THE COSMIC MICROWAVE BACKGROUND HAS NO BIOLOGICAL EFFECTS ON LIVING ORGANISMS, BUT IS CRUCIAL FOR COSMIC BIOLOGY: NEW FRONTIERS ON IONIZING RADIATION IN THE CENTRAL NERVOUS SYSTEM

G. Sonnino^1*, G. Barassi², F.M. Jahromi³, A. Coppola⁴, C. Genovesi⁵, G. Tete⁶, F. Pandolfi⁷ and P. Conti⁸

¹ Department of Theoretical Physics and Mathematics, Université Libre de Bruxelles (U.L.B.), Brussels, Belgium;
² Center for Physiotherapy, Rehabilitation and Re-Education (Ce.Fi.R.R.) Venue “G. d’Annunzio” University of Chieti-Pescara, Italy;
³  Shiraz University, Shiraz, Iran;
⁴ Private Practice, Studio Armando Coppola, Corso Garibaldi 246, Naples, Italy;
⁵ Skin Centres, Private Practice, Avezzano and Pescara, Italy;
⁶ Department of Human Sciences, “Sustainable Blue Economy and One Health”-XL Cycle, Law, and Economics “Leonardo da Vinci”, UNIDAV, Chieti, Italy;
⁷ Department of Internal Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy;
⁸ University of Chieti “G. D’Annunzio”, Chieti, Italy.

*Correspondence to:
Giorgio Sonnino,
Department of Theoretical Physics and Mathematics,
Université Libre de Bruxelles (U.L.B.),
Brussels, Belgium.
e-mail: giorgio.sonnino@ulb.be

Received: 05 December, 2025 Accepted: 13 March, 2026

ISSN 2279-5855 print ISSN 2974-6345 online. Copyright © by BIOLIFE 2026 This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.

ABSTRACT

The cosmic microwave background (CMB) is the relic electromagnetic radiation from the early universe, characterized by a black-body temperature of about 2.7 K and photon energies of approximately ~10⁻⁴ eV. Because these energies are far below those required to break chemical bonds or ionize atoms, the CMB is a form of non-ionizing radiation and has no measurable biological effects on living organisms. In particular, it cannot damage DNA or alter cellular structures in biological tissues, including those of the central nervous system (CNS). In contrast, ionizing radiation, such as X-rays, gamma rays, and high-energy cosmic rays, possesses sufficient energy to produce ionization events that can damage biological molecules. These interactions may directly disrupt DNA or indirectly generate reactive oxygen species (ROS) through water radiolysis, leading to oxidative stress, genomic instability, and cellular dysfunction. In the CNS, such processes can affect neurons, glial cells, and neural stem cells, potentially resulting in inflammation, impaired neurogenesis, and cognitive deficits depending on the absorbed radiation dose. This work examines the mechanisms and biological consequences of ionizing radiation in neural tissues and interprets radiation-induced injury within the framework of non-equilibrium thermodynamics, where energy deposition drives biological systems away from equilibrium and generates entropy through irreversible processes. Although the CMB has no direct biological effects, it remains crucial for cosmic biology because its primordial fluctuations shaped the formation of galaxies, stars, and the chemical elements necessary for life. By contrasting harmless cosmological radiation with biologically active ionizing radiation, this study provides a unified perspective linking radiobiology, thermodynamics, and the astrophysical conditions that ultimately enabled the emergence of life.

KEYWORDS: Cosmic wave background, cosmic biology, ionizing radiation, electromagnetic, neuron

INTRODUCTION

The cosmic microwave background (CMB), discovered by Arno Penzias and Robert Wilson in 1965, is the weak electromagnetic fossil radiation that has no significant effects on organisms and is a very weak microwave with a temperature of approximately 2.7 K. In contrast, cosmic rays are high-energy particles from space, such as protons and atomic nuclei, which can have biological effects. The CMB represents the thermal state of the early universe of the time of recombination when matter and radiation decoupled. These fluctuations determine the initial distribution of matter, influences the formation of galaxies and stars, and indirectly participates in the formation of our planet. The fluctuations observed in the CMB, the cosmic structures necessary for life would not have formed. The CMB is a “thermal background” of the universe; it is weak, located in the microwave range, and has very low photon energy. It is non-ionizing, so it does not damage DNA and does not produce appreciable biological effects. It is much weaker than sunlight, ambient infrared radiation, and cosmic rays. Cosmic rays are high-energy particles from space, such as protons and atomic nuclei, and have biological effects. Cosmic rays increase the risk of chromosomal mutations, have effects at high altitudes, and can harm astronauts. The CMB has no direct biological effects, but it is fundamental to cosmic biology because it informs us about the chemical elements necessary for life, such as carbon, oxygen, and nitrogen, about the initial structure of the universe, explains how galaxies formed, and how stars formed. The primordial fluctuations observed in the CMB allowed the formation of complex structures, but had no direct effect on biology, DNA, or evolution. However, the role of the cosmos was important for life. The CMB has no biologically significant effects and cannot damage DNA because it has such low energy (photons of about 10⁻⁴ eV), too low, and it is not ionizing. To cause DNA damage and bond breakage, an energy of at least 3–10 eV is required, while high-energy UV radiation can directly damage DNA. Radiation that can directly damage DNA includes high-energy ultraviolet (UV) rays, X-rays, and gamma rays. Because CMB radiation is millions of times weaker than the other rays mentioned above, it cannot cause damage to the DNA structure. Therefore, the CMB does not cause genetic mutations or pose biological damage, while cosmic rays, particles at high-energy coming from space, can modify genetic molecules. Therefore, high-energy cosmic rays at high altitudes can damage astronauts. The CMB, which has lower energy than even that of everyday objects, has no significant thermal effect and does not alter biological molecules as ionizing radiation does.

IONIZING RADIATION, NEUTRAL DAMAGE, AND ENTROPY PRODUCTION IN BIOLOGICAL SYSTEMS

Ionizing radiation is defined as radiation possessing sufficient energy to remove electrons from atoms or molecules, thereby producing ions. The relation determines the energy of a photon

E = hν = hc/λ

where h is the Planck constant, ν is the radiation frequency, λ is the wavelength, and c is the speed of light in vacuum, respectively. When the photon energy exceeds approximately 10 eV, comparable to the energy required to break many covalent chemical bonds, the radiation can ionize atoms and molecules. Electromagnetic radiation such as X-rays and gamma rays, as well as energetic particles including alpha particles, beta particles, and neutrons, therefore belong to the class of ionizing radiation and can produce biologically significant molecular damage (1-3). The boundary between ionizing and non-ionizing electromagnetic radiation can be estimated using the photon-energy relation. Assuming a minimum ionization energy of approximately E ≈ 10 eV, the corresponding wavelength is

λ = hc/E ≈ 124 nm.

Radiation with wavelengths shorter than about 124 nm, found in the far ultraviolet, X-ray, and gamma-ray regions, has enough energy to cause ionization. In contrast, electromagnetic radiation with longer wavelengths, such as visible light, infrared, and microwaves, is generally non-ionizing and cannot directly break molecular bonds in biological tissues (1). Ionizing radiation can produce significant biological effects mainly by damaging cellular DNA. This damage can occur through two main mechanisms: direct and indirect interactions. In direct interactions, radiation deposits energy directly into the DNA molecule, causing ionization events that can result in single-strand breaks, double-strand breaks, and point mutations. Double-strand breaks are especially serious because they are difficult for cellular repair systems to fix without errors (2). Indirect damage happens when ionizing radiation interacts with water molecules inside cells, generating highly reactive chemical species called reactive oxygen species (ROS). A typical ionization reaction is

H₂O + γ → H₂O⁺ + e⁻ ,

which subsequently leads to the formation of free radicals such as OH∙, O₂∙, and H₂O_2​. These reactive species can oxidize nucleic acid bases, modify DNA structure, and disrupt cellular metabolism, thereby contributing to mutagenesis or cell death (2,3). The biological impact of ionizing radiation depends on several factors, including the absorbed dose, duration of exposure, radiation quality, and physiological characteristics of the exposed individual. The absorbed dose D is defined as

D = E_abs/m,

where E_abs​ is the energy absorbed by the tissue and m is the mass of the irradiated material. The unit of absorbed dose is the gray (Gy). The biological effect of radiation exposure is often expressed through the equivalent dose

H = D w_R ​,

where w_R​ is a radiation weighting factor that accounts for the relative biological effectiveness of different radiation types; the unit is the sievert (Sv) (1). In radiobiology, the relationship between radiation dose and cell survival is frequently described using the linear–quadratic model

S(D) = exp[−(αD+βD²)],

where S(D) represents the surviving fraction of cells after an absorbed dose D, and α and β are empirical parameters that characterize cellular radiosensitivity. The linear term αD describes damage caused by a single radiation track, whereas the quadratic term βD² accounts for damage arising from the interaction of two independent radiation events. This model is widely used in radiobiology and radiation therapy to predict tissue responses to ionizing radiation (4). At the level of the central nervous system (CNS), ionizing radiation can affect both neurons and supporting cells. Mature neurons are largely non-dividing but are particularly sensitive to oxidative stress and metabolic disturbances. Radiation exposure may therefore induce neuronal dysfunction, inflammation, vascular injury, and demyelination. Neural stem cells located in the hippocampus are highly radiosensitive, and damage to these cells may lead to apoptosis, impaired neurogenesis, and long-term cognitive deficits (2,3). High or prolonged radiation doses can overwhelm cellular repair mechanisms and may result in permanent tissue injury, radiation necrosis, or an increased risk of tumor development. Clinical manifestations of significant brain irradiation may include headache, nausea, confusion, cerebral edema, and neurological impairment.

During embryonic development, the CNS is particularly vulnerable, and exposure to ionizing radiation can lead to developmental abnormalities or long-term neurocognitive impairment (1-3). By contrast, low-dose exposures such as those associated with diagnostic imaging procedures, including computed tomography (CT), generally present a very small risk because cellular repair mechanisms, particularly DNA repair pathways, can correct most radiation-induced lesions. Diagnostic exposures are typically in the millisievert range and are considered relatively safe when medically justified (3).

Therapeutic management of radiation-induced brain injury depends on the severity of the damage. Corticosteroids are commonly used to reduce inflammation and cerebral edema. Antioxidants, including vitamins C and E and N-acetylcysteine, may help mitigate oxidative stress caused by free radicals. In some cases, therapies targeting vascular endothelial growth factor (VEGF) may reduce abnormal vascular permeability and radiation-induced vascular changes. In severe situations involving radiation necrosis or mass effects, surgical intervention may be required (2).

It is important to distinguish ionizing radiation from non-ionizing radiation present in natural astrophysical environments. The photons of the CMB correspond to a black-body radiation field with a temperature T of approximately T=2.725 K. The characteristic photon energy can be estimated using

E ≈ k_BT,

with k_B denoting Boltzmann’s constant. This yields an energy of approximately 2×10⁻⁴ eV, many orders of magnitude smaller than the energy required to break chemical bonds or ionize atoms. Consequently, CMB radiation has no measurable biological effects on living organisms, whereas ionizing radiation such as X-rays, gamma rays, and energetic particles can damage DNA and other cellular structures, including neurons of the brain. From the perspective of Non-equilibrium Thermodynamics, radiation-induced biological damage may also be interpreted as an irreversible process associated with entropy production. When ionizing radiation deposits energy in biological tissue, it drives the system away from thermodynamic equilibrium by producing ionization events, molecular fragmentation, and chemically reactive species. These processes increase microscopic disorder and lead to a net production of entropy. Within the theoretical framework of irreversible thermodynamics developed by scientists such as Ilya Prigogine and Lars Onsager, the rate of entropy production in an open system can be expressed in compact form as

dS/dt = ∑_i J_i X_i,

where dS/dt represents the entropy production rate, J_i denotes the thermodynamic fluxes (such as diffusion of reactive species or energy transfer), and X_i represents the corresponding thermodynamic forces that drive the system away from equilibrium, respectively (5-7). In irradiated biological tissues, these forces originate from gradients in chemical potentials, concentrations of reactive species, and localized energy deposition. The resulting irreversible processes, such as radical diffusion, biochemical reactions, and cellular repair mechanisms, convert absorbed radiation energy into heat, chemical changes, and increased entropy, while biological regulatory systems work to maintain cellular organization. Recent theoretical research suggests that entropy production at mesoscopic scales may be subject to fundamental constraints and potential quantization properties, offering a deeper thermodynamic view of irreversible processes in small systems (8-10).

DISCUSSION

Ionizing radiation encompasses electromagnetic (X-rays, gamma rays) and particulate (alpha particles, beta particles, neutrons) forms characterized by energies sufficient to ionize atoms and disrupt molecular bonds (11). As detailed in the section Ionizing Radiation, Neural Damage, and Entropy Production in Biological Systems, the physical basis of this interaction lies in photon energies exceeding the ionization threshold (~10 eV), enabling direct bond cleavage and charge separation within biological macromolecules (12). Once absorbed by neural tissue, this energy initiates a cascade of physicochemical events that extend beyond immediate DNA damage to broader cellular and tissue-level dysfunction (13).

In the CNS, radiation injury is mediated by both direct genomic insult and indirect oxidative mechanisms. Double-strand DNA breaks represent a pivotal lesion, given their potential to induce apoptosis, senescence, or malignant transformation when misrepaired. However, neuronal damage is not exclusively genomic (14). Ionization of intracellular water leads to the formation of ROS, amplifying oxidative stress, lipid peroxidation, mitochondrial dysfunction, and neuroinflammatory signaling (15). These processes contribute to synaptic impairment, white matter injury, and disruption of the neurovascular unit. Although mature neurons are post-mitotic and relatively resistant to radiation-induced oncogenesis, they are metabolically demanding and particularly vulnerable to oxidative imbalance. In contrast, neural stem and progenitor cells, especially within the hippocampus, exhibit marked radiosensitivity (16). Injury to these proliferative populations compromises neurogenesis and has been linked to persistent cognitive deficits. The embryonic and developing brain is even more susceptible, reflecting high proliferative activity and critical windows of neurodevelopment, during which radiation exposure may lead to long-term structural and functional abnormalities.

Clinical manifestations of CNS irradiation depend strongly on dose, fractionation, and individual susceptibility. Acute or subacute effects may include cerebral edema, headache, nausea, confusion, and inflammatory responses (17). Chronic high-dose exposure can result in demyelination, vascular damage, and radiation necrosis (18). In contrast, low-dose diagnostic exposures, such as those from CT, are associated with a very small absolute risk when medically justified, owing to the efficiency of endogenous DNA repair and antioxidant systems (19). Therapeutic management remains primarily supportive and symptom-oriented. Corticosteroids are widely employed to control cerebral edema and inflammation (20). Anti-VEGF agents may reduce vascular permeability in selected cases of radiation necrosis (21). Antioxidant strategies have been investigated to counteract ROS-mediated injury, though clinical evidence remains variable. Surgical intervention is reserved for refractory necrotic lesions or significant mass effect. Emerging approaches, including stem cell–based therapies and regenerative strategies, are under active investigation but require further validation before routine clinical application. From a broader biophysical perspective, radiation-induced CNS injury can be interpreted as an irreversible process within the framework of non-equilibrium thermodynamics. Energy deposition drives neural tissue away from steady-state organization, generating chemical gradients, molecular fragmentation, and dissipative biochemical reactions. Entropy production, expressed in compact thermodynamic form as

dS/dt = ∑_i J_i X_i,

reflects the coupling between thermodynamic fluxes (e.g., diffusion of reactive species, metabolic heat flow) and their corresponding driving forces (22).  In this view, oxidative cascades, inflammatory responses, and repair mechanisms represent dissipative processes that convert absorbed radiation energy into heat and chemical transformations, while cellular regulatory systems strive to preserve structural and functional order. Integrating radiobiological mechanisms with thermodynamic principles provides a unifying conceptual framework linking molecular damage, cellular response, and tissue-level dysfunction (23). Such interdisciplinary integration may enhance predictive modeling of radiation effects, improve risk assessment, and guide the development of targeted neuroprotective strategies (24). Future research combining quantitative radiobiology, systems neuroscience, and mesoscopic thermodynamic modeling could further clarify thresholds of reversibility and optimize both preventive and therapeutic interventions in radiation-exposed populations.

CONCLUSIONS

In conclusion, it can be stated that the cosmic background of microwaves has no biological effects on living organisms, while ionizing radiation can damage DNA and other cellular structures, including neurons. The fundamental distinction lies in photon energy: radiation associated with the CMB, characterized by a temperature of approximately 2.7 K, possesses photon energies many orders of magnitude below the ionization threshold required to disrupt chemical bonds. In contrast, ionizing radiation, such as X-rays, gamma rays, and energetic particles, carries sufficient energy to remove electrons from atoms and initiate molecular instability within biological tissues. Within the CNS, radiation-induced injury reflects a complex interplay of direct DNA ionization, oxidative stress mediated by ROS, neuroinflammatory activation, and vascular impairment. Double-strand DNA breaks represent a critical lesion with potential long-term consequences, particularly when repair mechanisms are overwhelmed or inaccurate. Neural stem and progenitor cells exhibit marked radiosensitivity, and their damage may contribute to persistent cognitive impairment. Although mature neurons are post-mitotic, they remain highly vulnerable to oxidative and metabolic disturbances that may alter synaptic integrity and white matter structure.

The clinical impact of radiation exposure is strongly dose-dependent. Low-dose diagnostic exposures are associated with minimal absolute risk when appropriately justified, owing to efficient endogenous repair systems. Conversely, high or cumulative exposures can exceed biological repair capacity, leading to irreversible tissue injury, radiation necrosis, or increased oncogenic risk. Therapeutic strategies currently focus on mitigating inflammation, vascular dysfunction, and oxidative damage, while regenerative approaches remain under investigation. From a broader physical perspective, radiation-induced biological damage may be interpreted as an irreversible process within the framework of Non-equilibrium Thermodynamics. Energy deposition drives neural tissue away from thermodynamic equilibrium, generating molecular fragmentation, chemical gradients, and entropy production. The cellular response, including DNA repair, antioxidant activation, and metabolic adaptation, constitutes a dissipative effort to restore homeostasis while complying with the second law of thermodynamics. This interdisciplinary interpretation links radiobiology with fundamental physical principles and provides a coherent conceptual framework for understanding radiation-induced CNS injury. Future research integrating quantitative radiobiology, neuroscience, and thermodynamic modeling may improve risk stratification, optimize radioprotective strategies, and refine therapeutic interventions. A deeper understanding of the thresholds between reversible adaptation and irreversible damage will be essential for advancing both clinical management and theoretical insight into radiation–biological interactions.

Conflict of interest

The authors declare that they have no conflict of interest.

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