A brief review is given of mechanical property measurements on oxide films. This review is followed by a detailed discussion of the mechanical and fracture properties of anodic aluminum oxide films as observed in the author's laboratory. Extensive measurement of Young's modulus, E c ,and fracture strain, ε f , for separated films 3000Aå thick is reported as a function of environmental water vapor pressure. The fracture of these unsupported films is shown to occur by a brittle mechanism. Mechanical properties of adhering aluminum oxide films are given as a function of their thickness. These oxides were observed to fracture either at slip steps, or at right angles to the tensile axis in a regularly spaced fashion. A theory of adhering oxide fracture is discussed which accounts well for the observations. An equation which describes the spacing d of regular oxide fracture cracks as a function of substrate strain ε is given in the form ln ( ε / ε 0 ) = k √ t ( 1 / d − l / d 0 ) , where ( ε o , d o ) are the initial conditions for regular fracture, t is the oxide thickness, and k is a constant.

A comprehensive description of the mechanisms of fatigue in metals is given for the temperature range in which creep processes are not important. The general response of materials to cyclic loading is discussed, including fatigue hardening/softening and the development of inhomogeneous plastic strains. The generation of fatigue cracks is treated by listing first the common sites for initiation and then discussing the various mechanisms for initiation which have been observed. Fatigue crack growth is described generally in terms of propagation modes and the appearance of fracture surfaces. Then the mechanisms of crack advance are considered in detail, and the effects of multiple load amplitude are included. Predictive theories of fatigue, from early “damage” theories to recent crack growth laws, are discussed in the light of fatigue mechanisms knowledge. Included is a discussion of the effects of crystal structure on fatigue strength. Finally, the practical implications of fatigue mechanisms knowledge are presented as they affect nondestructive inspection, repair of fatigue damage, the choice of fatigue-resistant materials, and development of new materials. There are 68 references to the fatigue literature.

The fracture of brittle coatings on a strained substrate is examined from two points of view. In the first case, the substrate deforms continuously and regularly spaced fractures occur in the coating. The spacing d at any strain ε is given by In ε/ε0 = (4g/d) (1−d/d0), where d0, ε0 are any convenient set of data points, and g is a parameter having the units of length. In the second case, the substrate deforms by crystallographic slip and fracture of the oxide may or may not occur at the slip step. The criteria for fracture are that the interface adhesive stresses be too large for the coating to sustain the necessary peel stress. Quantitative relations are given in terms of the coating thickness, fracture strain, and the orientation of the slip step with respect to the surface. The results for both cases are compared with experiment and found to be in essential agreement.

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In order to investigate quantitatively the influence of point‐defect clusters on the saturation stress in metal fatigue, the yield stress for uni‐directional deformation was measured as a function of temperature between 78 and 300 °K on copper single crystals which had been fatigue‐hardened into saturation at room temperature. Weak beam transmission electron micrographs of these specimens revealed a cell‐like dislocation array with a low point‐defect cluster density in the dislocation‐poor interior and a high cluster density in the dislocation‐rich walls of the cells. The size distribution of the defect clusters was found to be exponential for both the cell interior and the cell walls. A quantitative analysis of the yield stress measurements together with the electron‐microscopical data showed that the saturation stress of fatigued copper single crystals is controlled by internal stresses and defect clusters within the interior of the cells which impede the dislocation motion through these regions.