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I explore the hypothesis that most intraplate earthquakes and their aftershock sequences are triggered by pore-fluid pressure increases. As proposed in this paper, data from the magnitude 5.7 Virginia earthquake of 23 August 2011 show that this is a two-step process. (1) First, from areas where there is greater than normal meteoric recharge, pore-fluid pressure diffusion by means of Biot slow waves transfers more pore-fluid pressure towards a future hypocentre. Here the cumulation of Biot slow waves produces a steady increase in pore-fluid overpressure until a main shock is triggered. (2) Then, aftershocks occur in the zone reaching from the depth of the main shock to a depth of a few kilometres below the land surface, preferring to localize in a weaker, pervasive anisotropic crustal fabric, in response to locally increased permeability and pore-fluid pressure transients caused by the main shock. The primary corrosive agent responsible for reducing the strength of silicate minerals in this upper crustal zone is water, so that quartz-rich crust tends to have lower values of Poisson’s ratio. I show here that increases in pore-fluid overpressure from normal groundwater recharge can start crack dilation leading to fracturing and the creation of new permeability. Previous chemical analyses across the Central Virginia Piedmont that hosted the 2011 Virginia shock show high upper crustal quartz content. This proposed two-step model for a main shock-aftershock sequence explains why intraplate earthquakes are rarely correlated with recognizable brittle faults at the Earth’s surface.

Supplementary material: A biography of John Costain is available at

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