Assessment of radio frequency fields in the 2.45 GHz band produced by smart home devices.

This paper describes the assessment of the electromagnetic fields produced by consumer "smart" devices used to control and monitor everyday equipment and appliances in a modern "smart" home. The assessment is based on the careful measurement of fields produced by a range of such devices in a laboratory environment configured to operate in a condition simulating high user activity. All devices included in this study operate in the 2.4 GHz band utilizing either Wi-Fi or Bluetooth connectivity. Overall results indicate very low levels of electromagnetic fields for all IoT smart devices in terms of human exposure safety standards (typically much less than 1%) with very low duty cycles (also less than 1%) resulting in even lower time-averaged exposure levels. These low levels of exposure, along with rapid reduction of levels with distance from the devices, suggests that the cumulative effect of multiple devices in a "smart" home are not significant.

Bioelectromagnetics Research within an Australian Context: The Australian Centre for Electromagnetic Bioeffects Research (ACEBR).

Mobile phone subscriptions continue to increase across the world, with the electromagnetic fields (EMF) emitted by these devices, as well as by related technologies such as Wi-Fi and smart meters, now ubiquitous. This increase in use and consequent exposure to mobile communication (MC)-related EMF has led to concern about possible health effects that could arise from this exposure. Although much research has been conducted since the introduction of these technologies, uncertainty about the impact on health remains. The Australian Centre for Electromagnetic Bioeffects Research (ACEBR) is a National Health and Medical Research Council Centre of Research Excellence that is undertaking research addressing the most important aspects of the MC-EMF health debate, with a strong focus on mechanisms, neurodegenerative diseases, cancer, and exposure dosimetry. This research takes as its starting point the current scientific status quo, but also addresses the adequacy of the evidence for the status quo. Risk communication research complements the above, and aims to ensure that whatever is found, it is communicated effectively and appropriately. This paper provides a summary of this ACEBR research (both completed and ongoing), and discusses the rationale for conducting it in light of the prevailing science.

Protein kinase D is increased and activated in lung epithelial cells and macrophages in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive and usually fatal lung disease of unknown etiology for which no effective treatments currently exist. Hence, there is a profound need for the identification of novel drugable targets to develop more specific and efficacious therapeutic intervention in IPF. In this study, we performed immunohistochemical analyses to assess the cell type-specific expression and activation of protein kinase D (PKD) family kinases in normal and IPF lung tissue sections. We also analyzed PKD activation and function in human lung epithelial cells. We found that PKD family kinases (PKD1, PKD2 and PKD3) were increased and activated in the hyperplastic and regenerative alveolar epithelial cells lining remodeled fibrotic alveolar septa and/or fibroblast foci in IPF lungs compared with normal controls. We also found that PKD family kinases were increased and activated in alveolar macrophages, bronchiolar epithelium, and honeycomb cysts in IPF lungs. Interestingly, PKD1 was highly expressed and activated in the cilia of IPF bronchiolar epithelial cells, while PKD2 and PKD3 were expressed in the cell cytoplasm and nuclei. In contrast, PKD family kinases were not apparently increased and activated in IPF fibroblasts or myofibroblasts. We lastly found that PKD was predominantly activated by poly-L-arginine, lysophosphatidic acid and thrombin in human lung epithelial cells and that PKD promoted epithelial barrier dysfunction. These findings suggest that PKD may participate in the pathogenesis of IPF and may be a novel target for therapeutic intervention in this disease.

Incidence of micronuclei in human peripheral blood lymphocytes exposed to modulated and unmodulated 2450 MHz radiofrequency fields.

Peripheral blood samples from four healthy volunteers were collected and aliquots were exposed in vitro for 2 h to either (i) modulated (wideband code division multiple access, WCDMA) or unmodulated continuous wave (CW) 2450 MHz radiofrequency (RF) fields at an average specific absorption rate of 10.9 W/kg or (ii) sham-exposed. Aliquots of the same samples that were exposed in vitro to an acute dose of 1.5 Gy ionizing gamma-radiation (GR) were used as positive controls. Half of the aliquots were treated with melatonin (Mel) to investigate if such treatment offers protection to the cells from the genetic damage, if any, induced by RF and GR. The cells in all samples were cultured for 72 h and the lymphocytes were examined to determine the extent of genetic damage assessed from the incidence of micronuclei (MN). The results indicated the following: (i) the incidence of MN was similar in incubator controls, and those exposed to RF/sham and Mel alone; (ii) there were no significant differences between WCDMA and CW RF exposures; (iii) positive control cells exposed to GR alone exhibited significantly increased MN; and (iv) Mel treatment had no effect on cells exposed to RF and sham, while such treatment significantly reduced the frequency of MN in GR-exposed cells.

Protein kinases D2 and D3 are novel growth regulators in HCC1806 triple-negative breast cancer cells.

AIM: The role of protein kinase D (PKD) in the context of breast cancer cell biology is not clear. MATERIALS AND METHODS: The expression of PKD isoforms was assessed in various breast cancer cell lines and PKD isoform-specific siRNAs and selective inhibitors were used to study the role of PKD in breast cancer cell growth. RESULTS: PKD2 and PKD3 were two major isoforms expressed at the highest levels in tumorgenic HCC1806 triple-negative breast cancer cells. Silencing PKD2 or PKD3 significantly inhibited HCC1806 cell proliferation, and PKD3 silencing had a higher inhibitory effect than PKD2 silencing on cell growth and PKD-mediated signaling. HCC1806 breast cancer cells were highly responsive to PKD inhibitors but not to a general protein kinase C (PKC) inhibitor. CONCLUSION: We have identified PKD2 and PKD3, especially PKD3, as novel cell growth regulators in HCC1806 triple-negative breast cancer cells. Targeting PKD instead of all PKCs effectively inhibited cell proliferation in a number of breast cancer cell lines.

A comparison of the effect of mobile phone use and alcohol consumption on driving simulation performance.

OBJECTIVE: The present study compared the effects of a variety of mobile phone usage conditions to different levels of alcohol intoxication on simulated driving performance and psychomotor vigilance. METHODS: Twelve healthy volunteers participated in a crossover design in which each participant completed a simulated driving task on 2 days, separated by a 1-week washout period. On the mobile phone day, participants performed the simulated driving task under each of 4 conditions: no phone usage, a hands-free naturalistic conversation, a hands-free cognitively demanding conversation, and texting. On the alcohol day, participants performed the simulated driving task at four different blood alcohol concentration (BAC) levels: 0.00, 0.04, 0.07, and 0.10. Driving performance was assessed by variables including time within target speed range, time spent speeding, braking reaction time, speed deviation, and lateral lane position deviation. RESULTS: In the BAC 0.07 and 0.10 alcohol conditions, participants spent less time in the target speed range and more time speeding and took longer to brake in the BAC 0.04, 0.07, and 0.10 than in the BAC 0.00 condition. In the mobile phone condition, participants took longer to brake in the natural hands-free conversation, cognitively demanding hands-free conversation and texting conditions and spent less time in the target speed range and more time speeding in the cognitively demanding, hands-free conversation, and texting conditions. When comparing the 2 conditions, the naturalistic conversation was comparable to the legally permissible BAC level (0.04), and the cognitively demanding and texting conversations were similar to the BAC 0.07 to 0.10 results. CONCLUSION: The findings of the current laboratory study suggest that very simple conversations on a mobile phone may not represent a significant driving risk (compared to legally permissible BAC levels), whereas cognitively demanding, hands-free conversation, and particularly texting represent significant risks to driving.

Individual differences in the effects of mobile phone exposure on human sleep: rethinking the problem.

Mobile phone exposure-related effects on the human electroencephalogram (EEG) have been shown during both waking and sleep states, albeit with slight differences in the frequency affected. This discrepancy, combined with studies that failed to find effects, has led many to conclude that no consistent effects exist. We hypothesised that these differences might partly be due to individual variability in response, and that mobile phone emissions may in fact have large but differential effects on human brain activity. Twenty volunteers from our previous study underwent an adaptation night followed by two experimental nights in which they were randomly exposed to two conditions (Active and Sham), followed by a full-night sleep episode. The EEG spectral power was increased in the sleep spindle frequency range in the first 30 min of non-rapid eye movement (non-REM) sleep following Active exposure. This increase was more prominent in the participants that showed an increase in the original study. These results confirm previous findings of mobile phone-like emissions affecting the EEG during non-REM sleep. Importantly, this low-level effect was also shown to be sensitive to individual variability. Furthermore, this indicates that previous negative results are not strong evidence for a lack of an effect and, given the far-reaching implications of mobile phone research, we may need to rethink the interpretation of results and the manner in which research is conducted in this field.

Assessment of SAR and thermal changes near a cochlear implant system for mobile phone type exposures.

A cochlear implant system is a device used to enable hearing in people with severe hearing loss and consists of an internal implant and external speech processor. This study considers the effect of scattered radiofrequency fields when these persons are subject to mobile phone type exposure. A worst-case scenario is considered where the antenna is operating at nominal full power, the speech processor is situated behind the ear using a metallic hook, and the antenna is adjacent to the hook and the internal ball electrode. The resultant energy deposition and thermal changes were determined through numerical modelling. With a 900 MHz half-wave dipole antenna producing continuous-wave (CW) 250 mW power, the maximum 10 g averaged SAR was 1.31 W/kg which occurred in the vicinity of the hook and the ball electrode. The maximum temperature increase was 0.33 degrees C in skin adjacent to the hook. For the 1800 MHz antenna, operating at 125 mW, the maximum 10 g averaged SAR was 0.93 W/kg in the pinna whilst the maximum temperature change was 0.16 degrees C. The analysis predicts that the wearer complies with the radiofrequency safety limits specified by the International Commission on Non-Ionizing Radiation Protection (ICNIRP), the Institute of Electrical and Electronics Engineers (IEEE), and the Australian Radiation Protection and Nuclear Safety Agency (ARPANSA) for 900 and 1800 MHz mobile phone type exposure and thus raises no cause for concern. The resultant temperature increase is well below the maximum rise of 1 degrees C recommended by ICNIRP. Effects in the cochlea were insignificant.

The effect of GSM-like ELF radiation on the alpha band of the human resting EEG.

Mobile phone handsets such as those operating in the GSM network emit extremely low frequency electromagnetic fields ranging from DC to at least 40 kHz. As a subpart of an extended protocol, the influence of these fields on the human resting EEG has been investigated in a fully counter balanced, double blind, cross-over design study that recruited 72 healthy volunteers. A decrease in the alpha frequency band was observed during the 20 minutes of ELF exposure in the exposed hemisphere only. This result suggests that ELF fields as emitted from GSM handsets during the DTX mode may have an effect on the resting alpha band of the human EEG.

A numerical evaluation of SAR distribution and temperature changes around a metallic plate in the head of a RF exposed worker.

The 1998 International Commission for Non-Ionising Radiation (ICNIRP) Guidelines for human exposure to radiofrequency (RF) fields contain a recommendation to assess the potential impact of metallic implants in workers exposed up to the allowable occupational field limits. This study provides an example of how numerical electromagnetic (EM) and thermal modelling can be used to determine whether scattered RF fields around metallic implants in workers exposed to allowable occupational ambient field limits will comply with the recommendations of relevant standards and guidelines. A case study is performed for plane wave exposures of a 50 mm diameter titanium cranioplasty plate, implanted around 5-6 mm under the surface of the forehead. The level of exposures was set to the ambient power flux density limits for occupational exposures specified in the 1998 ICNIRP guidelines and the current 1999 IEEE C95.1 standard over the frequency range 100-3000 MHz. Two distinct peak responses were observed. There was a resonant response for the whole implant at 200-300 MHz where the maximum dimension of the implant is around a third of the wavelength of the RF exposure. This, however, resulted in relatively low peak specific energy absorption rate (SAR) levels around the implant at the exposure limits. Between 2100-2800 MHz, a second SAR concentrating mechanism of constructive interference of the wave reflected back and forth between the air-scalp interface and the scalp-plate interface resulted in higher peak SARs that were within the allowable limits for the ICNIRP exposures, but not for the IEEE C95.1 exposures. Moreover, the IEEE peak SAR limits were also exceeded, to a lesser degree, even when the implant was not present. However, thermal modelling indicated that the peak SAR concentrations around the implant did not result in any peak temperature rise above 1 degrees C for occupational exposures recommended in the ICNIRP guidelines, and hence would not pose any significant health risk.

The distribution of 210Pb in human bone and its impact on methods for the retrospective estimation of 222Rn exposure from in vivo measurements.

It is possible to estimate radon exposure to man retrospectively by the in vivo measurement of the decay product (210)Pb, which accumulates in the bones. For in vivo methods, knowledge of the distribution of (210)Pb in the skeleton is needed to determine the optimal site for measurement, the skull or the knee. In this study the activity of (210)Pb in a variety of bone samples from 3 individuals have been measured in vitro using underground gamma-ray spectrometry. The individuals were unlikely to have had elevated intakes of Rn. These measurements give baseline data on the bone massic activity of (210)Pb. They show that the massic activity is similar for each of these people and there are similar massic activities of (210)Pb in the skull and the knee of the 2 individuals for which the skull was measured. Additionally for 2 of the individuals trabecular and cortical bone were separated and massic activities were found to be strongly correlated indicating that the (210)Pb is associated with the hydroxyapatite.