Effects of generalization descriptions on risk perception.

The study addresses the effects of generalization descriptions on risk perceptions. In a 1-factorial online experiment, 629 participants were randomly allocated to one of three groups. Group G1 received an excerpt of an original press release from the International Agency for Research on Cancer (IARC) regarding mobile phones and cancer, classifying RF EMF as possibly carcinogenic to humans. Group G2 received an additional explanatory text module, and Group G3 received a rewritten text, with both G2 and G3 highlighting that the possible cancer risk only refers to mobile phones. Risk perceptions regarding cell phones and related personal devices, base stations, and high voltage power lines were used as dependent variables measured before and after text reading. Further, the degree to which participants generalized from cell phone-related to other RF EMF exposures was assessed to determine whether this was predictive of their post-text risk perceptions. Regarding risk perceptions, no differences between the three groups were observed after reading the presented texts. Instead, all three experimental groups indicated increased risk perceptions for all electromagnetic field sources. However, we found significant differences according to the prevailing risk generalization belief. Respondents expressing a strong risk generalization belief showed significantly higher risk perceptions for all tested EMF sources (except mobile phones) than subjects with a weak risk generalization belief.

Effects of selective outcome reporting on risk perception.

The current study aimed to investigate how selective reporting of study results indicating increased health effects will influence its receiver's risk perception. Using the example of the Interphone Study from 2010 on mobile phone usage and cancer, an online experiment was conducted separating respondents into two groups. One group of subjects was informed selectively about a relationship between heavy mobile phone use and an elevated risk of glioma (brain cancer) only. The other group of subjects was informed about the full results of the analyses of glioma risk by cumulative call time, which suggests that other than for the heavy users, there were no statistically significant elevated risks related to mobile phone use. The results showed that selective reporting of risk information increased risk perception when compared to receiving the full information. Additionally, the selectively informed subjects revealed a stronger tendency towards overgeneralization of the 'elevated brain cancer risk' to all mobile phone users, although this did not extend to an overgeneralization to other electromagnetic field sources or differences in the perception of a usage time dependency for possible health risks. These results indicate that reporting of full results is an important factor in effective risk communication.

Framing effects in risk communication messages - Hazard identification vs. risk assessment.

The way in which risk communication messages are framed can influence recipients' risk perceptions. Despite this, there is a limited understanding of how framing is responsible for influencing risk perception. One particularly important element may be whether a risk communication message is framed as a completed 'risk assessment' (specifying a magnitude of risk to the public as a function of the exposure level), or as a 'hazard identification' (a statement regarding whether an environmental agent could in principle cause detrimental health effects in humans, without addressing whether such effects may occur in practice). The current study aimed to investigate for the first time whether framing a risk communication message regarding 'mobile phones and health' as a hazard identification or as a risk assessment affects the reader's risk perception. Using an online survey, participants were separated into three groups and shown either an original press release from the International Agency for Research on Cancer regarding mobile phones and cancer (Group 1), or the press release with additional text modules intended to frame the press release as either a risk assessment (Group 2) or a hazard identification (Group 3). The experimental manipulation was successful in that framing the message as a hazard identification reduced the number of people that believed the press release was a risk assessment, whereas framing it as a risk assessment was not able to increase the number of people who thought that it was a risk assessment. However, no differences in risk perception were found between the groups. In an attempt to ascertain the reason for this lack of framing effect on the radiofrequency electromagnetic fields risk perception measures, it was found that pre-existing interpretations of risk and hazard strongly predicted risk perception, regardless of experimental group. Participants who believed that the International Agency for Research on Cancer conducted a hazard identification perceived lower risks and were less convinced that radiofrequency electromagnetic field exposure from mobile phones increases cancer risks. The results of the study demonstrate the importance of understanding the distinction between a hazard identification and a risk assessment, and suggest that radiofrequency electromagnetic field risk communication needs to develop means for empowering the public to differentiate between hazards and risks.

Use of mobile phones and changes in cognitive function in adolescents.

BACKGROUND: Several studies have investigated the impact of mobile phone exposure on cognitive function in adults. However, children and adolescents are of special interest due to their developing nervous systems. METHODS: Data were derived from the Australian Mobile Radiofrequency Phone Exposed Users' Study (MoRPhEUS) which comprised a baseline examination of year 7 students during 2005/2006 and a 1-year follow-up. Sociodemographic and exposure data were collected with a questionnaire. Cognitive functions were assessed with a computerised test battery and the Stroop Color-Word test. RESULTS: 236 students participated in both examinations. The proportion of mobile phone owners and the number of voice calls and short message services (SMS) per week increased from baseline to follow-up. Participants with more voice calls and SMS at baseline showed less reductions in response times over the 1-year period in various computerised tasks. Furthermore, those with increased voice calls and SMS exposure over the 1-year period showed changes in response time in a simple reaction and a working memory task. No associations were seen between mobile phone exposure and the Stroop test. CONCLUSIONS: We have observed that some changes in cognitive function, particularly in response time rather than accuracy, occurred with a latency period of 1 year and that some changes were associated with increased exposure. However, the increased exposure was mainly applied to those who had fewer voice calls and SMS at baseline, suggesting that these changes over time may relate to statistical regression to the mean, and not be the effect of mobile phone exposure.

Effects of 2G and 3G mobile phones on human alpha rhythms: Resting EEG in adolescents, young adults, and the elderly.

The present study was conducted to determine whether adolescents and/or the elderly are more sensitive to mobile phone (MP)-related bioeffects than young adults, and to determine this for both 2nd generation (2G) GSM, and 3rd generation (3G) W-CDMA exposures. To test this, resting alpha activity (8-12 Hz band of the electroencephalogram) was assessed because numerous studies have now reported it to be enhanced by MP exposure. Forty-one 13-15 year olds, forty-two 19-40 year olds, and twenty 55-70 year olds were tested using a double-blind crossover design, where each participant received Sham, 2G and 3G exposures, separated by at least 4 days. Alpha activity, during exposure relative to baseline, was recorded and compared between conditions. Consistent with previous research, the young adults' alpha was greater in the 2G compared to Sham condition, however, no effect was seen in the adolescent or the elderly groups, and no effect of 3G exposures was found in any group. The results provide further support for an effect of 2G exposures on resting alpha activity in young adults, but fail to support a similar enhancement in adolescents or the elderly, or in any age group as a function of 3G exposure.

The effect of mobile phone electromagnetic fields on the alpha rhythm of human electroencephalogram.

Mobile phones (MP) emit low-level electromagnetic fields that have been reported to affect neural function in humans; however, demonstrations of such effects have not been conclusive. The purpose of the present study was to test one of the strongest findings in the literature; that of increased "alpha" power in response to MP-type radiation. Healthy participants (N = 120) were tested using a double-blind counterbalanced crossover design, with each receiving a 30-min Active and a 30-min Sham Exposure 1 week apart, while electroencephalogram (EEG) data were recorded. Resting alpha power (8-12 Hz) was then derived as a function of time, for periods both during and following exposure. Non-parametric analyses were employed as data could not be normalized. Previous reports of an overall alpha power enhancement during the MP exposure were confirmed (relative to Sham), with this effect larger at ipsilateral than contralateral sites over posterior regions. No overall change to alpha power was observed following exposure cessation; however, there was less alpha power contralateral to the exposure source during this period (relative to ipsilateral). Employing a strong methodology, the current findings support previous research that has reported an effect of MP exposure on EEG alpha power.

Mobile phones and brain tumours: a review of epidemiological research.

There has been a great deal of public concern regarding the possibility that the use of mobile phone-related technologies might result in adverse health effects. Corresponding to this, there has been substantial epidemiological research designed to determine whether the use of mobile phones (MP) has any effect on health, and in particular whether it increases the risk of developing head and neck tumours. Such literature is particularly heterogeneous, which makes it difficult to pool in a meta-analysis. This paper thus reviews the epidemiological literature pertaining to the use of mobile phones and mobile phone-related technologies, and head and neck tumours, in an attempt to consolidate the various reports. Although there have been individual reports of associations between MP-use and tumours, this research is not consistent and on balance does not provide evidence of an association. There are reports of small associations between MP-use ipsilateral to the tumour for greater than 10 years, for both acoustic neuroma and glioma, but the present paper argues that these are especially prone to confounding by recall bias. The reported associations are in need of replication with methods designed to minimise such bias before they can be treated as more than suggestive.

Effects of aging and depression on mnemonic discrimination ability.

Aging and depression have been found to be associated with poorer performance in mnemonic discrimination. In the current study, a two-response format mnemonic similarity test, Cognitive Drug Research MST, was used to compare these effects. Seventy-six participants were tested; with 52 participants in the young group, aged 18-35 years, and 24 participants in the elderly group, aged 55 years or older. Twenty-two young participants and 10 elderly participants met DSM-IV criteria for MDD or dysthymia. Age-related deficits were found for lure identification and speed of response. Differences in speed of responses to lure images were found for younger depressed participants, and depressive symptom severity was found to be negatively associated with lure identification accuracy in the elderly. These findings may be viewed as putative behavioral correlates of decreased pattern separation ability, which may be indicative of altered hippocampal neurogenesis in aging and depression.

ERP components associated with an indirect emotional stop signal task in healthy and depressed participants.

Recent research has provided evidence to suggest that emotional stimuli may interfere with response inhibition, due to automatic capture of attention. Whilst previous studies have provided data regarding changes to event-related potentials (ERPs) in emotional Go/NoGo tasks, few studies to-date have utilized an emotional stop signal task (SST). Thirty-five participants were included in the study; 21 healthy controls and 14 depressed. An indirect emotional SST was employed, which consisted of the presentation of neutral, negative or positive visual images. The primary two-choice reaction time task required responding to frame colour (blue or green), whilst in 33% of trials an auditory stop signal was presented, with stop signal delay adjusted according to an adaptive tracking procedure. ERPs associated with both the primary visual task and the auditory SST were analysed using temporal principle components analysis (tPCA). In the primary task, reaction times were found to be slower for negative compared to neutral images. Stop signal reaction time (SSRT) was not found to be affected by image category or depression status. However, the NoGo-N2 component was found to be reduced for positive images, whilst the NoGo-P3 component was reduced for both positive and negative images in comparison to neutral images in the stop signal task. This effect was found to be enhanced for the depressed participants, indicating that inhibitory processing in the presence of positive stimuli may be inhibited to a greater extent in depressed individuals than in healthy controls. These findings provide further evidence for the ability of emotional valence and major depressive disorder to influence inhibitory processing.

Comparison of the effects of continuous and pulsed mobile phone like RF exposure on the human EEG.

It is not clear yet whether Global System for Mobiles (GSM) mobile phone radiation has the ability to interfere with normal resting brain function. There have been reports that GSM exposure increases alpha band power, and does so only when the signal is modulated at low frequencies (Huber, R., Treyer, V., Borbely, A. A., Schuderer, J., Gottselig, J. M., Landolt, H.P., Werth, E., Berthold,T., Kuster, N., Buck, A and Achermann, P. Electromagnetic fields, such as those from mobile phones, alter regional cerebral blood flow and sleep and waking EEG. J Sleep Res 11, 289-295, 2002.) However, as that research employed exposure distributions that are not typical of normal GSM handset usage (deep brain areas were overexposed), it remains to be determined whether a similar result patterning would arise from a more representative exposure. In this fully counterbalanced cross-over design, we recruited 12 participants and tried to replicate the modulation linked post exposure alpha band power increase described above, but with an exposure source (dipole antenna) more closely resembling that of a real GSM handset. Exposures lasted for 15 minutes. No changes to alpha power were found for either modulated or unmodulated radiofrequency fields, and thus we failed to replicate the above results. Possible reasons for this failure to replicate are discussed, with the main reason argued to be the lower and more representative exposure distribution employed in the present study. In addition we investigated the possible GSM exposure related effects on the non-linear features of the resting electroencephalogram using the Approximate Entropy (ApEn) method of analysis. Again, no effect was demonstrated for either modulated or unmodulated radiofrequency exposures.

The effects of dexamphetamine on simulated driving performance.

RATIONALE: The number of road fatalities related to the presence of amphetamines in drivers has been relatively constant over the past 10 years. However, there remains uncertainty as to the extent that these drugs induce driving impairment, and whether any such impairments translate to an increase in road fatalities. OBJECTIVES: To examine the acute effects of 0.42 mg/kg dexamphetamine on simulated driving performance, and to establish which, if any, simulated driving abilities become impaired following dexamphetamine administration. METHODS: A repeated-measures, counter-balanced, double-blind, placebo-controlled design was employed. Twenty healthy volunteers completed two treatment conditions-0.42 mg/kg dexamphetamine and placebo. Performance was assessed using a driving simulator task. Blood and saliva samples were obtained prior to the driving tasks and immediately after task completion (120 min and 170 min post-drug administration, respectively). RESULTS: Mean dexamphetamine blood concentrations were 83 ng/ml and 98 ng/ml at 120 min and 170 min, respectively. Results indicated a decrease in overall simulated driving ability following dexamphetamine administration during the day-time but not the night-time scenario tasks. Contributing to this performance reduction, "incorrect signalling", "failing to stop at a red traffic light" and "slow reaction times" were the behaviours most strongly affected by dexamphetamine. CONCLUSIONS: The decrease in simulated driving ability observed during the day-time driving tasks are consistent with the perceptual narrowing or tunnel vision that is associated with dexamphetamine consumption.

Associations of P50 suppression and desensitization with perceptual and cognitive features of "unreality" in schizotypy.

BACKGROUND: P50 suppression is an electrophysiologic index of early sensory gating and has consistently been found deficient in schizophrenic patients. This gating deficit is thought to lead to sensory overload and cognitive fragmentation, and correspondingly many symptoms of the disorder. However, the link between P50 suppression deficits and symptomatology is yet to be established, and so this study was designed to determine whether such a relation is present within a nonclinical population. METHODS: P50 suppression and schizotypy measures were obtained from 36 healthy volunteers, and correlation analyses determined whether measures of schizotypy were related to P50 suppression. RESULTS: Consistent with the view that P50 gating deficits are related to schizophrenic symptoms, subjects with poorer P50 suppression reported more perceptual anomalies and magical ideation--an unreality syndrome--in contrast to other positive symptoms and to withdrawal. This study also found a trend to P50 suppression desensitization, and that whereas subjects low on "unreality" demonstrated desensitization to the second of the paired clicks, subjects high on "unreality" demonstrated sensitization. CONCLUSIONS: It is concluded that early sensory gating deficits, in the form of poor P50 suppression, are related to unreality aspects of schizotypy. This supports the view that poor P50 suppression in schizophrenia is related to symptomatology.

Electrophysiological evidence of serotonergic impairment in long-term MDMA ("ecstasy") users.

OBJECTIVE: "Ecstasy," or 3,4-methylenedioxymethamphetamine (MDMA), causes long-term impairment to the serotonin (5-HT) system in rats, dogs, and nonhuman primates. 5-HT dysfunction has also been observed in human recreational users of the drug, but whether 5-HT dysfunction in humans is caused by MDMA has not been established, since dysfunction may have preceded MDMA exposure. This ambiguity about causation is particularly important in MDMA research, because 5-HT deficiency is a predictor of risky behavior. METHOD: The 5-HT function of 22 long-term MDMA users was compared to that of 20 drug-naive comparison subjects and 19 cannabis users. 5-HT function was assessed with the intensity dependence paradigm, a tool that measures 5-HT-related attenuation of neural response to auditory stimuli (measured with EEG). RESULTS: Long-term MDMA users exhibited 5-HT dysfunction, relative to both cannabis users and drug-naive comparison subjects. This dysfunction was related to total MDMA consumption (after removing the effect of frequency of use) but not to frequency of use (after removing the effect of total consumption). CONCLUSIONS: These data show that 5-HT dysfunction occurs in MDMA users, is related to users' MDMA consumption, and is independent of cannabis use. The results do not suggest that self-medication explains this relationship, because the deficit was related to total MDMA consumption but not frequency of consumption. The results are thus consistent with the thesis that MDMA consumption causes 5-HT impairment in humans.

Chronic MDMA (ecstasy) use, cognition and mood.

RATIONALE: It has been suggested that 3,4-methylenedioxymethamphetamine (MDMA or ecstasy) causes damage to the serotonergic system, and that this damage results in cognitive and mood impairments. OBJECTIVES: To examine the effect of chronic MDMA usage on a wide battery of cognitive tests and psychological abilities and processes. METHODS: In the present study, the performance of 17 participants with a history of MDMA use was compared to the performance of 15 control subjects on a battery of neuropsychological tests. This battery included tests for depression, immediate word recall, delayed recall, attention and working memory. RESULTS: Results indicated that the MDMA group had significantly higher scores for depression than the control group, and displayed poorer delayed recall and verbal learning than controls after accounting statistically for the effects of cannabis and depression. CONCLUSIONS: These results suggest that MDMA users exhibit difficulties in coding information into long-term memory, display impaired verbal learning, are more easily distracted, and are less efficient at focusing attention on complex tasks.

The relative contributions of ecstasy and cannabis to cognitive impairment.

RATIONALE: (+/-)-3,4-methylenedioxymethamphet-amine (MDMA; 'ecstasy'), a commonly used recreational drug, has typically been found to be related to poor cognitive function in humans. However, cannabis consumption may not have been adequately controlled for in these studies. OBJECTIVE: The present study was designed to further elucidate the relation between MDMA and cannabis in cognitive impairment. METHODS: Subjects who had used neither MDMA nor cannabis (controls; n=31), cannabis but not MDMA (cannabis users; n=18) and both MDMA and cannabis (MDMA/cannabis users; n=11) were compared on a battery of neuropsychological tests. RESULTS: The cannabis and MDMA/cannabis groups did not differ on any of the tests, whereas the combined cannabis and MDMA/cannabis groups performed more poorly than controls on tests of memory, learning, word fluency, speed of processing and manual dexterity. Further, apart from speed of processing where higher MDMA consumption predicted slower processing, covariate analysis revealed that the deficits were more closely related to cannabis than MDMA usage. CONCLUSION: The results suggest that cannabis is an important confound in studies of MDMA-related cognitive impairment, and that previously reported cognitive impairment in MDMA users may have been caused by coincident cannabis use.

Reperitonealization and invagination of the lesser curvature of the stomach following proximal gastric vagotomy.

Lesser curve necrosis usually presents as free perforation. A case of large gastric ulcer occurring very shortly after proximal gastric vagotomy (PGV) for a duodenal ulcer that was almost certainly due to ischemic necrosis of the lesser curve is presented here. Reperitonealization and invagination of the lesser curve is recommended following PGV so that, if necrosis occurs, it will take place within the stomach and not into the free peritoneal cavity. This maneuver may also avoid possible vagal reinnervation and the formation of dense adhesions between the stomach and liver.

EOG correction: comparing different calibration methods, and determining the number of epochs required in a calibration average.

OBJECTIVE: A form of EOG correction called the 'aligned-artifact average' (AAA) method has been advanced by the authors. In contrast to many previous methods, this used a correction coefficient (B), based on an average of eye movements rather than raw data, to remove eye movement related contamination from the EEG. The first part of this study was aimed at determining whether a variation of this procedure that is more easily implemented would produce a similar correction. The second part was designed to determine the number of epochs needed in an average to correct adequately. METHODS: Subjects performed a series of eye movement tasks whilst EEG and EOG data were recorded. Data were manipulated according to either the AAA or an alternate new ERP method (NERP) and the resultant Bs were compared in part A. In part B, averages were created from varying numbers of epochs, and the resultant r(2)-values were compared. RESULTS: The AAA and NERP methods produced the same Bs, and averages with at least 40 epochs were required for adequate B estimation for both VEOG and HEOG. CONCLUSION: There is no difference between the AAA and NERP methods and thus it is acceptable to use the more easily implemented NERP method for EOG correction. It is recommended that when applying this procedure, at least 40 epochs should be used to make up the averages from which to calculate correction coefficients.

EOG correction of blinks with saccade coefficients: a test and revision of the aligned-artefact average solution.

OBJECTIVE: The 'aligned-artefact average' (AAA) procedure was advanced by the authors as a technique suitable for removing eye movement-related artefacts from the EEG. It was proposed that this method would correct both blink and non-blink artefact from the EEG, using the same set of correction coefficients (Bs). However, recent evidence suggests that this simplification is not always accurate. Thus, we test here a revision of the AAA, including an appropriate allowance for the radial EOG (REOG) component, that does allow the use of the same Bs for the correction of blink and non-blink artefact. METHODS: Blink (and saccade) ERP data from 15 subjects were corrected using the AAA method, with Bs calculated from the same blink (and saccade) data set (referent waveforms), or a different set of blink (and saccade) data, or using the new revised AAA procedure (RAAA). RESULTS: AAA Bs calculated from saccades corrected blinks poorly (and vice versa). However, the RAAA Bs corrected blink ERPs better than blink-derived Bs, and saccade ERPs better than saccade-derived Bs. It was also found that irrespective of correction type, inclusion of REOG improved correction. CONCLUSION: EOG correction is more accurate when the radial channel is included, but inclusion of REOG (and/or HEOG) is not sufficient to resolve the discrepancy between blink and saccade correction. Using the RAAA procedure, both blink and non-blink data can be corrected using the same set of Bs.

Removal of ocular artifact from the EEG: a review.

Eye movements cause changes to the electric fields around the eyes, and consequently over the scalp. As a result, EEG recordings are often significantly distorted, and their interpretation problematic. A number of methods have been proposed to overcome this problem, ranging from the rejection of data corresponding temporally to large eye movements, to the removal of the estimated effect of ocular activity from the EEG (EOG correction). This paper reviews a number of such methods of dealing with ocular artifact in the EEG, focusing on the relative merits of a variety of EOG correction procedures. Issues discussed include the distinction between frequency and time domain approaches, the number of EOG channels required for adequate correction, estimating correction coefficients from raw versus averaged data, differential correction of different types of eye movement, the most suitable statistical procedure for estimating correction coefficients, the use of calibration trials for the estimation of correction coefficients, and the distinction between 'coefficient estimation' and 'correction phase' error. A suggested EOG correction algorithm is also described.

The use of a 'phantom scalp' to assess the possible direct pickup of mobile phone handset emissions by electroencephalogram electrode leads.

A 'Phantom Scalp' was constructed from a conducting foam mat to form a layer under a 62-electrode electroencephalogram cap closely approximating the electrical properties of a human scalp. The mat was placed over a polystyrene manikin head to preserve a correct anatomical arrangement. Electrical signals were recorded with a Global System for Mobile (GSM) communications mobile phone handset in place against the side of the 'head'. Amplitude spectra were compared for three phone conditions: 'off', 'standby' and 'transmit'. At 217 Hz, significant differences were obtained between 'transmit' and the other two conditions, but no significant differences were noted for the physiologically important range 0.5-30 Hz. An anomalous difference was noted for one electrode in the range 30-45 Hz.