Joseph J. Morrissey

How well do adolescents recall use of mobile telephones? Results of a validation study

BackgroundIn the last decade mobile telephone use has become more widespread among children. Concerns expressed about possible health risks have led to epidemiological studies investigating adverse health outcomes associated with mobile telephone use. Most epidemiological studies have relied on self reported questionnaire responses to determine individual exposure. We sought to validate the accuracy of self reported adolescent mobile telephone use.MethodsParticipants were recruited from year 7 secondary school students in Melbourne, Australia. Adolescent recall of mobile telephone use was assessed using a self administered questionnaire which asked about number and average duration of calls per week. Validation of self reports was undertaken using Software Modified Phones (SMPs) which logged exposure details such as number and duration of calls.ResultsA total of 59 adolescents participated (39% boys, 61% girls). Overall a modest but significant rank correlation was found between self and validated number of voice calls (ρ = 0.3, P = 0.04) with a sensitivity of 57% and specificity of 66%. Agreement between SMP measured and self reported duration of calls was poorer (ρ = 0.1, P = 0.37). Participants whose parents belonged to the 4th socioeconomic stratum recalled mobile phone use better than others (ρ = 0.6, P = 0.01).ConclusionAdolescent recall of mobile telephone use was only modestly accurate. Caution is warranted in interpreting results of epidemiological studies investigating health effects of mobile phone use in this age group.

Characterization of electromagnetic interference of medical devices in the hospital due to cell phones.

Concern over electromagnetic interference with medical devices due to cell phone emissions has stemmed from anecdotal reports and unpublished observations of hospital staff. In an effort to characterize electromagnetic interference concerns, representative medical devices from four large teaching hospitals were exposed to standard North American and European communication signal emissions. Of 33 medical devices tested, only 4 showed disruption of critical function due to cell phone emissions at a distance of 25 cm or greater. Although other cases of electromagnetic interference were observed, these were not critically disruptive and mainly occurred when the transmitters were at full power and placed 5 cm or closer to the medical device. Overall, no cell phone signal was exempt from producing electromagnetic interference effects. While sensitive medical devices were often affected by more than one signal type, the effects were not entirely predictable based upon the results of other signals or related medical device units or models. Because a comprehensive analysis of all medical devices in all possible electromagnetic environments was not performed, the data presented here are only intended to provide a general idea of the magnitude of electromagnetic interference effects that might be encountered in a hospital environment, as well as a standard protocol for clinical engineering groups to perform ad hoc electromagnetic interference surveys and methods to manage and/or eliminate electromagnetic interference with appropriate system engineering design including supplementary communication infrastructure, medical device shielding and positioning, and appropriate cell phone user guidelines.

Dosimetry in mice exposed to 1.6 GHz microwaves in a carrousel irradiator.

We have developed a carrousel irradiator for mice which delivers a head-first and near-field radiofrequency exposure that more closely simulates cellular telephone and radio use than conventional whole body exposure systems. Mouse cadavers were placed on the carrousel irradiator and exposed with their noses 5 mm from the feedpoint of a 1.6 GHz antenna. Local measured specific absorption rates (SAR) in brain regions corresponding to the frontal cortex, medial caudate putamen, and midhippocampal areas were 2.9, 2.4, and 2.2 W/kg per watt of irradiated power, respectively. In addition, average SAR was estimated to be 3.4 W/kg per watt along the sagittal plane of the brain, 2.0 W/kg per watt along the sagittal plane of the body, and between 6.8 and 8.1 W/kg per watt at peak locations along the sagittal plane at the body surface. This detailed SAR information in mice is critical to the interpretation of biological studies of IRIDIUM exposure, and similar analysis should be included for all studies of in vivo exposure of small animals to microwaves.

Mobile phones in the hospital: improved mobile communication and mitigation of EMI concerns can lead to an overall benefit to healthcare.

There is a growing trend in hospitals throughout the world to incorporate mobile phones and other wireless technology to offer more efficient, cost effective, and higher quality healthcare. Misunderstanding of mobile phone systems, electromagnetic interference with medical devices, and available management solutions, however, has led to a wide range of inconsistent hospital policies. Recent reviews and commentaries on the subject have provided inconsistent and in some cases factually incorrect information that confuses the issue. At one extreme, unmanaged use of mobile phones in areas where life-critical medical devices are in operation can result in atypical situations that may place patients at risk. At the other extreme, overly-restrictive policies based upon speculation may deny benefits by acting as an obstacle to technology. Overly-restrictive policies may also not address growing and legitimate communication needs of patients and visitors in times of crisis. While it may not be feasible for hospitals to manage every mobile phone handset that is randomly brought into their facility without certain limits on use in areas where life-critical devices are commonly in operation, restrictions are not usually necessary throughout the entire facility. Restrictive policies are also better facilitated when easily accessible areas are designated where mobile phone use is encouraged. Controlled mobile phone systems for use by doctors and staff for hospital-specific communication, by contrast, can operate compatibly throughout the entire hospital facility with appropriate system design and management, even in sensitive areas, and such systems have already been deployed in a number of hospitals throughout the U.S.

The FEL (AF-4) protein donates transcriptional activation sequences to Hrx-Fel fusion proteins in leukemias containing T(4;11)(Q21;Q23) chromosomal translocations

The t(4;11) chromosomal translocation marks a subset of acute lymphoblastic and secondary myeloid leukemias. It results in the fusion of the FEL (AF-4) gene on chromosome band 4q21 with the HRX (MLL) gene on chromosome band 11q23. This translocation results in the expression of fusion transcripts from both translocated chromosomes, with the derivative 11 product (fusing the amino-terminal third of the Hrx protein to the C-terminal two-thirds of the Fel protein) thought to be involved in leukemic transformation. The mechanism of transformation by Hrx-Fel in leukemic cells, however, is unknown and the specific leukemogenic contributions of Fel have not been defined. In this study, we demonstrate that Fel is capable of activating transcription from a minimal adenoviral E1b promoter as a Gal4-Fel fusion protein in transient transcriptional assays. The Fel transactivating sequences were localized to amino acids 365-572 which are consistently retained by Hrx-Fel fusion proteins created by t(4;11) translocations in leukemias. Furthermore, we demonstrate that the transactivation properties of Fel vary in different cell types. While Gal4-Fel constructs strongly activated transcription in Cos-7 cells and the MCF-7 breast tumor cell line, they displayed low to no activity in the precursor B-cell line REH, breast tumor cell line Gl-101A and epithelial-derived A431 cells. These data are consistent with a potential role of Hrx-Fel as a chimeric transcription factor in which Fel contributes transcriptional effector properties and suggest the requirement for cell-specific accessory factors.

A METASTATIC BREAST TUMOR CELL LINE, GI-101A, IS ESTROGEN RECEPTOR POSITIVE AND RESPONSIVE TO ESTROGEN BUT RESISTANT TO TAMOXIFEN

The progression of human breast cancer is often associated with a loss of estrogen dependence for growth, a resistance to estrogen antagonists such as tamoxifen, and the metastatic spread of the disease to secondary sites. Cell lines developed from such advanced breast tumors are often metastatic in athymic mice, show a loss of estrogen receptor mRNA and protein (ER−), and do not respond to 17β‐estradiol. However many advanced human breast tumors do express significant amounts of ER transcript, especially when analyzed by more sensitive methods of detection including RT‐PCR and Ribonuclease Protection Assay (RPA). No metastatic, ER+breast tumor cell line has previously existed to examine the role of ER in metastatic progression and acquired drug (tamoxifen) resistance. The GI‐101A cell line was recently developed from a metastatic breast tumor xenograft and is both tumorogenic and metastatic to the lungs and lymph node when injected into athymic mice, a pattern similar to that seen in patients. While Western blot analysis initially indicated that GI‐101A was ER−, analysis of ER mRNA by RT‐PCR and RPA have demonstrated the expression of ER (as well as EGF receptor and neu oncogene) transcripts. Functional ER in GI‐101A was confirmed by a clear growth response to 17β‐estradiol in culture. Optimal 17β‐estradiol concentrations were significantly lower for GI101A than for MCF‐7 (1nmas opposed to ≥10nm), and GI‐101A growth was inhibited at 17β‐estradiol concentrations above 10nm. Unlike MCF‐7 cells, GI‐101A shows constitutive expression of pS2 protein in hormone depleted media with no apparent induction by 17β‐estradiol supplimentation, as well as a resistance to the anti‐estrogen tamoxifen at concentrations up to 10nm. Finally, ER transcripts which likely represent an alternately spliced ER variant which has previously been shown to encode a constitutively active ER protein have been detected in GI‐101A at levels similar to the wild type transcript, and offer a possible mechanism for estrogen independence, tamoxifen resistance, and constitutive pS2 expression.

Effects of 1.6 GHz Microwaves (Continuous and Pulsed Wave) on c-Fos, Epidermal Growth Factor Receptor, and NSCL-1 Gene Expression in the Mouse Brain

The effect of high level microwave irradiation in experimental animal systems has been analyzed in detail, and these studies have been used to help set occupational and public exposure standards. The FCC has adopted tentative guidelines for the general public specific for microwaves used in communication applications based on recommendations from the Institute of Electrical Engineers (IEEE) and the National Council for Radiation Protection (NCRP), and has established a maximal SAR of 1.6 mW/g averaged over 1 g of tissue over a 30 minute period (1). The long term effectof low level RF exposure, however, has become an issue of public concern due to the increased use of mobile telephones. Some recent studies have suggested biological effects of low level exposure to electromagnetic fields using frequencies from 27 MHz to 2.45 GHz on various endpoints, while others have not. While positive effectshave been attributed to athermal interactions of the microwaves with brain tissue, similar exposure conditions (1mW/cm2 with 0.5 to 2.0 mW/g local SAR) have been shown to have a thermal effect on body temperature in rats with bacterial endotoxin induced hypothermia and impaired thermoregulatory ability (2). These exposures may, therefore, result in localized temperature increases in the brain and/or body of healthy animals which are not detected by a total body temperature increase, and which can lead to a stress response as a result of the restraining apparatus plus thermoregulation and/or the perception of heat. Deliberate hyperthermic exposure of rats to 2.45 GHz at SARs of over 5 W/kg (whole body average) has been reported to elevate the expression of c-fos in the thalamus, hypothalamus, and deep cortical regions of the brain (3). This exposure was also accompanied by a behavioral change (loss of ability to discriminate between objects), and was proposed by the authors to be a heat stress phenomenon due to the induction of hsp 70 protein as well as the reverse of c-fos induction when naltrexone was administered immediately before exposure (4).

In Vitro Laboratory Experiments Related to Cellular Telephone Communication

The dramatic expansion of wireless communications technology, particularly personal mobile telephones, has cast attention on the possible health effects of electromagnetic field exposure in the radiofrequency range. Largely anecdotal information has led to speculation about possible associations with cancer, headaches, sleep disorders and various other symptoms and health conditions. While a large and decisive body of literature exists on the biological effects of high-level microwave radiation, the biological database on the effects of low-level microwave exposure on cancer and other suggested health responses is not as substantial. The available literature contains a limited number of in vivo studies using microwave frequencies and modulation characteristics representative of wireless telephones. While some of these studies suggest an effect of microwaves on malignant and non-malignant disease in animal models, these findings are inconsistent in their reporting of disease type. Moreover, just as many studies have shown a lack of any detectable effect of microwaves on survival, disease incidence, and disease latency. In response to the safety-related questions that have been raised, a number of additional studies have been initiated over the last few years. Some have been completed and are making their way into the scientific literature. Even more are under way or planned. These various studies address the effects of wireless telephone-specific emissions on tumorogenesis, mutagenesis, tumour promotion, implanted tumour growth, DNA and chromosomal damage, neurochemistry, gene expression, and immunologic responses. These studies are listed below along with a brief introduction to quality research design specific for this field.

Epidemiologic Studies Related to Cellular Telephone Communication

In vivo animal studies (and to a lesser extent in vitro studies) are important for the short term hazard assessment of physical and chemical agents. The initial identification of environmental and behavioral risk factors, however, has historically been accomplished through epidemiological studies. Further, epidemiological studies provide the only direct confirmation and assessment of human health risk. Epidemiologic studies can be broadly classified as experimental or observational. Experimental studies involve the intentional, but random, exposure of subjects. Observational studies are non-experimental investigations which can be either analytic (cohort, case-control) or descriptive (ecologic correlation) depending upon whether exposure to individuals is known. To date, few epidemiologic studies have been conducted on the possible health effects associated with radio frequency exposures from cellular telephones1,2, but the number is expected to increase3,4. Definite answers about possible health effects related to the use of radiotelephones from these studies, however, are unlikely to come about in the short term. This is because the validity of any study, no matter how well designed, is made stronger through replication. Further, a disease latency on the order of decades could make immediate detection impossible since the widespread use of mobile telephones is a relatively recent phenomena. Therefore, careful surveillance of populations exposed to radio frequency emissions coupled with comprehensive animal and cellular studies are necessary for an unambiguous determination of possible health effects of cellular telephone exposure.