2013 Conference of the International Medical Geology Association (25–29 August 2013)

Paper No. 7
Presentation Time: 4:50 PM


CROSBY, Lynn M.1, DEVERA, Christina2, CHARLES, Kaylene1 and OREM, William H.3, (1)US Geological Survey, Eastern Energy Resources Science Center, Mail Stop 956, National Center, 12201 Sunrise Valley Dr, Reston, VA 20192, (2)U.S. Geological Survey, 956 National Center, Reston, VA 20192, (3)Eastern Energy Resources Science Center, U.S. Geological Survey, 12201 Sunrise Valley Dr, MS 956, Reston, VA 20192, lcrosby@usgs.gov

Studies of the potential health impacts of water used in hydraulic fracturing are very limited. This water is stored in man-made ponds for extended periods prior to injection, pumped to tanks where biocide is added, then transferred to a blender where sand and chemicals such as polyacrylamide and sugar-based polymers are added. Injecting these fluids into shale exposes them to anoxic conditions and elevates temperatures for up to several months during which time organic matter, chlorides, iron and radon may enter the fluid. Flowback returns an estimated 30-70% of the fluids from the well. Compared to water used to prepare the injected fluids, salinity, alkalinity, sulfate, iron and total dissolved solids concentrations in returned waters are elevated.

In the present study, we investigated the effects of hydraulic fracturing flowback waters from eight sites on human cells. Toxicity at full-strength and 1:10 was severe for four sites sampled and in full-strength only for two additional sites. In a post-injection time series exposed cells were 20% viable. An intensive study of a subset of two samples revealed severe, significant wound closure inhibition occurred at 1:10, remaining significant at 1:100 but without effect at 1:1000. Cells behind the wound edge lost cell-cell continuity indicating aberrant healing. At 1:100, glutathione transferase kappa (GSTκ1) and arylhydrocarbon receptor (AhR) proteins were increased. AhR is a transcription factor activated by many toxic contaminants including dioxins. Mice engineered to lack GSTκ1 develop glomerulonephropathies therefore loss of function could compromise contaminant detoxification, leading to renal impairment. GSTµ1/2, involved in protection against oxidative stress and DNA damage repair, and CYP1A1 (AhR ligands regulate mRNA expression of CYP1A1) protein expression decreased similar to a known kidney carcinogen. Although it is unclear whether accidental discharges will occur, the possibility remains and recycling or treatment, if possible, could forestall toxic consequences.

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