Radiation damage
Radiation damage refers to the irreversible changes in the atomic, molecular, or supramolecular structure of materials or biological systems induced by the energy transfer from ionizing radiation, primarily through mechanisms of atomic displacement, ionization, and excitation.[1][2] In solid materials, the primary process involves elastic collisions where incident particles or recoil atoms impart sufficient kinetic energy—typically exceeding a threshold of 10–100 eV depending on the material—to eject lattice atoms from their sites, generating cascades of vacancies and interstitial defects that degrade mechanical properties such as ductility and fracture toughness.[3][4] These defects accumulate over time, quantified in displacements per atom (dpa), and can lead to macroscopic effects like swelling, embrittlement, or altered thermal conductivity, limiting the operational lifespan of nuclear reactor components and space vehicle structures.[5] In biological contexts, radiation damage manifests as direct breaks in DNA strands or indirect oxidative stress from radiolysis products like hydroxyl radicals, triggering cellular responses including apoptosis, senescence, or mutagenesis, with severity scaling with absorbed dose in grays (Gy).[6][7] Empirical models, such as the Kinchin-Pease approximation for displacement damage, enable prediction of defect production rates via R = \Phi \Sigma = \Phi \sigma \rho_A, where \Phi is particle flux, \sigma the displacement cross-section, and \rho_A atomic density, underscoring the causal primacy of ballistic collisions over mere electronic stopping in dense cascades.[2] While repair mechanisms mitigate low-dose effects in living systems, high-fluence exposures in engineered materials reveal persistent defect clusters resistant to annealing, informing designs for radiation-tolerant alloys through first-principles simulations of defect dynamics.[8]Fundamentals
Definition and Classification
Radiation damage refers to the microscopic defects and structural alterations induced in matter by exposure to ionizing radiation, encompassing both atomic displacements and electronic excitations that disrupt lattice integrity or molecular bonds. These changes occur on timescales of picoseconds following initial particle interactions, forming the primary damage state before annealing or aggregation modifies the defect population.[2][9] Damage mechanisms are primarily classified into displacement (non-ionizing) and ionization (electronic) types. Displacement damage arises from elastic collisions where incident particles, such as neutrons or ions, transfer kinetic energy exceeding the displacement threshold (typically 10-100 eV depending on the material) to target atoms, creating primary knock-on atoms (PKAs) that generate cascades of further displacements, often resulting in thousands of defects per event in metals.[10][11] Ionization damage, dominant for photons, electrons, or lightly ionizing particles, involves inelastic energy loss through electron ejection, leading to charge buildup, trapped holes, or radiolytic decomposition, with effects pronounced in wide-bandgap materials where recombination is inefficient.[12][13] Defects are further classified by morphology: point defects include vacancies (missing atoms), self-interstitials (extra atoms in non-lattice sites), and Frenkel pairs (vacancy-interstitial combinations); extended defects encompass dislocation loops from coalesced interstitials, voids from vacancy clustering under stress, and amorphous zones in ceramics from overlapping cascades.[14][15] In biological contexts, analogous classifications apply to DNA strand breaks (single- or double-strand from direct ionization or indirect radical attack) versus clustered damage from high-LET particles, though macroscopic effects like mutagenesis stem from repair failures rather than isolated defects.[16][2]Physical and Chemical Mechanisms
Radiation damage arises primarily through physical mechanisms involving atomic displacements and electronic excitations. In displacement damage, incident particles such as neutrons, protons, or heavy ions transfer kinetic energy via elastic nuclear collisions to lattice atoms, ejecting them from their positions if the energy exceeds the material-specific displacement threshold, typically 10–50 eV (equivalent to 2–8 × 10⁻¹⁸ J). This process generates Frenkel defects, pairs of vacancies and self-interstitial atoms, which disrupt the crystal structure and degrade mechanical properties like ductility.[10] The non-ionizing energy loss (NIEL) quantifies the energy partitioned into such displacements, distinct from ionizing losses that produce electron-hole pairs, with NIEL-driven defects causing permanent lattice perturbations in semiconductors and metals.[11] A single displaced atom, termed the primary knock-on atom (PKA), can trigger a cascade of secondary displacements, forming dense clusters or "spikes" of defects within nanoseconds; the approximate number of displaced atoms scales as the PKA energy divided by twice the threshold energy, leading to localized melting-like conditions and amorphization in severe cases.[10] Neutrons, prevalent in nuclear environments, efficiently induce these cascades through elastic scattering, while lighter particles like electrons require higher energies (e.g., >1 MeV via Compton scattering) to surpass displacement thresholds.[11] Transmutation effects complement displacements, as neutron absorption reactions (e.g., (n,α) in stainless steel alloys) produce helium atoms that migrate, coalesce into bubbles, and drive void swelling under irradiation.[10] Chemical mechanisms stem from ionization and excitation, where radiation breaks molecular bonds directly or indirectly via reactive intermediates, altering composition without net atomic relocation. Radiolysis, the dissociation of molecules by ionizing particles, generates free radicals, ions, and excited states that initiate chain reactions; in liquids like water, yields include hydroxyl radicals (G-value ~2.7 molecules/100 eV), hydrated electrons (~2.6), and hydrogen peroxide, which oxidize nearby biomolecules or materials.[17] In solids and polymers, electronic energy deposition cleaves covalent bonds, forming trapped charges, color centers (e.g., F-centers in alkali halides), or cross-links, with damage amplified by diffusion of radicals over micrometer scales.[18] These processes often dominate in molecular or biological systems, contrasting with the ballistic displacements in crystalline solids, though synergies occur where radiolytic species enhance defect recombination or precipitation.[2]Historical Development
The study of radiation damage originated with the discovery of X-rays by Wilhelm Conrad Röntgen on November 8, 1895, when he observed their ability to penetrate matter and produce fluorescence, leading to immediate reports of biological effects such as skin erythema and hair loss in experimenters exposed during early imaging trials.[19] In 1896, Henri Becquerel identified natural radioactivity in uranium salts, and subsequent work by Marie and Pierre Curie isolated polonium and radium, revealing alpha, beta, and gamma emissions; these findings prompted observations of tissue damage, including burns and cataracts, among researchers like Thomas Edison and Nikola Tesla, who noted eye irritations after prolonged exposure.[20][21] By the 1920s, radiation's mutagenic effects were recognized through experiments on fruit flies by Hermann Muller, who in 1927 demonstrated induced genetic mutations in Drosophila melanogaster using X-rays, establishing ionizing radiation as a tool for genetic research while highlighting heritable damage risks.[22] Studies expanded to chemical changes, with papers by 1928 documenting phenomenological effects on diverse materials, including polymers and gases, via ionization and excitation processes.[23] International guidelines emerged in the 1930s, such as the International X-ray and Radium Protection Committee recommendations in 1928 and 1934, driven by accumulating evidence of acute injuries among medical and industrial workers.[20] The advent of nuclear fission in 1938 and wartime reactor development accelerated research into material damage, with early observations in the 1940s revealing embrittlement and dimensional changes in metals and graphite under neutron bombardment in pilot reactors like Chicago Pile-1.[24] Post-World War II, the Manhattan Project's aftermath and atomic testing programs spurred systematic investigations, including displacement cascades in solids theorized by 1950s models, while biological studies quantified dose-response relationships for cellular damage.[25] By the 1956 Annual Review of Nuclear Science, effects on mechanical properties—such as increased yield strength and reduced ductility in irradiated steels—were cataloged from reactor surveillance data.[26] These efforts laid the foundation for modern radiation hardness assessments in nuclear and space applications.Effects on Non-Biological Materials
Damage to Metals and Alloys
Neutron irradiation primarily damages metals and alloys through atomic displacements caused by elastic scattering events, where incident neutrons transfer sufficient kinetic energy to lattice atoms to exceed the threshold displacement energy, which ranges from 25 eV in copper to 40 eV in iron.[27][28] These collisions generate primary knock-on atoms (PKAs) that initiate displacement cascades, producing clusters of Frenkel defects—vacancies paired with self-interstitial atoms—in densities up to thousands per cascade for PKAs with energies of several keV.[29] The extent of damage is quantified in displacements per atom (dpa), with 1 dpa corresponding to each atom in the material being displaced once on average.[30] At irradiation temperatures below approximately one-third of the absolute melting point, these point defects remain largely immobile and accumulate, obstructing dislocation motion and causing irradiation hardening; for example, neutron fluences of 10^{19} to 10^{20} n/cm² (equivalent to ~0.1-1 dpa for fast neutrons) can increase yield strength in ferritic steels by 50-200% while reducing uniform elongation to near zero.[31][32] This hardening contributes to embrittlement, shifting the ductile-to-brittle transition temperature upward by 50-150°C in reactor pressure vessel alloys, limiting service life in nuclear reactors.[33] Radiation-enhanced diffusion and segregation of alloying elements to defect sinks further promote precipitation of phases like copper-rich clusters in low-alloy steels, exacerbating brittleness.[34] At higher temperatures (0.4-0.6 T_m), defect mobility enables recombination, clustering into dislocation loops, and void nucleation, leading to radiation-induced swelling from supersaturated vacancies coalescing into voids under bias-driven absorption differences between voids and dislocations.[35] In austenitic stainless steels like 304 or 316, swelling initiates after an incubation dose of 10-50 dpa, proceeds at a terminal rate of about 1% volume increase per dpa, and can accumulate to 10-30% at 100-150 dpa and temperatures of 300-600°C, causing dimensional instability in fuel cladding and core internals.[36][37] Swelling above 10% severely degrades tensile strength and promotes intergranular fracture.[38] Irradiation creep, a stress-directed anisotropic deformation, arises from similar defect fluxes, with rates enhanced by factors of 10^4-10^6 over thermal creep in alloys under neutron fluxes.[31] Alloying strategies, such as adding oversize elements like titanium or niobium to stabilize voids or precipitate transmutants like helium, mitigate swelling and embrittlement; for instance, 20Cr-35Ni-Ti alloys exhibit swelling rates below 0.5%/dpa up to 110 dpa.[36] In refractory metals like tungsten for fusion applications, low-temperature hardening dominates due to high cascade densities, with yield strength doubling at 0.1-1 dpa from loop formation.[39] Post-irradiation annealing partially recovers ductility by defect annihilation, though full restoration requires temperatures exceeding 0.5 T_m.[4]Damage to Ceramics, Concrete, and Glasses
Ceramics exposed to ionizing radiation, particularly neutrons or heavy ions, undergo atomic displacements through elastic collisions, generating point defects, dislocation loops, and Frenkel pairs that accumulate into cascades.[40] In crystalline oxides like Al₂O₃ and ZrO₂, this displacement damage leads to volumetric swelling, typically a few percent at high fluences, alongside embrittlement and reduced fracture toughness due to microcracking.[41] [42] Thermal conductivity decreases markedly from phonon scattering by defects, while electrical conductivity may increase initially from charge carrier generation before saturating.[43] Amorphization occurs in susceptible phases, such as pyrochlores or zirconolite, at doses around 0.1-1 displacements per atom (dpa), transforming ordered structures into disordered states with higher stored energy.[44] Heavy-ion irradiation induces continuous ion tracks via electronic excitation, promoting radiolytic damage in materials like CeO₂, where track radii reach 5-10 nm at energies above 1 MeV/amu.[45] Concrete in nuclear facilities, such as reactor biological shields, suffers neutron-induced degradation primarily in siliceous aggregates, where fast neutrons (E > 1 MeV) cause metamictization of quartz and feldspars, resulting in radiation-induced volumetric expansion (RIVE) up to 1-2% at fluences of 10¹⁹-10²⁰ n/cm².[46] [47] This expansion exerts internal stresses, leading to microcracking in the cement paste and overall loss of compressive strength by 20-50% and modulus of elasticity by similar margins beyond 1 × 10¹⁹ n/cm².[48] Gamma radiation contributes via radiolytic water decomposition and radiogenic heating, exacerbating drying and shrinkage, though neutron effects dominate structural integrity loss.[49] Aggregate swelling predominates over paste damage, with synergistic neutron-gamma interactions remaining poorly quantified but potentially amplifying cracking under combined exposures up to 10¹⁸ n/cm² and 10²¹ Gy.[50] [49] Glasses, being amorphous, resist amorphization but experience ballistic disordering and electronic excitation effects, leading to densification (up to 1-3% volume reduction) at low doses from structural relaxation, followed by expansion at higher fluences due to defect percolation.[51] In borosilicate nuclear waste glasses, alpha-decay recoils (from actinides) at 10¹⁸-10¹⁹ events/g induce cascade overlap, altering network polymerization and increasing leach rates by factors of 2-10 via track formation and phase separation.[52] Heavy-ion tracks in glasses create cylindrical damage zones with radii of 2-5 nm, softening the material and reducing chemical durability, as evidenced by enhanced boron and silicon dissolution in simulated high-level waste forms.[52] Mechanical properties like hardness decline modestly, with fracture toughness potentially improving from flaw blunting, though overall radiation tolerance depends on composition, with aluminoborosilicates showing stability up to 10²¹ Gy equivalent dose.[53] In glass-ceramics like zirconolite-based composites, irradiation accelerates amorphization of crystalline phases at fluences as low as 10¹² ions/cm² for 21 MeV Au, exacerbating helium accumulation and swelling.[53]Damage to Polymers and Organics
Ionizing radiation induces damage in polymers primarily through the generation of reactive intermediates such as free radicals, ions, and excited states via energy deposition from ionization and electronic excitation. These processes lead to two dominant chemical reactions: main-chain scission, which fragments polymer chains and reduces molecular weight, and intermolecular cross-linking, which forms covalent bonds between chains, increasing molecular weight and potentially creating insoluble gel networks.[4][54] The prevalence of each reaction depends on the polymer's chemical structure; for instance, polyethylene and polyvinyl chloride predominantly undergo cross-linking under anaerobic conditions, enhancing tensile strength but reducing elongation at break, while polymethyl methacrylate and polystyrene favor chain scission, resulting in embrittlement and weight loss.[4][55] In the presence of oxygen, radiation damage is exacerbated by oxidative mechanisms, where initial radicals react with O₂ to form peroxyl radicals, propagating chain reactions that produce peroxides, hydroperoxides, and oxygenated functional groups like carbonyls and carboxyls. This radiolytic oxidation causes yellowing, surface cracking, and accelerated loss of mechanical integrity, with degradation yields often quantified by G-values (molecules reacted per 100 eV absorbed); for example, polyethylene exhibits a G-value for oxidation of approximately 10-15 under gamma irradiation at doses exceeding 1 MGy.[56][57] Post-irradiation effects further contribute, as trapped radicals persist and react with atmospheric oxygen over time, leading to continued embrittlement even after exposure ceases.[58] For non-polymeric organic materials, such as lubricants or solvents, radiation primarily drives radiolysis, fragmenting C-H and C-C bonds to yield smaller hydrocarbons, hydrogen gas, and unsaturated compounds, often with polymerization of monomers into dimers or oligomers. In organic liquids like hydrocarbons, doses above 0.1 MGy from gamma rays can reduce viscosity by 20-50% due to bond breaking, while aromatic organics like benzene show higher resistance via resonance stabilization, with decomposition yields below 1 molecule/100 eV.[57] Empirical data from nuclear reactor environments indicate that unirradiated polymers like EPR (ethylene-propylene rubber) retain >80% elongation after 1 MGy, but oxidative exposure halves this value, underscoring the role of environment in damage accumulation.[59] These effects limit polymer use in high-radiation settings, such as reactor cabling, where stabilizers like antioxidants mitigate but do not eliminate degradation.[58]Damage to Gases and Liquids
Ionizing radiation induces damage in gases through direct interactions such as ionization, excitation, and electron capture, transferring energy from particles like electrons, α-particles, or γ-rays to gas molecules and producing ion pairs, free radicals, and excited species.[60] These primary events initiate secondary chain reactions, including dissociation, polymerization, or oxidation, often yielding stable products like smaller molecules or polymers depending on the gas composition and pressure.[60] In dilute gases, reactions proceed via homogeneous kinetics with high species mobility and minimal overlap of reaction zones, contrasting with denser media; the energy required per ion pair (W-value) typically ranges from 25–35 eV, as seen in air or noble gases.[61] Examples include the radiolysis of methane (CH₄), where irradiation produces hydrogen (H₂), ethane (C₂H₆), and ethylene (C₂H₄) as primary decomposition products through C–H bond cleavage and radical recombination.[62] In sulfur dioxide (SO₂)-containing gases, radiation enhances oxidation to sulfuric acid precursors, useful for applications like flue gas treatment but demonstrating damage via unwanted byproduct formation.[60] Yields are quantified by G-values (molecules per 100 eV absorbed) or ionization efficiencies, though these vary with linear energy transfer (LET); low-LET radiation favors radical production over molecular products compared to high-LET particles.[60] In liquids, damage arises from similar ionization and excitation but is amplified by the medium's density, creating dense ionization tracks and short-lived "spurs" (radii ~10–100 nm) where radicals form at high local concentrations, promoting recombination or diffusion-controlled reactions.[17] Radiolysis dissociates molecules into transient species that drive oxidative or reductive changes, with water serving as the canonical example: under ⁶⁰Co γ-irradiation at 25°C, primary yields include G(eₐq⁻) = 2.65, G(●OH) = 2.80, G(H●) = 0.60, G(H₂) = 0.45, and G(H₂O₂) = 0.68 molecules/100 eV, reflecting the net decomposition G(–H₂O) ≈ 4.15.[17] These species—hydrated electrons (eₐq⁻), hydroxyl radicals (●OH), hydrogen atoms (H●), and molecular hydrogen (H₂) or peroxide (H₂O₂)—propagate damage by abstracting hydrogen or adding to solutes, as in nuclear reactor coolant corrosion.[17] Liquid-phase reactions differ from gases due to restricted diffusion and solvation effects, yielding higher molecular product fractions under high-LET conditions (e.g., α-particles) via intraspur recombination; temperature dependence alters G-values, with yields for eₐq⁻, ●OH, and H₂ increasing ~50% from 25°C to 300°C in γ-irradiated water.[63] In organic liquids like hydrocarbons, analogous processes form peroxides or cross-links, while ionic liquids exhibit tailored stability against radiolytic decomposition for advanced applications.[64] Overall, liquid damage emphasizes localized chemistry, enabling both destructive effects (e.g., polymer degradation) and synthetic utility (e.g., radiation-induced grafting).[61]Impacts on Electronic Devices and Semiconductors
Radiation damage to electronic devices and semiconductors primarily arises from two mechanisms: total ionizing dose (TID) effects, where ionizing radiation generates electron-hole pairs that become trapped in insulating layers, and displacement damage dose (DDD), where high-energy particles displace atoms from lattice sites, creating defects that degrade carrier transport. TID leads to parametric shifts such as increased leakage currents and threshold voltage alterations in metal-oxide-semiconductor field-effect transistors (MOSFETs), potentially causing functional failure after cumulative exposures on the order of 10-100 krad(Si). DDD predominantly affects bipolar junction transistors and optoelectronic devices by reducing minority carrier lifetime, with silicon devices showing significant degradation at fluences exceeding 10^12-10^14 neutrons/cm² depending on energy.[65][66][67] In integrated circuits, TID induces oxide charge buildup, shifting flat-band voltage by up to several volts in unhardened CMOS technologies, which exacerbates power consumption and timing errors; for instance, commercial-off-the-shelf (COTS) devices may fail at 50 krad(Si) in low-Earth orbit environments. Displacement damage in silicon lattices forms vacancy-interstitial pairs, reducing transistor current gain (h_FE) by factors of 10-100 in bipolar amplifiers under proton irradiation typical of space (e.g., 10^11 protons/cm² at 50 MeV). Single event effects (SEE), a transient subset, include upsets flipping memory bits (SEU) at linear energy transfer (LET) thresholds around 10-50 MeV·cm²/mg, leading to data corruption in SRAM without error correction.[68][69][70] Nuclear reactor environments amplify these impacts through neutron fluxes causing bulk displacement damage, with fast neutrons (E > 1 MeV) producing up to 10^15 displacements per atom (dpa) over operational lifetimes, severely degrading power MOSFETs and diodes via increased on-resistance. In space, galactic cosmic rays and solar particle events contribute to SEE rates of 10^-3 to 10^-6 errors/device/day for geosynchronous orbits, as observed in satellite anomalies since the 1970s. Combined effects in mixed radiation fields, such as those in fission reactors or Jupiter's magnetosphere, exhibit synergy where TID sensitizes devices to subsequent DDD, accelerating failure beyond additive models.[71][72][73] Wide-bandgap semiconductors like silicon carbide (SiC) and gallium nitride (GaN) demonstrate superior resilience, tolerating TID up to 1 Mrad(Si) with minimal threshold shifts due to lower displacement cross-sections, enabling their use in high-radiation missions such as NASA's Europa Clipper. However, even hardened devices require techniques like silicon-on-insulator (SOI) structures to isolate active layers, reducing SEE susceptibility by isolating charge collection volumes.[74][75][76]Biological Effects
Cellular and Molecular Damage
Ionizing radiation damages cells by depositing energy that ionizes atoms in biomolecules, either directly or indirectly through the production of reactive species. Direct effects involve ionization of DNA, proteins, or lipids, leading to molecular disruptions such as strand breaks or cross-links. Indirect effects, predominant in hydrated cellular environments, arise from the radiolysis of water, generating reactive oxygen species (ROS) like hydroxyl radicals (•OH), hydrogen radicals (•H), and hydrated electrons (e⁻_aq), which diffuse and react with nearby targets. Approximately two-thirds of cellular damage in mammalian cells stems from these indirect mechanisms due to the high water content (about 70-80%) in cytoplasm and nucleus.[6][77] At the molecular level, DNA is the primary target, sustaining oxidative lesions to bases (e.g., 8-oxoguanine, thymine glycol), abasic sites, and phosphodiester backbone disruptions. Single-strand breaks (SSBs) occur frequently but are generally reparable, whereas double-strand breaks (DSBs)—where both strands are severed within 10-20 base pairs—are induced at yields of about 20-40 DSBs per gray per cell in human fibroblasts and pose severe threats due to their potential for misrepair into translocations or deletions. Clustered damage, involving multiple lesions within a single helical turn (e.g., DSBs with adjacent base damage), complicates repair and arises from high linear energy transfer (LET) radiation like alpha particles, which deposit energy densely.[78][79][80] Proteins undergo denaturation, fragmentation, or aggregation via radical-induced oxidation of amino acids (e.g., cysteine sulfhydryl groups forming disulfides) or direct ionization, impairing enzymatic functions and signaling pathways. Lipids in cell membranes experience peroxidation, where •OH abstracts allylic hydrogens from polyunsaturated fatty acids, propagating chain reactions that compromise membrane integrity and trigger inflammatory cascades. These molecular alterations collectively disrupt cellular homeostasis, with DSBs and clustered lesions being the most cytotoxic, as evidenced by survival curves showing linear-quadratic dependence on dose for low-LET radiation like X-rays.[6][77][6]Tissue and Organ Responses
Ionizing radiation primarily damages tissues and organs through deterministic effects, which occur above specific threshold absorbed doses and exhibit severity proportional to the dose received. These effects arise from the killing of parenchymal cells, disruption of vascular endothelium, and inflammatory responses, leading to impaired organ function such as hypoplasia, atrophy, ulceration, or fibrosis.[81] Tissues with high cell turnover rates, such as those in the bone marrow and gastrointestinal tract, manifest responses at lower doses (typically 1-10 Gy) compared to quiescent tissues like muscle or nerve (often >50 Gy).[82] The Bergonié-Tribondeau law explains this radiosensitivity: undifferentiated cells undergoing mitosis are most vulnerable due to their inability to repair DNA damage efficiently before division.[83] In the hematopoietic system, doses exceeding 1 Gy suppress bone marrow stem cells, causing lymphocytopenia within hours and subsequent pancytopenia, which compromises immunity and increases infection risk; at 2-6 Gy, this contributes to the prodromal phase of acute radiation syndrome.[84] Gastrointestinal responses emerge above 6-10 Gy, where crypt cell sterilization leads to mucosal denudation, electrolyte imbalance, and barrier breakdown, potentially fatal without supportive care.[85] Skin exhibits erythema at 2-6 Gy due to vascular dilation and inflammatory cytokine release, progressing to dry or moist desquamation and temporary epilation above 7 Gy, with late fibrosis possible.[81] Lung tissue responds with pneumonitis 1-6 months post-exposure above 8-10 Gy, characterized by alveolar inflammation and exudation from endothelial damage, potentially evolving into fibrosis that reduces compliance.[86] Renal effects, including glomerular sclerosis, occur above 10-20 Gy, impairing filtration and leading to hypertension; hepatic responses involve sinusoidal endothelial damage and veno-occlusive disease at similar thresholds.[87] Neural tissues show limited acute responses due to low proliferation but vascular compromise at >50 Gy can cause edema and necrosis.[82] Ocular lens opacification (cataracts) develops deterministically above 0.5-2 Gy, depending on fractionation, via epithelial cell death and fiber disruption.[88]| Relative Sensitivity | Examples of Tissues/Organs | Typical Threshold for Observable Effects (Gy, whole-body or local) |
|---|---|---|
| High | Bone marrow, lymphoid organs, intestinal epithelium | 1-2 |
| Moderate | Skin, lung, kidney, liver, ovary/testis | 5-10 |
| Low | Muscle, brain, spinal cord | >30 |