The evaluation of toxic effects induced by exposure of mammals to oil sands process-affected water and its organic fraction

• Author / Creator

  Li, Chao

• Oil sands process-affected water (OSPW) produced by the surface-mining oil sands industry in Alberta, has been shown to be toxic to a variety of organisms. Much of this toxicity has been attributed to the dissolved organic compounds, primarily naphthenic acids (NAs). Under a no-release practice, OSPW is stored on-site in tailings ponds with the understanding that eventual reclamation of this water must be undertaken. Successful remediation of OSPW is expected to require a reduction in total dissolved organics (including NAs) and the removal of other compounds that may contribute to OSPW toxicity. Ozonation is currently identified as one of the promising methods for reduction of OSPW toxicity. However, there is concern regarding the possible hazardous byproducts that may be created by ozonation. To date, most toxicological data of OSPW were generated using aquatic organisms, while information on the effects of OSPW exposure in mammals is limited. The overall objective of my research was to determine possible adverse effects of whole OSPW and its organic fraction (OSPW-OF) in a representative mammal, using in vitro and in vivo assessments, and evaluate the effectiveness of ozone treatment in reducing OSPW toxicity. The raw OSPW and OSPW-OF were chemically analyzed, revealing that classical NAs (CnH2n+zO2) and oxy-NAs (CnH2n+zOx, x=3-6) accounted for 37.9% of the total mass of OSPW-OF. In vitro assays using RAW 264.7 mouse macrophage-like cell line demonstrated that whole OSPW, and not OSPW-OF, reduced cell viability at NAs ≥ 14 mg/L that was related to the cell membrane damage, and suppressed cellular proliferation. Whole OSPW (10 mg/L NAs content) also modulated the antimicrobial function of RAW 264.7 cells by altering NO production and subsequent release of pro-inflammatory mediators. Furthermore, this dose of OSPW induced higher mRNA levels of heme oxygenase 1 (hmox1) in RAW 264.7 cells, suggesting that oxidative stress were induced by the constituents in tailing ponds water. Despite ~ 90% reduction of NAs after ozonation, this treatment failed to ameliorate the toxicity of OSPW. These results suggest that in addition to NAs, other components in OSPW (other organic substances or the constituent(s) of the inorganic fraction) or the additive and/or synergistic effects between the constituents present in whole OSPW are responsible for the observed toxic effects. In vivo toxicity studies using BALB/c mice revealed that acute exposure during the gestation and sub-chronic exposure throughout gestation and lactation had minimal effects on the reproduction of female mice. Mating behavior, pregnancy success, embryonic implantation, gestation length, and litter size were not affected by NA doses up to 100 mg/kg body weight/week. The growth and development of the offspring was similar between pups from OSPW-OF orally exposed and sham-treated non-exposed mothers. Changes in pregnancy-associated hormones (progesterone, 17β-estradiol, prolactin and aldosterone) and immune response (T helper 1 (Th1)/Th2 cytokines shift) were observed in non-exposed pregnant mice, which promoted maternal tolerance of the fetus. OSPW-OF exposure did not bring about significant changes in plasma hormone levels and cytokine protein secretion, consistent with normal reproductive performance. The gene expression analysis suggested that liver was the main target organ for OSPW-OF. Acute exposure to OSPW-OF at 55 mg/L NAs down-regulated the expression of glutathione-S-transferase genes (gstp1 and gstm1) in the liver, suggesting that cellular detoxification functions may be impaired. The expression of ogg1 (8-oxoguanine DNA glycosylase), a gene involved in DNA repair, was also suppressed in mice after acute exposure to OSPW-OF (55 mg/L NAs). However, these inhibitory effects were transitory and not observed after sub chronic (6 week) exposure of mice to OSPW-OF. Following sub-chronic exposure to OSPW-OF at high dose, an elevated mRNA level of uracil-DNA glycosylase (ung) was observed, indicating a possible increase in OSPW-OF induced mutagenesis. The results of my thesis research present the first comprehensive analysis of mammalian toxicity associated with OSPW and OSPW-OF exposure, using a series of in vitro and in vivo bioassays. Additionally, it provides important information regarding the feasibility of ozonation as an option to reduce OSPW contaminants and associated toxicity.

• Subjects / Keywords

  • Organic fraction
  • OSPW
  • Mammals
  • Toxicity

• Graduation date

  Spring 2018

• Type of Item

  Thesis

• Degree

  Doctor of Philosophy

• DOI

  https://doi.org/10.7939/R34B2XM0J

• License

  This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.