Hydraulic fracturing (HF) has emerged as a major method of unconventional oil and gas recovery. The toxicity of hydraulic fracturing flowback and produced water (HF-FPW) has not been previously reported and is complicated by the combined complexity of organic and inorganic constituents in HF fluids and deep formation water. In this study, we characterized the solids, salts, and organic signatures in an HF-FPW sample from the Duvernay Formation, Alberta, Canada. Untargeted HPLC-Orbitrap revealed numerous unknown dissolved polar organics. Among the most prominent peaks, a substituted tri-phenyl phosphate was identified which is likely an oxidation product of a common polymer antioxidant. Acute toxicity of zebrafish embryo was attributable to high salinity and organic contaminants in HF-FPW with LC50 values ranging from 0.6% to 3.9%, depending on the HF-FPW fractions and embryo developmental stages. Induction of ethoxyresorufin-O-deethylase (EROD) activity was detected, due in part to polycyclic aromatic hydrocarbons (PAHs), and suspended solids might have a synergistic effect on EROD induction. This study demonstrates that toxicological profiling of real HF-FPW sample presents great challenges for assessing the potential risks and impacts posed by HF-FPW spills.

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There is increasing environmental concern about the volume of oil sands process-affected water (OSPW) produced by the oil sands industry in Alberta, Canada. There is limited knowledge of the toxic effects of OSPW and one of the primary organic constituents, naphthenic acids (NAs), which are thought to be one of the toxic constituents of OSPW. OSPW and NAs can have endocrine disrupting potential. The NAs in OSPW are persistent, but ozonation can significantly reduce concentrations of NA, while increasing their biodegradability, and consequently reduce OSPW toxicity. However, it is of concern that OSPW ozonation might generate hydroxylated cycloaliphatics with endocrine disrupting potential. In this study, the estrogen receptor- (ER) and androgen receptor- (AR) mediated effects of OSPW and ozone-treated OSPW were investigated in vitro by use of T47D-kbluc (estrogen responsive) and MDA-kb2 (androgen responsive) cells. Ozonation neither attenuated nor intensified the estrogenicity of OSPW. The estrogenic responses to untreated OSPW and ozone treated OSPW were 2.58(±0.22)-fold and 2.48(±0.13)-fold greater than those of controls, respectively. Exposure to untreated OSPW produced significant antiandrogenicity in the presence of 0.01, 0.05, or 0.1 nM testosterone (T), while ozone-treated OSPW produced significant antiandrogenicity in the presence of 0.01 or 0.05 nM T. Exposure to untreated and ozone-treated OSPW also caused potentiation of androgen receptor-mediated effects of T. OSPW could cause estrogenic and antiandrogenic effects through receptor mediated pathways, and ozonation can partially mitigate the OSPW antiandrogenicity as well as androgen potentiating effect, without increasing estrogen potency.

There is increasing concern over the risk of environmentally relevant doses of bisphenol A (BPA) on human endocrine systems. Effects of BPA on steroidogenesis and the related molecular mechanisms were investigated in H295R human adenocarcinoma cells. This immortal cell line is unique in expressing all the enzymes of the steroidogenic pathways. The effects of BPA on steroidogenesis, 17β-estradiol (E2) metabolism, and aromatase activity were examined in H295R cells exposed to BPA from 3.0 × 10(-1) to 3.0 × 10(3) ng/ml. Concentrations of BPA in basic cell culture materials were verified. Stable CYP17A-knockdown H295R cells were developed to verify the mechanism of inhibited steroidogenesis by BPA. Background concentrations of BPA in control cell culture media ranged from 0.03 to 0.38 ng/ml. Significantly lesser concentrations of androstenedione, testosterone, cortisol, and cortisone were caused by exposure to 30-3000 ng BPA/ml. In contrast, sconcentrations of estrone (E1) and E2 were significantly greater in BPA-exposed H295R cells. Lesser production of androstenedione and testosterone by H295R cells exposed to BPA was the most sensitive endpoint (no observable effect concentrations < 30 ng BPA/ml). CYP17A knockdown in H295R cells resulted in less production of both 17α hydroxyprogesterone and androstenedione. The results are consistent with the hypothesis that in H295R cells, BPA selectively inhibits 17,20-lyase but not 17α-hydroxylase. The primary mechanism causing increased E2 in the medium was inhibition of E2 metabolism rather than greater aromatase (CYP19) activity. These results suggest that BPA has the potential to interfere with cellular steroidogenesis in humans through multiple molecular mechanisms.

Per- and polyfluoroalkyl substances (PFASs) have been manufactured and widely used for over 60 years. Currently, there are thousands of marketed PFASs, but only dozens of them are routinely monitored. This work involved target, nontarget, and suspect screening of PFASs in the liver of Indo-Pacific humpback dolphin (Sousa chinensis) and finless porpoise (Neophocaena phocaenoides), two resident marine mammals in the South China Sea, stranded between 2012 and 2018. Among the 21 target PFASs, perfluorooctane sulfonate and 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFESA) predominated in the samples, accounting for 46 and 30% of the total PFASs, respectively. Significantly higher total target PFAS concentrations (p < 0.05) were found in dolphin liver samples [3.23 × 103 ± 2.63 × 103 ng/g dry weight (dw)] than in porpoise liver samples (2.63 × 103 ± 1.10 × 103 ng/g dw). Significant increasing temporal trends (p < 0.05) were found in the concentrations of two emerging PFASs, perfluoroethylcyclohexane sulfonate and 2,3,3,3-tetrafluoro-2-propanoate in porpoises, indicating increasing pollution by these emerging PFASs. Forty-four PFASs from 9 classes were additionally identified by nontarget and suspect screening, among which 15 compounds were reported for the first time in marine mammals. A primary risk assessment showed that the emerging PFAS 6:2 Cl-PFESA could have possible adverse effects in terms of reproductive injury potential on most of the investigated cetaceans.