New developments in cosmetic applications of electromagnetic fields: Client and occupational hazard assessment.

Energy-based devices are used to improve features of appearance for aesthetic reasons while avoiding more invasive methods. Examples of treatment targets are the reduction of wrinkles, sagging, unwanted skin lesions, body hair and excess fatty tissue, and the enhancement of muscle tissue. One treatment modality is the use of electromagnetic fields (EMF, 0‒300 GHz). The present work aims to give an up-to-date survey of cosmetic applications of EMF for professional use with an assessment of client and worker exposure and possible adverse effects. A systematic search was conducted for peer-reviewed articles (2007-2022), patents, premarket notifications, manufacturer data, and adverse effects reports. Five categories of cosmetic EMF device with increasing frequency were identified: sinusoid low frequency magnetic fields for lipolysis; pulsed low frequency magnetic fields for skin rejuvenation; pulsed low frequency magnetic fields for muscle building; radiofrequency EMF for lipolysis or skin rejuvenation; microwaves for hair removal or hyperhidrosis. In the vicinity of the last four device categories, there is a potential for exceeding the occupational exposure limits in the European Union EMF Directive, which could lead to nerve or muscle stimulation, burns or overheating. There are also potential hazards for clients or workers wearing active or passive medical devices. The severity of reported adverse effects increases with EMF frequency.

Protection of Workers Exposed to Radiofrequency Electromagnetic Fields: A Perspective on Open Questions in the Context of the New ICNIRP 2020 Guidelines.

Workers in occupational settings are usually exposed to numerous sources of electromagnetic fields (EMF) and to different physical agents. Risk assessment for industrial workplaces concerning EMF is not only relevant to operators of devices or machinery emitting EMF, but also to support-workers, bystanders, service and maintenance personnel, and even visitors. Radiofrequency EMF guidelines published in 2020 by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) may also be indirectly applied to assess risks emerging from EMF sources at workplaces by technical standards or legislation. To review the applicability and adequacy to assess exposure to EMF in occupational settings in the European Union, the most current ICNIRP guidelines on radiofrequency EMF are reviewed. Relevant ICNIRP fundamentals and principles are introduced, followed by practical aspects of exposure assessment. To conclude, open questions are formulated pointing out gaps between the guidelines' principles and occupational practice, such as the impact of hot and humid environments and physical activity or controversies around ICNIRPS's reduction factors in view of assessment uncertainty in general. Thus, the article aims to provide scientific policy advisors, labor inspectors, or experts developing standards with a profound understanding about ICNIRP guidelines' applicability to assess hazards related to radiofrequency EMF in occupational settings.

Occupational exposure to radiofrequency electromagnetic fields.

High exposures to radiofrequency electromagnetic fields (RF EMF) are possible in workplaces involving sources used for broadcasting, telecommunication, security and identification, remote sensing and the heating and drying of goods. A systematic literature review of occupational RF EMF exposure measurements could help to clarify where more attention to occupational safety may be needed. This review identifies specific sources of occupational RF EMF exposure and compares the published maximum exposures to occupational exposure limits. A systematic search for peer-reviewed publications was conducted via PubMed and Scopus. Relevant grey literature was collected via web searches. For each publication, the highest measured electric field strength, magnetic flux density or power density was extracted. Maximum exposures exceeding the limits were reported for dielectric heating, scanners for security and radiofrequency identification, plasma devices and broadcasting and telecommunication transmitters. Occupational exposure exceeding the limits was rare for microwave heating and radar applications. Some publications concerned cases studies of occupational accidents followed by a medical investigation of thermal health effects. These were found for broadcasting antennas, radar installations and a microwave oven and often involved maintenance personnel. New sources of occupational exposure such as those in fifth generation telecommunication systems or energy transition will require further assessment.

Occupational exposure to electromagnetic fields from medical sources.

High exposures to electromagnetic fields (EMF) can occur near certain medical devices in the hospital environment. A systematic assessment of medical occupational EMF exposure could help to clarify where more attention to occupational safety may be needed. This paper seeks to identify sources of high exposure for hospital workers and compare the published exposure data to occupational limits in the European Union. A systematic search for peer-reviewed publications was conducted via PubMed and Scopus databases. Relevant grey literature was collected via a web search. For each publication, the highest measured magnetic flux density or internal electric field strength per device and main frequency component was extracted. For low frequency fields, high action levels may be exceeded for magnetic stimulation, MRI gradient fields and movement in MRI static fields. For radiofrequency fields, the action levels may be exceeded near devices for diathermy, electrosurgery and hyperthermia and in the radiofrequency field inside MRI scanners. The exposure limit values for internal electric field may be exceeded for MRI and magnetic stimulation. For MRI and magnetic stimulation, practical measures can limit worker exposure. For diathermy, electrosurgery and hyperthermia, additional calculations are necessary to determine if SAR limits may be exceeded in some scenarios.

The revised electromagnetic fields directive and worker exposure in environments with high magnetic flux densities.

Some of the strongest electromagnetic fields (EMF) are found in the workplace. A European Directive sets limits to workers' exposure to EMF. This review summarizes its origin and contents and compares magnetic field exposure levels in high-risk workplaces with the limits set in the revised Directive. Pubmed, Scopus, grey literature databases, and websites of organizations involved in occupational exposure measurements were searched. The focus was on EMF with frequencies up to 10 MHz, which can cause stimulation of the nervous system. Selected studies had to provide individual maximum exposure levels at the workplace, either in terms of the external magnetic field strength or flux density or as induced electric field strength or current density. Indicative action levels and the corresponding exposure limit values for magnetic fields in the revised European Directive will be higher than those in the previous version. Nevertheless, magnetic flux densities in excess of the action levels for peripheral nerve stimulation are reported for workers involved in welding, induction heating, transcranial magnetic stimulation, and magnetic resonance imaging (MRI). The corresponding health effects exposure limit values for the electric fields in the worker's body can be exceeded for welding and MRI, but calculations for induction heating and transcranial magnetic stimulation are lacking. Since the revised European Directive conditionally exempts MRI-related activities from the exposure limits, measures to reduce exposure may be necessary for welding, induction heating, and transcranial nerve stimulation. Since such measures can be complicated, there is a clear need for exposure databases for different workplace scenarios with significant EMF exposure and guidance on good practices.

Electromagnetic fields and the blood-brain barrier.

The mammalian blood-brain barrier (BBB) consists of endothelial cells, linked by tight junctions, and the adjoining pericytes and extracellular matrix. It helps maintain a highly stable extracellular environment necessary for accurate synaptic transmission and protects nervous tissue from injury. An increase in its normally low permeability for hydrophilic and charged molecules could potentially be detrimental. Methods to assess the permeability of the BBB include histological staining for marker molecules in brain sections and measurement of the concentration of marker molecules in blood and brain tissue. Their advantages and disadvantages are discussed. Exposure to levels of radiofrequency electromagnetic fields (EMF) that increase brain temperature by more than 1°C can reversibly increase the permeability of the BBB for macromolecules. The balance of experimental evidence does not support an effect of 'non-thermal' radiofrequency fields with microwave and mobile phone frequencies on BBB permeability. Evidence for an effect of the EMF generated by magnetic resonance imaging on permeability is conflicting and conclusions are hampered by potential confounders and simultaneous exposure to different types and frequencies of EMF. The literature on effects of low frequency EMF, which do not cause tissue heating, is sparse and does not yet permit any conclusions on permeability changes. Studies on the potential effect of EMF exposure on permeability of the BBB in humans are virtually absent. Future permeability studies should focus on low frequency effects and effects in humans. Care should be taken to avoid the methodological limitations of earlier studies and to determine the pathophysiological relevance of any changes found.

Altered neuropeptide Y and neurokinin messenger RNA expression and receptor binding in stress-sensitised rats.

A single session of footshocks in rats causes long-lasting sensitisation of behavioural, hormonal and autonomic responses to subsequent novel stressful challenges as well as altered pain sensitivity. These changes mimic aspects of post-traumatic stress disorder in humans. Our aim was to identify neuropeptide substrates in the central nervous system involved in stress sensitisation. Male Wistar rats were exposed to ten footshocks in 15 min (preshocked) or placed in the same cage without shocks (control). Two weeks later, rats were placed in a novel cage, subjected to 5 min of 85 dB noise, and returned to their home cage. Rats were killed either before or 1 h after noise and their brains processed for in situ hybridization for neuropeptide Y (NPY) and beta-preprotachykinin-I (PPT) mRNA. Additional groups of rats were killed under basal conditions and brains processed for NPY and neurokinin receptor binding with radiolabelled ligands. Two weeks after footshock treatment NPY mRNA expression was increased in the basolateral amygdala and showed preshockxnoise interaction in the locus coeruleus (down after noise in controls, lower basal and unchanged after noise in preshocked). PPT expression in the lateral parabrachial nucleus also showed preshockxnoise interaction (up after noise in controls, higher basal and down after noise in preshocked), and was increased after noise in the periaquaeductal grey. NK1 receptor binding in the agranular insular cortex and arcuate nucleus of the hypothalamus and NK2 receptor binding in the amygdala was lower in preshocked rats than in controls. Altered expression of NPY in the basolateral amygdala and locus coeruleus could contribute to or compensate for behavioural and autonomic sensitisation in preshocked rats. Altered PPT expression in the parabrachial nucleus may be involved in the altered pain processing seen in this model. Lower NK1 and NK2 receptor numbers in cortex, hypothalamus and amygdala may reflect secondary adaptations to altered neuropeptide release. These long-term changes in brain neuropeptide systems could offer novel leads for pharmacological modulation of long-term stress-induced sensitisation.

Duodenal pain and spinal morphine induce conditioned taste aversion in rats.

Conditioned taste aversion (CTA) is a behavioural response essential to the survival of an individual. The combination of taste and odour of most foods provides a strong conditioned stimulus (CS) for an animal to respond in an appropriate way to any harmful unconditioned stimuli (US) that follow. The most widely used conditioned stimuli are drinkable sweet solutions, such as saccharin and sucrose. CTA-like responses are also found for environmental unconditioned stimuli, but these usually take longer training. In the present study, the aversive nature of a duodenal distention with an implanted balloon catheter was studied in freely moving rats using either CTA against a sucrose solution, or a light-dark passive avoidance (PA) paradigm. In addition, the effect of spinal morphine on CTA and the cardiovascular response to duodenal distention were studied. CTA could be induced by a single, but long-lasting 20-minute duodenal distention, which did not induce PA behaviour in a light-dark box. Spinal infusion of morphine alone induced CTA, suggesting that the model is unsuitable to investigate spinal pharmacological modulation of visceral pain. Spinal morphine did reduce the cardiovascular response to duodenal distention, strengthening its validity as a visceral pain model. Since CTA is a complicating factor in the field of chemotherapy in cancer patients and spinal morphine causes nausea and vomiting in humans, CTA may also complicate spinal drug treatment or anaesthesia.

PTSD and stress sensitisation: a tale of brain and body Part 2: animal models.

Animal models that are characterised by long-lasting conditioned fear responses as well as generalised behavioural sensitisation to novel stimuli following short-lasting but intense stress have a phenomenology that resembles that of PTSD in humans. These models include brief sessions of shocks, social confrontations, and a short sequence of different stressors. Subgroups of animals with different behavioural traits or coping styles during stress exposure show a different degree or pattern of long-term sensitisation. Weeks to months after the trauma, treated animals on average also show a sensitisation to novel stressful stimuli of neuroendocrine, cardiovascular and gastrointestinal motility responses as well as altered pain sensitivity and immune function. Functional neuroanatomical and pharmacological studies in these animal models have provided evidence for involvement of amygdala and medial prefrontal cortex, and of brain stem areas regulating neuroendocrine and autonomic function and pain processing. They have also generated a number of neurotransmitter and neuropeptide targets that could provide novel avenues for treatment in PTSD.

PTSD and stress sensitisation: a tale of brain and body Part 1: human studies.

Post-traumatic stress disorder (PTSD) is a chronic, debilitating psychiatric disorder that can follow exposure to extreme stressful experiences. It is characterised by hyperarousal and increased startle responses, re-experiencing of the traumatic event, withdrawal or avoidance behaviour and emotional numbing. The focus of this review is on aspects that have received less attention. PTSD develops only in a substantial minority of people exposed to traumatic stress, and possible individual traits that increase vulnerability are discussed. An overview is given of the wide variety of physiological disturbances that accompany PTSD and may contribute to disability, including neuroendocrine, cardiovascular, gastrointestinal and immune function and pain sensitivity. Brain imaging and pharmacological studies have generated some insight into the circuitry that may be involved in the generation of PTSD symptoms. Major limitations of human studies so far are the issue of causality and our lack of understanding of the underlying molecular substrates in the brain, which are easier to address in relevant animal models and will be discussed in a companion paper.

Involvement of group II metabotropic glutamate receptors in stress-induced behavioural sensitization.

RATIONALE: A short session of repeated foot shocks in rats causes long-lasting sensitization of behavioural, hormonal and autonomic responses to novel stressful challenges. The behavioural sensitization can be reduced by anxiolytics and mimics aspects of stress-induced changes in patients with post-traumatic stress disorder. OBJECTIVES: The aim of this study was to test the efficacy of a group II metabotropic glutamate receptor (mGluR) agonist and assess altered brain mGluR receptor expression in shock-sensitized rats. MATERIALS AND METHODS: Male Wistar rats were exposed to a 15-min session with ten 6-s foot shocks (preshocked). One and 2 weeks later, rats were intraperitoneally injected with the group II metabotropic glutamate receptor agonist (2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC) or vehicle, and 30 min later exposed to 5 min of 85 dB noise. For in situ hybridization with probes for mGluR1, mGluR2, mGluR3 and mGluR5, preshocked and control rats were killed under basal conditions 2 weeks after foot shocks and their brains cryosectioned. RESULTS: APDC had no clear effect in controls, but dose-dependently reduced high immobility and increased low locomotion and rearing seen in preshocked rats to the levels of controls. mGluR3 expression was increased in the basolateral nucleus of the amygdala, and mGluR2 expression was increased in the agranular insular cortex of preshocked rats compared to controls. CONCLUSIONS: Shock-induced behavioural sensitization in rats is reduced by acute treatment with a group II metabotropic glutamate receptor agonist. This effect may depend on the increased expression of amygdala mGluR3, which could be hypothesized as an endogenous mechanism to counteract stress-induced neuronal sensitization.

Individual reactivity to the open-field predicts the expression of stress-induced behavioural and somatic pain sensitisation.

Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder. It is associated with somatic complaints like pain problems. Only a proportion of persons exposed to traumatic events develop PTSD. Several factors, like genetic predisposition, stressor intensity, cognitive appraisal mechanisms and coping processes influence the likelihood of developing PTSD after exposure to a trauma. We used a single session of footshocks in rats, an animal model with a high degree of validity for PTSD, to study whether individual behavioural traits predict long-term stress-induced sensitisation of behavioural responsivity and somatic pain sensitivity and therefore can act as a vulnerability factor. Rats were selected for low (LA) and high (HA) open-field locomotor reactivity and then underwent a single session of footshocks. Two to 5 weeks after footshocks, behavioural sensitisation was investigated using a noise challenge, an electrified prod challenge and a forced swim test. Somatic pain sensitivity was measured using a tail-immersion test. During exposure to noise in a novel cage, footshocked rats showed increased immobility compared to controls, which was significantly greater in LA than in HA rats. Footshocked rats showed increased burying in the electrified prod challenge and no effect was found in the forced swim test. Footshocks caused hyperalgesia in LA rats, but hypoalgesia in HA rats. We conclude that low open-field locomotor reactivity predicts the degree of stress-induced behavioural sensitisation and the direction of altered somatic pain sensitivity, suggesting that an anxiety-prone personality or passive coping style may increase the risk of developing stress-related psychosomatic disorders.

Individual reactivity to the open-field predicts the expression of cardiovascular and behavioural sensitisation to novel stress.

Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder. It is associated with cardiovascular disorders and irritable bowel syndrome (IBS). Besides stressful life-events, a prior history of gastrointestinal infection is a predisposing factor for the development of IBS. Only a proportion of persons exposed to traumatic events develop PTSD. Several factors, like genetic predisposition, stressor intensity, cognitive appraisal mechanisms and coping processes influence the likelihood of developing PTSD after exposure to a trauma. We used a single session of footshocks in rats, an animal model with a high degree of validity for PTSD, to study whether transient colonic inflammation alters local and distal visceral sensitivity, and whether reactivity to the open-field (low (LA) or high (HA) active) predicts long-term stress-induced behavioural and cardiovascular sensitisation and altered visceral pain sensitivity. A distention series and noise challenge were given 2 weeks after foot-shocks, followed by a transient colonic inflammation period and a second distention series and noise challenge 4 weeks after foot-shocks. During exposure to noise, both before and after inflammation, footshocked rats showed increased immobility compared to controls, which was significantly greater in LA rats than in HA rats. LA preshocked rats also showed a greater blood pressure response to the noise test, but this only became evident in the second noise-test. Neither footshocks nor colonic inflammation affected duodenal pain sensitivity. The results provide additional evidence for long-lasting cardiovascular hyperresponsivity after a stressful event and indicate that its degree is predicted by personality traits or coping style.

Physiological and behavioural responses to duodenal pain in freely moving rats.

Luminal distention of the intestine can be aversive in humans and laboratory animals, and hypersensitivity to distention is found in functional gastrointestinal disorders. Current animal models either require anaesthesia or acute balloon intubation or use implanted balloons of irritant materials, for which the aversive quality of distention and physiological responses have not been well characterised. We report here that silicone balloon catheters implanted in the duodenum via the stomach have long patency without obvious tissue damage. Balloon inflation in freely moving rats caused passive avoidance learning and classic 'pain' postures, as well as graded cardiovascular responses which can be recorded telemetrically. The method should make long-lasting studies of pharmacological and environmental effects on visceral sensitivity more feasible.

Long-lasting changes in central nervous system responsivity to colonic distention after stress in rats.

BACKGROUND & AIMS: The highly prevalent functional gastrointestinal disorders involve visceral pain and disturbed bowel habit and are associated with preceding stressful experiences, although causality and biological mechanisms remain unclear. The aim of the present study was to establish whether stress can directly and lastingly alter central nervous system responsivity to colonic distention in the rat as well as which neural pathways are likely to be involved. METHODS: Rats were treated with a brief session of stressful foot shocks known to induce long-term behavioral and autonomic sensitization. Two weeks later, after induction of inhalation anesthesia, a balloon catheter was inserted in the distal colon and repeatedly inflated with brief, constant-pressure air pulses. RESULTS: Reflex decreases in blood pressure and heart rate indicative of visceral afferent activation were greater in previously shocked rats than in controls. Colonic distention increased the expression of Fos, a marker of neuronal activation, in the sacral spinal cord and caudal brain stem. In the central amygdala and several cortical areas (prelimbic, infralimbic, agranular insular, cingulate), previously shocked rats showed reduced Fos expression following colonic distention compared with relevant controls. CONCLUSIONS: The results indicate that a brief but intense stressful experience causes long-lasting alterations in higher-order central nervous system responsivity to colonic distention even in the absence of conscious affective responses, pointing to basic alterations in the neural pathways involved.

Variability factors in the expression of stress-induced behavioural sensitisation.

Altered behavioural and physiological responsivity following a short session of foot shocks in the rat has proven to be a stable and clinically relevant model of stress-induced sensitisation. However, a number of key factors influencing effect size or direction have not previously been reported. Rats underwent a single, 15-min session of foot shocks and were exposed to a variety of novel stressful challenges 1 or 2 weeks later. Sensitised behavioural responses (increased immobility) in preshocked rats remained present over 3 days of repeated exposure to noise stress. In mild novel challenges (open field, empty cage), behavioural sensitisation and defecation was most clearly expressed at the beginning of the dark phase (evening). Higher-arousal challenges (prod, noise) caused increased behavioural inhibition in preshocked rats at all three time points (morning, afternoon, evening). Female preshocked rats showed a different pattern of behavioural and defecation sensitisation than preshocked males. The robustness of the model makes it suitable for further investigations into the mechanisms and vulnerability factors involved in the long-term consequences of stress.