQ, Lee JS, Kim TH, Pack JK, Jang JJ, Seo JS. · 2005
The study used 80 male ICR mice initiated with DMBA and then exposed to 849 MHz or 1,763 MHz RF radiation at 0.4 W/kg SAR for 19 weeks. No skin tumors were observed in the sham or RF-exposed groups, while the TPA positive control group had a 95% tumor incidence. Pathological examination and PCNA staining showed no differences between sham and RF-exposed groups, and cyclin D1 and c-fos expression was only detected in TPA-induced tumors. The researchers concluded that RF radiation does not act as a tumor promoter for skin tumors in this model.
Christensen et al. · 2005
Researchers conducted a nationwide population-based case-control study in Denmark. Cellular telephone use was associated with lower risk for high-grade glioma (OR 0.58, 95% CI 0.37-0.90). Risk estimates were near unity for low-grade glioma (OR 1.08) and meningioma (OR 1.00). The results did not support an association between cellular telephone use and risk for glioma or meningioma.
Lahkola A, Salminen T, Auvinen A. · 2005
Researchers evaluated selection bias in a Finnish case-control study of mobile phone use and brain tumors by comparing full and incomplete participants. Among controls, 83% of full participants and 73% of incomplete participants regularly used a mobile phone, while among cases the figures were 76% and 64%. The odds ratio for brain tumor based on the combined group was slightly closer to unity than that based only on full participants. Selection bias tends to distort effect estimates below unity, while analyses based on more comprehensive material gave results close to unity.
Hardell L, Eriksson M, Carlberg M, Sundstrom C, Mild KH. · 2005
B-cell non-Hodgkin's lymphoma was not associated with the use of cellular or cordless telephones. For T-cell non-Hodgkin's lymphoma with a latency period of more than five years, cordless phone use showed an odds ratio of 2.47 with a 95% confidence interval of 1.09 to 5.60. The authors noted that the results indicate an association between T-cell NHL and phone use but are based on low numbers and must be interpreted with caution.
Hardell L, Carlberg M, Hansson Mild K. · 2005
Researchers conducted a case-control study of benign brain tumors with 413 cases and 692 controls. For meningioma, analogue phone use yielded an odds ratio of 1.7 (95% CI 0.97-3.0), which increased to 2.1 (95% CI 1.1-4.3) with a latency period greater than 10 years. For acoustic neuroma, analogue phone use gave an odds ratio of 4.2 (95% CI 1.8-10) that rose to 8.4 (95% CI 1.6-45) with a latency period greater than 15 years, though based on low numbers. Digital phone use was associated with an odds ratio of 2.0 (95% CI 1.05-3.8) for acoustic neuroma, while cordless phone use did not show a significant increase. In multivariate analysis, analogue phones were a significant risk factor for acoustic neuroma.
Hardell L, Carlberg M, Hansson Mild K. · 2005
Researchers investigated the association between cellular or cordless telephone use and brain tumour risk in urban and rural areas of Sweden. The study included 1429 cases and 1470 controls aged 20 to 80 years diagnosed between 1997 and 2000. Use of different phone types was assessed by questionnaire with one control matched for sex and age per case. Rural residence with digital phone use showed an odds ratio of 1.4 increasing to 3.2 with longer latency, while urban residence showed odds ratios of 0.9. The effect was most obvious for malignant brain tumours.
Caraglia M et al. · 2005
Researchers exposed human epidermoid cancer KB cells to non-thermal microwave electromagnetic fields at 1.95 MHz. The exposure induced time-dependent apoptosis reaching 45% after 3 hours, accompanied by a roughly 2.5-fold decrease in expression of ras and Raf-1 and activity of ras and Erk-1/2. A 2.5-fold increase in ubiquitination of ras and Raf-1 was observed, and proteasome inhibition with lactacystin counteracted the degradation, indicating proteasome-dependent degradation. MW-EMF differentially activated stress pathways, increasing JNK-1 activity and HSP70 and HSP27 expression while reducing p38 kinase activity and HSP90 expression; overexpression of HSP90 completely blocked apoptosis and the inactivation of the ras-Erk survival signal, while Erk inhibition reversed this protection.
Anghileri LJ, Mayayo E, Domingo JL, Thouvenot P. · 2005
Mice were treated with 1 hour per week of radiofrequency exposure for 4 months while a sham-exposed group served as controls. The evolution of carcinogenesis was followed up to 18 months, and the maximal life span of control mice was about 24 months. All dead animals were clinically and histologically examined to give an age-determined comparative quantification of the evolving carcinogenesis. A radiocalcium tracer method permitted the evaluation of radiofrequency effects on transmembrane transport of extracellular calcium at 1 and 24 hours after exposure, and the determination of induced lipid peroxidation completed this second study.
Anderson, L. · 2004
Researchers conducted a two-year chronic bioassay to determine whether long-term exposure to a 1.6 GHz radiofrequency field would affect cancer incidence in Fischer 344 rats. Timed-pregnant rats were assigned to far-field RF Iridium or sham groups, with whole-body exposures starting at 19 days gestation for 2 hours per day, 7 days per week until weaning. Offspring then received near-field head-first exposures 2 hours per day, 5 days per week from 36 days old until 2 years of age at brain SAR levels of 1.6 W/kg, 0.16 W/kg, or sham. No statistically significant differences were seen among groups for live pups per litter, survival index, weaning weights, clinical signs, or neoplastic lesions, and male survival was similar across groups while female cage controls had reduced survival time.
Unknown authors · 2004
Researchers compared two Sprague-Dawley substrains, SD1 and SD2, for magnetic field effects on cell proliferation, susceptibility to DMBA-induced mammary cancer, and tumor development in the DMBA model. The SD1 substrain was considered MF-sensitive and was compared with SD2 from the same breeder. Magnetic field exposure significantly increased mammary tumor development and growth in SD1 rats but not in SD2 rats. No enhanced cell proliferation was determined after magnetic field exposure in SD2 rats, unlike in SD1 rats. The researchers concluded that genetic background plays a pivotal role in magnetic field exposure effects.
Unknown authors · 2004
Researchers conducted a population-based case-control study in Norway to assess residential and occupational exposure to 50-Hz magnetic fields and breast cancer risk. Cases of breast cancer diagnosed from 1980 to 1996 were identified in a cohort of women living near a high-voltage power line, and each case was matched to two controls by year of birth, municipality, and cohort entry year. Residential exposure was calculated from the magnetic fields generated by the power lines before diagnosis, while occupational exposure was based on an exposure matrix. Women with residential exposure had an odds ratio of 1.58 (95% CI: 1.30, 1.92) for breast cancer, whereas the highest occupational exposure yielded an odds ratio of 1.13 (95% CI: 0.91, 1.40).
Unknown authors · 2004
Ionizing radiation has been the subject of intense epidemiological investigation. The Life Span Study of atomic bomb survivors is the predominant source of evidence, supplemented by studies of medical, occupational, and environmental exposures. Notable studied groups include underground miners exposed to radon, patients receiving therapeutic radiation, and nuclear weapons program workers in the former USSR. Low-level exposure risk is contentious but evidence suggests increased risk approximately proportional to dose. Ultraviolet radiation is established as a cause of skin cancer, while evidence for mobile phone or power line radiation is not convincing, though a childhood leukemia link to extremely low-frequency fields cannot be dismissed.
Unknown authors · 2004
Researchers reviewed Swedish melanoma incidence, mortality, charter travel statistics, and FM broadcasting network expansion across all counties. Melanoma trend break occurred in 1955, while increased charter sun travel began seven years later. Counties with delayed FM network rollout had stable melanoma mortality during the delay period.
Unknown authors · 2004
No increased risks were found for leukemia, brain tumors, or breast cancer among the utility workers. Utility workers showed a significantly increased ALS mortality rate that rose with longer employment and higher EMF exposure. The mobile phone cohort showed no increased risk for brain tumors, acoustic neuroma, salivary gland tumors, or leukemia.
Sommer AM, Streckert J, Bitz AK, Hansen VW, Lerchl A · 2004
Survival rate and lymphoma incidence did not differ between exposed and sham-exposed mice. Exposed mice gained more weight than sham-exposed mice. The data do not support the hypothesis that 900 MHz fields are a significant risk factor for lymphoma in this genetically predisposed strain.