Abstract
Graphene inherently possesses defect sites and grain boundaries that are vulnerable to chemical etching by hydrogen radicals. In this study, an etch-mitigation method is presented to selectively passivate these sites using atomic layer deposition (ALD) of a H etch-resistant material. First, as a reference experiment, pristine exfoliated graphitic layers are exposed to H radicals to determine the lateral etch rate from defect sites. Next, these samples are compared to graphitic layers in which the defects are selectively passivated by Al2O3, in the same exposure conditions, using atomic force microscopy at every step in the experiment. The results show that etching is slowed down by local deposition of Al2O3 ALD at sites vulnerable to H radical etching.
Highlights
Graphene is an exceptional material, owing to its marvellous electronic properties, high optical transparency, thermal conductivity, and theoretical mechanical strength [1,2,3,4]
Al2O3 atomic layer deposition (ALD) was performed on highly oriented pyrolytic graphite (HOPG) flakes to selectively passivate the defect sites
The Al2O3 ALD decorated HOPG was exposed to H radicals to test the extent to which ALD passivation of defects reduces the etch rate
Summary
Graphene is an exceptional material, owing to its marvellous electronic properties, high optical transparency, thermal conductivity, and theoretical mechanical strength [1,2,3,4]. Free-standing graphene layers have been considered for various applications, including energy storage device applications [5] and particle filtering membranes inserted into optical beam paths for e.g. light element x-ray transmission windows [6] and extreme ultraviolet (EUV) lithography pellicles [7]. Simulations by Despiau-Pujo et al suggest that chemical-etching mechanisms of defect-free graphene by H ions start to play a role for ion energies of 5 eV and higher [9]. Already degrades in H radical environments starting from its structural defects, such as grain boundaries and point defects [10], which are vulnerable sites for etching due to their enhanced reactivity towards H radicals [11,12,13,14]
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