Intrinsic defect formation in amorphous ${\text{SiO}}_2$ by electronic excitation: Bond dissociation versus Frenkel mechanisms

Two competing mechanisms of intrinsic defect formation in amorphous ${\text{SiO}}_2$ $\left(a{\text{-SiO}}_2\right)$, i.e., the vacancy-interstitial (Frenkel) mechanism and Si-O bond dissociation to form silicon and oxygen dangling bonds, were compared under $\gamma$-ray electronic excitation. The Frenkel mechanism was found to be dominant. The concentrations of both kinds of defects strongly correlate with the degree of the structural disorder of $a{\text{-SiO}}_2$, providing experimental evidence that both types of intrinsic defect pairs are formed mainly from the strained Si-O-Si bonds. The bond dissociation mechanism is more susceptible to the structural disorder than the vacancy-interstitial mechanism.

Figure 1

Optical absorption spectra (resolution of 1 nm) of the DryF samples heated at $900°\text{C}$ and irradiated with ${}^{60}\text{C}\text{o}$ $\gamma$ rays. The inset shows the induced absorption spectra at a cumulative dose of $\sim 5.3\times {10}^7\text{Gy}$, obtained by subtracting the spectrum of the unirradiated sample from the original spectrum. The induced absorption spectrum is fitted with a linear combination of Gaussian-shaped bands of NBOHC, divalent Si, $E^{\prime }$ center, and Si-Si bond by least-squares fitting. The peak parameters used for the fitting is listed in Table .

Figure 2

Induced optical-absorption spectra of the DryF samples preannealed at 900 or $1400°\text{C}$ and exposed to $\sim 5.3\times {10}^7\text{Gy}$ $\gamma$ rays. The inset shows IR PL spectra of interstitial ${\text{O}}_2$ excited at 765 nm.

Figure 3

(Color online) Variations in concentrations $C$ of NBOHC, $E^{\prime }$ center, Si-Si bond, and interstitial ${\text{O}}_2$ with $\gamma$-ray absorbed dose $D$ (${\text{SiO}}_2$ equivalent) in the (a) DryF and (b) WetF samples annealed at 900 or $1400°\text{C}$. The dotted lines illustrate theoretical curves calculated at semiarbitrarily chosen values of the formation rate $\left(5\times {10}^{11}{\text{cm}}^{-3}{\text{Gy}}^{-1}\right)$ and equilibrium concentration $\left(5\times {10}^{17}{\text{cm}}^{-3}\right)$. The theoretical curve represents the single exponential defect formation kinetics and the derivation is described in the Appendix.

Figure 4

(a) Typical simulated curves of time-dependent change in normalized concentration of products $A_1$ and $A_2$ generated by the mechanism [Eq. (A1)]. Curves for no [$k^{\prime }=0$ in Eq. (A3)], first-order [$k^{\prime }=k$ in Eq. (A3)], and second-order [$k^{\prime }=k/C_0$ in Eq. (A6)] backward reactions are drawn at $k={10}^{-3}$. (b) Effect of overlap of defect formation processes of different time constants $\tau$. Each $\tau$ component is shown with thin lines. Two examples, where the saturation concentration of the components is constant and increases with $\tau$ (solid and dashed lines, respectively), are exhibited. In the total concentration changes (thick lines), sublinear concentration dependence on time is clearly seen.