INTRODUCTION
Radio waves are a type of electromagnetic radiation with wavelengths in the electromagnetic spectrum longer than infrared light. Radio waves have frequencies from 300 GHz to as low as 3 kHz, and corresponding wavelengths ranging from 1 millimeter to 100 kilometers. Artificially generated radio waves are used for fixed and mobile radio communication, broadcasting, radar and other navigation systems, communications satellites, computer networks and innumerable other applications.
The primary damage mechanism of non-ionizing radio waves is thermal, by dielectric heating. This heating effect varies with the power and the frequency of the electromagnetic energy and an increase of the body temperature is the noticeable effect.
EFFECTS
1) Membrane fluidity
It is known that temperature influences cellular membrane fluidity, acting on the composition of membrane fatty acids (Molecular Control of Membrane Properties During Temperature Acclimation. Fatty Acid Desaturase Regulation of Membrane Fluidity in Acclimating Tetrahymena Cells, 1976.
It was also observed that the homeoviscous compensation of membrane function is an important component of temperature adaptation, in fact it is possible that the necessity of eurythermal fish species to tolerate and adapt to relatively large seasonal fluctuations in environmental temperature has placed a constraint upon their ability to modulate membrane dynamic structure for a change of environmental temperature and hence may be viewed as the price that must be paid for a eurythermal capacity. By contrast, species that exist in relatively unchanging thermal environments can permit specialization of their membranous structures to particular temperatures without having to exhibit seasonal flexibility, resulting in a more complete adaptation of membrane structure to that temperature.
(Evolutionary adaptation of membranes to temperature, 1978).
2) Role Of Heat Shock Proteins
An important role is played by Heat Shock Proteins (HSPs) which are a group of proteins induced by heat shock.
HSPs have different functions, the most important role is related to folding and unfolding protein.
It is also suggested that sHSP (small heat shock proteins)-mediated membrane stabilisation precedes the thermal adaptation that occurs by adjustment of the lipid composition. The fluidity and microdomain organisation of membranes are decisive factors in the perception and transduction of stresses into signals that trigger the activation of specific heat shock genes. Conversely, the membrane association of specific HSPs may result in the inactivation of membrane-perturbing signals, and thereby switch off the heat shock response.
(Membrane fluidity matters: hyperthermia from the aspects of lipids and membranes, 2013)
3) Protein Denaturation
Temperatures above the range that cells tend to live in will cause thermally unstable protein to unfold or denaturate. A fully denatured protein lacks both tertiary and secondary structure and loses its biological functions. So cells cannot work in a correct way and in the worst case they die by necrosis.
4) Role Of Cardiolipin And ROS Formation
An increase in fractions of cardiolipin and other phosholipids (phosphatidylserine, phosphatidic acid and lysophospholipids) were detected in mitochondria after heat stress. (Phospholipid composition of the liver mitochondrial membrane in thermal stress, 1994).
Moreover cardiolipin remodeling occurs with aging, specifically an increase in highly unsaturated fatty acids (more susceptible to ROS peroxidation) (Selective remodeling of cardiolipin fatty acids in the aged rat heart, 2006).
Mitochondrial superoxide production is increased with increasing temperature and in a time-dependent manner and as a consequence it was found that cardiolipin peroxidation was increased in a temperature-dependent manner and it was mediated by mitochondrial ROS (The Role of Mitochondria-Derived Reactive Oxygen Species in Hyperthermia-Induced Platelet Apoptosis, 2013).
The precise mechanisms responsible for how hyperthermia causes increased levels of mitochondrial ROS remain undetermined. The reasons may be manifold. On the one hand, hyperthermia might increase mitochondrial ROS generation. But it has also been reported that hyperthermia could induce mitochondrial dysfunction and thus augment mitochondrial ROS production (Mitochondrial dysfunction induced by heat stress in cultured rat CNS neurons, 2012).
The oxidized cardiolipin transfers from the inner membrane to the outer membrane, and then helps to form a permeable pore which releases cytochrome c into the cytosol.
In the cytosol cyochrome c activates caspase 9 which activates caspase 3 and caspase 7, which are responsible for destroying the cell from within by apoptosis.
5) Intracellular Calcium
Hyperthermia causes a large (three-to fivefold) increase in intracellular free calcium ([Ca2+]i) in HA-1 fibroblasts. Increased [Ca2+]i appears initially to be due to release of Ca2+ from an internal store, probably located in the endoplasmic reticulum. A subsequent influx of Ca2+ from the extracellular medium is then observed. These heat-induced changes in Ca2+ homeostasis are correlated with turnover of the phosphoinositides (PI), a class of phospholipids whose metabolism has been shown to regulate Ca2+ in a wide variety of cells (Effects of heat on cell calcium and inositol lipid metabolism, 1988).
Furthermore there is convincing evidence that the calcium ion can play a critical role in cell killing in the central nervous system and other tissues. Some researches have established some of the biochemical mechanisms by which intracellular Ca2+ overload can trigger either necrotic or apoptotic cell death (The calcium ion and cell death, 1994)
6) Other Effects
- The thermal effects on the eye are well known and include cataracts, corneal edema, endothelial cell loss and retinal degeneration (Effects of mobile phones and radar radiofrequencies on the eye, 2009).
- Metabolic rate increases as a result of increasing the body temperature.
- Blood flow increases to keep the body temperature constant (thermoregulation).
- Radio frequence enhances mitochondrial reactive oxygen species generation by human spermatozoa (known to be particularly vulnerable to oxidative stress by virtue of the abundant availability of substrates for free radical attack and the lack of cytoplasmic space to accommodate antioxidant enzymes), decreasing the motility and vitality of these cells while stimulating DNA base adduct formation and, ultimately DNA fragmentation. Thus the induction of oxidative stress in these cells not only perturbs their capacity for fertilization but also contributes to sperm DNA damage. The latter has, in turn, been linked with poor fertility, an increased incidence of miscarriage and morbidity in the offspring, including childhood cancer (Mobile Phone Radiation Induces Reactive Oxygen Species Production and DNA Damage in Human Spermatozoa In Vitro, 2009).
CONCLUSIONS
We consider that radio waves, after these evidences, are dangerous (especially for long exposition) for human body because, even if they are not unhealthy in a short period, they can cause cells’ death by apoptosis and necrosis and DNA damage. Thus they can cause organs failure and generalized problems to organism.
In order to decrease these complications it is important reduce the exposition especially on high-risk workers.
Piano Andrea, Rubatto Marco
