Comparison of the Ames Salmonella Assay and Mutatox Genotoxicity Assay for Assessing the Mutagenicity of Polycyclic Aromatic Compounds in Porewater from Athabasca Oil Sands Mature Fine Tailings

Abstract

The oil sands in the Athabasca region of northeastern Alberta, Canada, represent a significant hydrocarbon resource that is currently exploited by mining, followed by separation of bitumen from sand using hot water flotation. This process generates large quantities of bitumen-contaminated tailings. Current research involves an assessment of whether the tailings ponds can ultimately be converted to biologically productive lakes, with one unresolved issue being the toxicity of the polycyclic aromatic compounds (PACs) that might be released from the tailings. In this paper, we have identified several polycyclic aromatic hydrocarbons in the porewater from oil sands mature fine tailings and have compared the responses of 17 PACs in the Ames and Mutatox genotoxicity assays. The Mutatox assay was unsuitable as a surrogate for the Ames test in this application; poor (50%) concordance between the two assays occurred because the mechanism of light emission in the Mutatox assay is uncertain, leading to positive responses that could not be unambiguously associated with genotoxicity. Benzo[a]pyrene equivalency factors (BEFs) in the Ames assay were determined for a large number of PACs, from this work and from literature data, to express the genotoxic potencies of environmental mixtures in terms of benzo[a]pyrene equivalent concentrations (BEQs). In the case of porewater samples obtained from the mature fine tailings, even extracts concentrated 10,000-fold were below the detection limit of 1 μg/L BEQ, consistent with the value of 0.14 μg/L calculated using BEFs of PACs identified in the porewater.

Mutagenicity of selected polycyclic aromatic hydrocarbons (PAHs)

“…These observations corroborate the procarcinogen status of PAHs, whose metabolites through the CYP450 metabolic pathway produce diols and epoxides that form DNA adducts leading to mutations (Shimada et al, 2001;Rubin et al, 2005;Locasale and Cantley, 2011;Chapman et al, 2020). Similarly, the findings are consistent with the report that implicates the metabolites of benzo[a]pyrene and 2-methylnaphthalene in causing base-pair mutation, acre mutation, sister chromatid exchange, chromatid breaks, and frameshift mutation (Madill et al, 1999;Kulka et al, 1988;EPA, 2016). No information is available on the mutagenicity of phenazine via the Ames assay, and the available data was on the comet assay by McGuigan and Li (2014).…”

Concentrations, Sources and Health Risk Assessment of Polycyclic Aromatic Hydrocarbons in Chinese Herbal Medicines

“…Traditionally, carcinogenic toxicity assessments have been used to evaluate the health risk of an individual’s exposure to a carcinogen. The toxic equivalency assessment of PAHs is based on the toxic equivalency factor (TEF) of benzo [a]pyrene, which is set to 1, and the toxic equivalency of other PAHs is calculated according to the formula of the conversion factor [ 40 , 41 , 42 ]. The formula for calculating the toxic equivalent quotient (TEQ) concentration of PAHs (TEQBaP) is as follows (1): where TEQ BaP denotes the toxic equivalence of PAHs converted to benzo[a]pyrene, ng/kg; C i denotes the concentration of PAHs in CHMs, μg/kg; TEF i denotes the TEF value of PAHs in CHMs.…”

Polycyclic aromatic hydrocarbons residues and the carcinogenic risk assessment to pregnant women in Nantong, China using QuEChERS method and HPLC—A pilot case study

“…From the serum PAH concentrations in the test results and the TEFs of PAHs (Brownlee et al, 1999;Nisbet & Lagoy, 1992;Stroomberg et al, 1999), the total carcinogenicity equivalent concentration t i in the serum of pregnant women can be calculated. From the detected concentrations of the 16 PAHs, the carcinogenicity contribution rates (R, %) can be calculated (Table 4).…”