When X-rays interact with matter, they can create low-energy electrons that can damage DNA and cause mutations. The process of ionization, in which an electron is removed from an atom, is one of the primary mechanisms by which X-rays can create these harmful electrons. The electrons produced through ionization have kinetic energies in the range from tens of electronvolts to a few tens of kiloelectronvolts (see Figure 5). If an electron escapes from the site of ionization with a relatively low energy of less than ∼34 eV [8]—it becomes a so-called “slow” or “subexcitation” electron (also called a "low-energy electron", LEE)—the electron may stay localized and undergo energy degradation while traveling only short distances in water [9], but can cause extensive tissue damage [10–13]. However, not just any subexcitation electron causes these harmful biological effects. There is convincing evidence, both experimental and theoretical, that those subexcitation electrons which possess an *additional* property will lead to DNA fragmentation or strand breaks. This distinguishing property is that the subexcitation electrons must *resonate* with the π or π* molecular orbitals [1, 14] (also called “lone-pair states”)—a resonance phenomenon predicted long ago by Platzman [15]. Thus, those “resonance subexcitation electrons” which can become trapped will cause strand breaks. Such resonances can occur for molecules including those in DNA base pairs and in the sugar phosphate backbone—with thymine (T) as most notable and guanine (G) as least efficient base in creating strand breaks [1]. Although many details of this damage remain unresolved, there is growing recognition that resonance excitation in water vapor and solid DNA components could account for much (and possibly most) of the strand break production and the corresponding cell death and mutations produced by ionizing radiation at environmental exposure levels.

In summary, although a high-energy (≳34 eV) primary electron generated by radiation or by photoemission has a high probability of forming DNA base damage products such as thymine glycol and its dimer through direct Coulombic repulsive forces when undergoing fast deceleration [15–19], the lower energy primary electron does so with much reduced efficiency via indirect damage via the production of hydroxyl radicals by excitation of water and by a minor effect due to hydrogen abstraction and by addition to thymidine. On the other hand, low-energy electrons (≤34 eV) generated via the subexcitation process can indeed produce substantial levels of strand breaks (and related lesions), but only those which happen to efficiently resonate with specific unoccupied, weakly antibonding π* electronic states. Since low-energy electron formation has a considerably larger cross section than direct double strand break, low-energy electron damage might, in environmental exposures and at radiation therapy doses become competitive with high-energy electron–mediated double-strand breaks.