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Atomic‐Scale Observation of Irradiation‐Induced Surface Oxidation by In Situ Transmission Electron Microscopy
Author(s) -
Huang Xing,
Jones Travis,
Fan Hua,
Willinger MarcGeorg
Publication year - 2016
Publication title -
advanced materials interfaces
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.671
H-Index - 65
ISSN - 2196-7350
DOI - 10.1002/admi.201600751
Subject(s) - materials science , irradiation , transmission electron microscopy , chemical physics , amorphous solid , oxygen , chemical engineering , carbon fibers , electron beam processing , vacancy defect , nanotechnology , crystallography , chemistry , composite material , organic chemistry , physics , composite number , nuclear physics , engineering
Irradiation of materials with high energy particles can induce structural transitions or trigger chemical reactions. Understanding the underlying mechanism for irradiation‐induced phenomena is of both scientific and technical importance. Here, CdS nanoribbons are used as a model system to study structural and chemical evolution under electron‐beam irradiation by in situ transmission electron microscopy. Real‐time imaging clearly shows that upon irradiation, CdS is transformed to CdO with the formation of orientation‐dependent relationships at surface. The structural transition can always be triggered with a dose rate beyond 601 e/Å 2 s in this system. A lower dose rate instead leads to the deposition of an amorphous carbon layer on the surface. Based on real‐time observations and density functional theory calculations, a mechanism for the oxidation of CdS to CdO is proposed. It is essentially a thermodynamically driven process that is mediated by the formation of sulfur vacancies due to the electron‐beam irradiation. It is also demonstrated that the surface oxidation can be suppressed by pre‐depositing a conductive carbon layer on the CdS surface. The carbon coating can effectively reduce the rate of sulfur vacancy creation, thus decreasing defect‐mediated oxidation. In addition, it isolates the active oxygen radicals from the ribbon, blocking the pathway for oxygen diffusion.