Neural Effects of Fracking Sand Dust Aerosols
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2019/03/01
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Description:Hydraulic fracturing (fracking) is a process to recover oil and gas from shale rock formation. The technique involves fracturing the oil- and natural gas-laden rock with pressurized liquids. Water and fine mesh sand (proppant) generally make up 98 to 99.5 % of the fluid used during fracking. The transportation and handling of proppant at well sites generates aerosols, and, there is concern of worker exposure to such fracking sand dust (FSD) by inhalation. FSD are generally composed of silica in the respirable range, and other silicate/non-silicate minerals depending on the geological source of the proppant material. Field investigations by NIOSH suggest that the levels of respirable crystalline silica at well sites can exceed the permissible exposure limits. Thus, from an occupational safety perspective, it is of critical importance to evaluate the potential toxicological risks associated with FSD. To determine if FSD poses a neurological risk, male Sprague Dawley rats (8 weeks old) were exposed to FSD (10 or 30 mg/m3; 6 h/d × 4 d) by whole-body inhalation. At 1, 7, 27 or 90 d post-exposure, neuroinflammatory mediators, blood-brain barrier (BBB), synaptic, and glial markers were evaluated as indices of neural injury. FSD elicited neuroinflammation (increased Nos2, IL6 mRNAs) and altered the expression of BBB-related markers (increased or decreased Mmp9, Cldn1 and Cldn3 mRNAs) in the olfactory bulb, hippocampus and cerebellum. Increased glial fibrillary acidic protein and altered expression of myelin basic protein was also seen in these brain areas. An intriguing observation was the persistent reduction (25-42 % decrease at 7, 27, 90 d post-exposure; P < 0.05) of Synaptophysin 1 (SYP) and Synaptotagmin 1 (SYT) proteins in the cerebellum, suggestive of long-term synaptic changes. SYP and SYT are critical players in the exocytosis of synaptic vesicles, neurotransmitter release and synaptic plasticity. Synaptic loss and impaired synaptic plasticity are often associated with the functional decline of the nervous system. Whether such molecular aberrations will lead to neurodegeneration-like pathological changes remains unknown. Further, it needs to be determined if such effects follow direct FSD particulate translocation to the brain or an indirect neurogenic/systemic response. Thus, additional studies are warranted to investigate FSD translocation and evaluate the long-term neurological effects, including functional and behavioral outcomes, of FSD exposure. [Description provided by NIOSH]
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ISSN:1096-6080
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Pages in Document:19
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Volume:168
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Issue:1
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NIOSHTIC Number:nn:20054889
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Citation:Toxicologist 2019 Mar; 168(1):19
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CAS Registry Number:
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Federal Fiscal Year:2019
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Peer Reviewed:False
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Source Full Name:The Toxicologist. Society of Toxicology 58th Annual Meeting and ToxExpo, March 10-14, 2019, Baltimore, Maryland
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Main Document Checksum:urn:sha-512:75314602e39e9654886dc585e7e5e302e668c5c4bbc3a5738c2249e3922d6d1bfcd484b1fa99a8943b90bfd1ea0b5daec51f6e2cfe20b8300c96ad617e391fb0
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