Earthquakes are observed to occur in subduction zones to depths of approximately 680 km, even though unassisted brittle failure is inhibited at depths greater than about 50 km, owing to the high pressures and temperatures. It is thought that such earthquakes (particularly those at intermediate depths of 50-300 km) may instead be triggered by embrittlement accompanying dehydration of hydrous minerals, principally serpentine. A problem with failure by serpentine dehydration is that the volume change accompanying dehydration becomes negative at pressures of 2-4 GPa (60-120 km depth), above which brittle fracture mechanics predicts that the instability should be quenched. Here we show that dehydration of antigorite serpentinite under stress results in faults delineated by ultrafine-grained solid reaction products formed during dehydration. This phenomenon was observed under all conditions tested (pressures of 1-6 GPa; temperatures of 650-820 degrees C), independent of the sign of the volume change of reaction. Although this result contradicts expectations from fracture mechanics, it can be explained by separation of fluid from solid residue before and during faulting, a hypothesis supported by our observations. These observations confirm that dehydration embrittlement is a viable mechanism for nucleating earthquakes independent of depth, as long as there are hydrous minerals breaking down under a differential stress.
Intermediate-depth earthquakes (30–300 km) have been extensively documented within subducting oceanic slabs, but their mechanics remains enigmatic. Here we decipher the mechanism of these earthquakes by performing deformation experiments on dehydrating serpentinized peridotites (synthetic antigorite-olivine aggregates, minerals representative of subduction zones lithologies) at upper mantle conditions. At a pressure of 1.1 gigapascals, dehydration of deforming samples containing only 5 vol% of antigorite suffices to trigger acoustic emissions, a laboratory-scale analogue of earthquakes. At 3.5 gigapascals, acoustic emissions are recorded from samples with up to 50 vol% of antigorite. Experimentally produced faults, observed post-mortem, are sealed by fluid-bearing micro-pseudotachylytes. Microstructural observations demonstrate that antigorite dehydration triggered dynamic shear failure of the olivine load-bearing network. These laboratory analogues of intermediate-depth earthquakes demonstrate that little dehydration is required to trigger embrittlement. We propose an alternative model to dehydration-embrittlement in which dehydration-driven stress transfer, rather than fluid overpressure, causes embrittlement.
Cigarette smoking remains a significant health threat for smokers and nonsmokers alike. Secondhand smoke (SHS) is intrinsically more toxic than directly inhaled smoke. Recently, a new threat has been discovered – Thirdhand smoke (THS) – the accumulation of SHS on surfaces that ages with time, becoming progressively more toxic. THS is a potential health threat to children, spouses of smokers and workers in environments where smoking is or has been allowed. The goal of this study is to investigate the effects of THS on liver, lung, skin healing, and behavior, using an animal model exposed to THS under conditions that mimic exposure of humans. THS-exposed mice show alterations in multiple organ systems and excrete levels of NNAL (a tobacco-specific carcinogen biomarker) similar to those found in children exposed to SHS (and consequently to THS). In liver, THS leads to increased lipid levels and non-alcoholic fatty liver disease, a precursor to cirrhosis and cancer and a potential contributor to cardiovascular disease. In lung, THS stimulates excess collagen production and high levels of inflammatory cytokines, suggesting propensity for fibrosis with implications for inflammation-induced diseases such as chronic obstructive pulmonary disease and asthma. In wounded skin, healing in THS-exposed mice has many characteristics of the poor healing of surgical incisions observed in human smokers. Lastly, behavioral tests show that THS-exposed mice become hyperactive. The latter data, combined with emerging associated behavioral problems in children exposed to SHS/THS, suggest that, with prolonged exposure, they may be at significant risk for developing more severe neurological disorders. These results provide a basis for studies on the toxic effects of THS in humans and inform potential regulatory policies to prevent involuntary exposure to THS.
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