Effect of Fe content on the fracture behaviour of Al–Si–Cu cast alloys

• Impact testing of Al–Si–Cu cast alloys in relation to Fe content.
• Effect of Sr modification and cooling rate on the fracture mode.
• Role of Fe intermetallics on the fracture behaviour of 319-type alloys.
• Role of porosity on the fracture behaviour of 319-type alloys.

Castings were prepared from 319.2 alloy melts, containing Fe levels of 0.2–1.0 wt%. Sr-modified (∼200 ppm) melts were also prepared for each alloy Fe level. The end-chilled refractory mold used provided directional solidification and a range of cooling rates (or dendrite arm spacings, DAS) within the same casting. Impact test samples were machined from specimen blanks sectioned from the castings at various heights above the chill end provided DASs of 23–85μm. All samples were T6-heat-treated before testing keeping with Aluminum Association recommendations. The results show that at low Fe levels and high cooling rates (0.4% Fe, 23 μm DAS), crack initiation and propagation in unmodified 319 alloys occurs through the cleavage of β-Al5FeSi platelets (rather than by their decohesion from the matrix). The morphology and the size of the platelets (individual or branched) are important in determining the direction of crack propagation. Increasing the DAS to 83μm leads to cleavage fracture. In this case, the fracture path follows a transgranular plane that is usually a well-defined crystallographic plane as judged by the relatively large smooth surfaces of the β-Al5FeSi phase platelets. Cracks also propagate through the fracture of undissolved CuAl2 or other Cu-intermetallics, as well as through fragmented Si particles. In Sr-modified 319 alloys, cracks are mostly initiated by the fragmentation or cleavage of perforated β-phase platelets, in addition to that of coarse Si particles and undissolved Cu-intermetallics.The amount of undissolved Cu- intermetallics is directly related to the applied cooling rate. Slow cooling rate (DAS ≈83µm) results in the precipitation of Cu- containing phases on the β-platelets, amplifying the likehood for crack propagation through these loacations.

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