Dysregulated Purinergic Signalling in Fragile X Syndrome Cortical Astrocytes.

The symptoms of fragile X syndrome (FXS), caused by a single gene mutation to Fmr1, have been increasingly linked to disordered astrocyte signalling within the cerebral cortex. We have recently demonstrated that the purinergic signalling pathway, which utilizes nucleoside triphosphates and their metabolites to facilitate bidirectional glial and glial-neuronal interactions, is upregulated in cortical astrocytes derived from the Fmr1 knockout (KO) mouse model of FXS. Heightened Fmr1 KO P2Y purinergic receptor levels were correlated with prolonged intracellular calcium release, elevated synaptogenic protein secretion, and hyperactivity of developing circuits. However, due to the relative lack of sensitive and reproducible quantification methods available for measuring purines and pyrimidines, determining the abundance of these factors in Fmr1 KO astrocytes was limited. We therefore developed a hydrophilic interaction liquid chromatography protocol coupled with mass spectrometry to compare the abundance of intracellular and extracellular purinergic molecules between wildtype and Fmr1 KO mouse astrocytes. Significant differences in the concentrations of UDP, ATP, AMP, and adenosine intracellular stores were found within Fmr1 KO astrocytes relative to WT. The extracellular level of adenosine was also significantly elevated in Fmr1 KO astrocyte-conditioned media in comparison to media collected from WT astrocytes. Glycosylation of the astrocyte membrane-bound CD39 ectonucleotidase, which facilitates ligand breakdown following synaptic release, was also elevated in Fmr1 KO astrocyte cultures. Together, these differences demonstrated further dysregulation of the purinergic signalling system within Fmr1 KO cortical astrocytes, potentially leading to significant alterations in FXS purinergic receptor activation and cellular pathology.

Cohort profile: DNA methylation in the Northern Ireland Cohort for the Longitudinal Study of Ageing (NICOLA) - recruitment and participant characteristics.

PURPOSE: Epigenetic modifications including DNA methylation (DNAm) are proposed mechanisms by which social or environmental exposures may influence health and behaviours as we age. The Northern Ireland Cohort for the Longitudinal Study of Ageing (NICOLA) DNAm cohort, established in 2013, is one of several worldwide, nationally representative prospective studies of ageing with biological samples from participants who consented to multiomic analysis. PARTICIPANTS: NICOLA recruited 8478 participants (8283 aged 50 years or older and 195 spouses or partners at the same address aged under 50 years). Computer-Assisted Personal Interviews, Self-Completion Questionnaires and detailed Health Assessments (HA) were completed. Of the 3471 (44.1%) participants who attended the HA in wave 1, which included venous blood sampling, 2000 were identified for the DNAm cohort. Following technical and data quality control checks, DNAm data are currently available for n=1870. FINDINGS TO DATE: There was no significant difference based on age, self-reported gender, education, employment, smoking or alcohol status and subjective health reports between the DNAm cohort and other HA attendees. Participants were more likely to be in the DNAm group if they lived with one other person (OR 1.26, 95% CI 1.07 to 1.49). The DNAm group had a lower proportion of depressed participants and those meeting criteria for post-traumatic stress disorder (11.7% and 4.4% vs 13.5% and 4.5%, respectively) categorised by objective assessment tools but this was not significant (OR 0.84, 95% CI 0.69 to 1.02 and OR 0.87, 95% CI 0.64 to 1.19). FUTURE PLANS: The deeply phenotyped DNAm cohort in NICOLA with planned prospective follow-up and additional multiomic data releases will increase the cohort's utility for research into ageing. The genomic and epigenetic data for the DNAm cohort has been deposited on the European Genome-Phenome Archive, increasing the profile of this cohort and data availability to researchers.

A Phase I Trial of Allogeneic γδ T Lymphocytes From Haploidentical Donors in Patients With Refractory or Relapsed Acute Myeloid Leukemia.

Introduction We report the results of a phase I clinical trial NCT03790072 of an adoptive transfer of γδ T lymphocytes from haploidentical donors in patients with refractory/relapsed acute myeloid leukemia after lymphodepletion regimen. Patients and methods Healthy donor mononuclear cells collected by leukapheresis were consistently expanded to generate products of 109 to 1010 γδ T cells. Seven patients received donor-derived T cell product at doses of 106/kg (n = 3), 107/kg (n = 3), and 108/kg (n = 1). Results Four patients had bone marrow evaluation at day 28. One patient had a complete remission, one was classified as morphologic leukemia-free state, one had stable disease and one had no evidence of response. In one patient, there was evidence of disease control with repeat infusions up to 100 days after first dosing. There were no treatment-related serious adverse events or treatment-related Common Terminology Criteria for Adverse Events grade 3 or greater toxicities at any dose level. Allogeneic Vγ9Vδ2 T cell infusion was shown to be safe and feasible up to a cell dose of 108/kg. Discussion In agreement with previously published studies, the infusion of allogeneic Vγ9Vδ2 cells was safe. The contribution of lymphodepleting chemotherapy to responses seen cannot be ruled out. Main limitation of the study is the low number of patients and interruption due to COVID-19 pandemic. Conclusion These positive Phase 1 results support progression to phase II clinical trials.

Converging purinergic and immune signaling pathways drive IL-6 secretion by Fragile X cortical astrocytes via STAT3.

The symptoms of Fragile X syndrome (FXS) are driven in part by abnormal glial-mediated function. FXS astrocytes release elevated levels of immune-related factors interleukin-6 (IL-6) and tenascin C (TNC), and also demonstrate increased purinergic signaling, a pathway linked to signaling factor release. Here, in cortical astrocytes from the Fmr1 knockout (KO) FXS mouse model, purinergic agonism enhanced TNC secretion and STAT3 phosphorylation, two processes linked to elevated IL-6 secretion in FXS, while STAT3 knockdown and TLR4 antagonism normalized Fmr1 KO IL-6 release. We therefore suggest that purinergic signaling and immune regulatory pathways converge to drive FXS cortical pro-inflammatory responses.

Transition From an ICU Ventilator to a Portable Home Ventilator in Children.

BACKGROUND: The transition from an ICU ventilator to a portable home ventilator (PHV) for children requiring long-term mechanical ventilation is a crucial step in preparing for discharge home and may not be successful on the first attempt. A review of this process at our institution revealed that some children required multiple trials before they were able to tolerate a PHV. A protocol was developed to standardize the transition process and reduce the number of failed attempts. Key features of the protocol included a transition readiness assessment and criteria for changing to the PHV. METHODS: A retrospective chart review was completed to evaluate the process of changing to a PHV before and after the protocol was in place during the time period of 2011-2018. Primary outcome measures included the number of transition attempts and the length of time to achieve successful transition. A successful transition attempt was defined as the ability to tolerate a PHV for 14 d. RESULTS: The study included 56 children ≤ 3 y old with a tracheostomy who required long-term ventilator support. The majority of subjects were from the neonatal ICU and had a diagnosis of bronchopulmonary dysplasia. There was a significant decrease in the number of attempts (P = .005) and in the length of time (P = .01) to successfully transition to a PHV for those who underwent the protocol. CONCLUSIONS: The process of changing from an ICU ventilator to a PHV in children requiring long-term mechanical ventilation was improved through the use of a standardized protocol. Both the number of failed attempts and the length of time to achieve successful transition were reduced when the protocol was applied. Further study is needed to evaluate other medical and nonmedical factors that may affect successful transition to a PHV.

Bioaccumulation potential of naphthenic acids and other ionizable dissolved organics in oil sands process water (OSPW) - A review.

Bitumen recovery via mining in Alberta's Athabasca region generates large quantities of oil sands process water (OSPW). Aquatic toxicity of OSPW has been well-studied and the class of organic compounds referred to as naphthenic acids (NAs) are consistently implicated as the primary driver. Proposed lease closure options include treated produced waters in reclaimed landscapes such as pit lakes and wetlands. Consequently, it is crucial to understand the bioaccumulation potential of NAs and other OSPW dissolved organics in these environments. Early studies were focussed only on NAs due to analytical limitations, however, later studies investigated additional classes of dissolved organics in OSPW. Reported bioconcentration factors (BCFs) for NAs in fish and amphibians range from 0.24 to 53 L/kg wet-weight. Most quantitative assessments of NAs bioaccumulation potential evaluated commercial NAs mixtures as a surrogate for OSPW and used using single-ion monitoring for measuring NAs concentrations. The resulting BCF values are based on the NA isomers that conform to the formula, C13H22O2. More recently, an advanced analytical technique capable of determining the profile of different isomer classes in OSPW showed that NAs and other OSPW ionizable dissolved organics (OSPW-IDO) have low partitioning to simulated biological storage lipids, suggesting low bioaccumulation potential. Using the same analytical technique to assess in vivo fish exposures, a subsequent study reported a range of BCFs for OSPW NAs between 0.7 and 53 L/kg wet-weight and heteroatomic isomer classes containing S or N heteroatoms had BCFs between 0.6 and 28 L/kg wet-weight. Reported BCFs for all isomer classes of the OSPW-IDO fraction were less than the Canadian standard for bioaccumulative designation (i.e., BCF ≥ 5000).

Regulation of catecholamine release from the adrenal medulla is altered in deer mice (Peromyscus maniculatus) native to high altitudes.

High-altitude natives have evolved to overcome environmental hypoxia and provide a compelling system to understand physiological function during reductions in oxygen availability. The sympathoadrenal system plays a key role in responses to acute hypoxia, but prolonged activation of this system in chronic hypoxia may be maladaptive. Here, we examined how chronic hypoxia exposure alters adrenal catecholamine secretion and how adrenal function is altered further in high-altitude natives. Populations of deer mice (Peromyscus maniculatus) native to low and high altitudes were each born and raised in captivity at sea level, and adults from each population were exposed to normoxia or hypobaric hypoxia for 5 mo. Using carbon fiber amperometry on adrenal slices, catecholamine secretion evoked by low doses of nicotine (10 µM) or acute hypoxia (Po2 ∼15-20 mmHg) was reduced in lowlanders exposed to hypobaric hypoxia, which was attributable mainly to a decrease in quantal charge rather than event frequency. However, secretion evoked by high doses of nicotine (50 µM) was unaffected. Hypobaric hypoxia also reduced plasma epinephrine and protein expression of 3,4-dihydroxyphenylalanine (DOPA) decarboxylase in the adrenal medulla of lowlanders. In contrast, highlanders were unresponsive to hypobaric hypoxia, exhibiting typically low adrenal catecholamine secretion, plasma epinephrine, and DOPA decarboxylase. Highlanders also had consistently lower catecholamine secretion evoked by high nicotine, smaller adrenal medullae with fewer chromaffin cells, and a larger adrenal cortex compared with lowlanders across both acclimation environments. Our results suggest that plastic responses to chronic hypoxia along with evolved changes in adrenal function attenuate catecholamine release in deer mice at high altitude.

Genetic features of myelodysplastic syndrome and aplastic anemia in pediatric and young adult patients.

The clinical and histopathological distinctions between inherited versus acquired bone marrow failure and myelodysplastic syndromes are challenging. The identification of inherited bone marrow failure/myelodysplastic syndromes is critical to inform appropriate clinical management. To investigate whether a subset of pediatric and young adults undergoing transplant for aplastic anemia or myelodysplastic syndrome have germline mutations in bone marrow failure/myelodysplastic syndrome genes, we performed a targeted genetic screen of samples obtained between 1990-2012 from children and young adults with aplastic anemia or myelodysplastic syndrome transplanted at the Fred Hutchinson Cancer Research Center. Mutations in inherited bone marrow failure/myelodysplastic syndrome genes were found in 5.1% (5/98) of aplastic anemia patients and 13.6% (15/110) of myelodysplastic syndrome patients. While the majority of mutations were constitutional, a RUNX1 mutation present in the peripheral blood at a 51% variant allele fraction was confirmed to be somatically acquired in one myelodysplastic syndrome patient. This highlights the importance of distinguishing germline versus somatic mutations by sequencing DNA from a second tissue or from parents. Pathological mutations were present in DKC1, MPL, and TP53 among the aplastic anemia cohort, and in FANCA, GATA2, MPL, RTEL1, RUNX1, SBDS, TERT, TINF2, and TP53 among the myelodysplastic syndrome cohort. Family history or physical examination failed to reliably predict the presence of germline mutations. This study shows that while any single specific bone marrow failure/myelodysplastic syndrome genetic disorder is rare, screening for these disorders in aggregate identifies a significant subset of patients with inherited bone marrow failure/myelodysplastic syndrome.

Burden of Cancer in a Large Consortium of Prospective Cohorts in Europe.

BACKGROUND: Disability-adjusted life-years (DALYs) are an indicator of mortality, morbidity, and disability. We calculated DALYs for cancer in middle-aged and older adults participating in the Consortium on Health and Ageing Network of Cohorts in Europe and the United States (CHANCES) consortium. METHODS: A total of 90 199 participants from five European cohorts with 10 455 incident cancers and 4399 deaths were included in this study. DALYs were calculated as the sum of the years of life lost because of premature mortality (YLLs) and the years lost because of disability (YLDs). Population-attributable fractions (PAFs) were also estimated for five cancer risk factors, ie, smoking, adiposity, physical inactivity, alcohol intake, and type II diabetes. RESULTS: After a median follow-up of 12 years, the total number of DALYs lost from cancer was 34 474 (382 per 1000 individuals) with a similar distribution by sex. Lung cancer was responsible for the largest number of lost DALYs (22.9%), followed by colorectal (15.3%), prostate (10.2%), and breast cancer (8.7%). Mortality (81.6% of DALYs) predominated over disability. Ever cigarette smoking was the risk factor responsible for the greatest total cancer burden (24.0%, 95% confidence interval [CI] = 22.2% to 26.0%), followed by physical inactivity (4.9%, 95% CI = 0.8% to 8.1%) and adiposity (1.8%, 95% CI = 0.2% to 2.8%). CONCLUSIONS: DALYs lost from cancer were substantial in this large European sample of middle-aged and older adults. Even if the burden of disease because of cancer is predominantly caused by mortality, some cancers have sizeable consequences for disability. Smoking remained the predominant risk factor for total cancer burden.

Quantification of the smoking-associated cancer risk with rate advancement periods: meta-analysis of individual participant data from cohorts of the CHANCES consortium.

BACKGROUND: Smoking is the most important individual risk factor for many cancer sites but its association with breast and prostate cancer is not entirely clear. Rate advancement periods (RAPs) may enhance communication of smoking related risk to the general population. Thus, we estimated RAPs for the association of smoking exposure (smoking status, time since smoking cessation, smoking intensity, and duration) with total and site-specific (lung, breast, colorectal, prostate, gastric, head and neck, and pancreatic) cancer incidence and mortality. METHODS: This is a meta-analysis of 19 population-based prospective cohort studies with individual participant data for 897,021 European and American adults. For each cohort we calculated hazard ratios (HRs) for the association of smoking exposure with cancer outcomes using Cox regression adjusted for a common set of the most important potential confounding variables. RAPs (in years) were calculated as the ratio of the logarithms of the HRs for a given smoking exposure variable and age. Meta-analyses were employed to summarize cohort-specific HRs and RAPs. RESULTS: Overall, 140,205 subjects had a first incident cancer, and 53,164 died from cancer, during an average follow-up of 12 years. Current smoking advanced the overall risk of developing and dying from cancer by eight and ten years, respectively, compared with never smokers. The greatest advancements in cancer risk and mortality were seen for lung cancer and the least for breast cancer. Smoking cessation was statistically significantly associated with delays in the risk of cancer development and mortality compared with continued smoking. CONCLUSIONS: This investigation shows that smoking, even among older adults, considerably advances, and cessation delays, the risk of developing and dying from cancer. These findings may be helpful in more effectively communicating the harmful effects of smoking and the beneficial effect of smoking cessation.

Severe combined immunodeficiency (SCID) presenting with neonatal aplastic anemia.

Aplastic anemia in the neonate is rare. We report a case of severe combined immunodeficiency (SCID) presenting with neonatal aplastic anemia. This report highlights the importance of considering SCID early in the evaluation of neonatal aplastic anemia prior to the development of infectious complications.

The characteristics of physical activity and gait in patients receiving radiotherapy in cancer induced bone pain.

BACKGROUND AND PURPOSE: An objective measure of pain relief may add important information to patients' self assessment, particularly after a treatment. The study aims were to determine whether measures of physical activity and/or gait can be used in characterizing cancer-induced bone pain (CIBP) and whether these biomarkers are sensitive to treatment response, in patients receiving radiotherapy (XRT) for CIBP. MATERIALS AND METHODS: Patients were assessed before (baseline) and 6-8weeks after XRT (follow up). The following assessments were done: Brief Pain Inventory (BPI), activPAL™ activity meter, and GAITRite® electronic walkway (measure of gait). Wilcoxon, Mann-Whitney and Pearson statistical analyses were done. RESULTS: Sixty patients were assessed at baseline; median worst pain was 7 and walking interference was 5. At follow up 42 patients were assessed. BPI worst pain, average pain, walking interference and total functional interference all improved (p<0.001). An improvement in functional interference correlated with aspects of physical activity (daily hours standing r=0.469, p=0.002) and gait (cadence r=0.341, p=0.03). The activPAL and GAITRite parameters did not change following XRT (p>0.05). In responder analyses there were no differences in activPAL and GAITRite parameters (p>0.05). CONCLUSION: Assessment of physical activity and gait allow a characterization of the functional aspects of CIBP, but not in the evaluation of XRT.

Physical activity monitoring: a responsive and meaningful patient-centered outcome for surgery, chemotherapy, or radiotherapy?

CONTEXT: In surgical and clinical oncology, there is a growing need for patient-centered outcomes that are responsive, meaningful, and fit for purpose. OBJECTIVES: The aim of this study was to validate physical activity (PA) monitoring as a responsive outcome measure at different stages of disease and treatment, by verifying correlations between PA, performance score, and quality of life (QoL). METHODS: Daily life PA of 162 cancer patients, monitored by a device that records time sitting/lying, time standing, time walking, number of steps taken, and walking cadence, was compared with 20 healthy volunteers. In a subgroup of patients, functional status and QoL were assessed using the World Health Organization/Eastern Cooperative Oncology Group and the Karnofsky Performance Status scores and the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30) questionnaire. RESULTS: The PA of patients with resectable gastrointestinal cancer did not differ significantly from controls. In contrast, patients with advanced cancer took 45% fewer steps and spent an extra 2.8 hours/day lying/sitting (P=0.001). Patients undergoing neoadjuvant chemotherapy and surgery (5-6 weeks after operation) experienced a similar reduction in PA. There were significant correlations between PA and the physical and role domains as well as fatigue subscale of the EORTC QLQ-C30 scale. CONCLUSION: Objective PA scores correlate significantly with disease stage, functional status, and QoL of patients with cancer. Therefore, activity monitoring can make meaningful objective estimates of patient function in response to cancer and its treatment and may provide surrogate outcomes of QoL.

Pain, depression, and fatigue as a symptom cluster in advanced cancer.

CONTEXT: Pain, depression, and fatigue are common symptoms in cancer populations. They often coexist and have been suggested as a specific symptom cluster. Systemic inflammation (SI) may be a possible common mechanism. OBJECTIVE: This study examined whether pain, depression, and fatigue exist as a symptom cluster in advanced cancer patients with cachexia and might be related to the presence of SI. METHODS: Secondary data analysis was undertaken of two clinical trials in patients with cancer cachexia (n = 654). Pain, depression, and fatigue were assessed using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30. Plasma C-reactive protein (CRP) was measured as a marker of SI in a subgroup (n = 436). Multivariate analysis and a series of regression analyses were undertaken relating pain, depression, fatigue, and CRP. RESULTS: Pain, depression, and fatigue clustered, with between two and four times as many patients having all three symptoms as would be expected if the symptoms only coexist by chance (P < 0.001). CRP was not related to the symptom cluster. There was a strong relationship between the pattern of symptoms and physical functioning (P < 0.001). CONCLUSION: Pain, depression, and fatigue is an identifiable symptom cluster in a cohort of cachexic cancer patients and is associated with reduced physical functioning.

Cancer pain and its relationship to systemic inflammation: an exploratory study.

Pain is the commonest symptom in cancer patients, whereas inflammation is implicated in cancer development and progression. The relationship between pain and inflammation in cancer is therefore of interest; however, it is challenging to examine because multiple factors may affect these variables. This study assessed the relationship between cancer pain and systemic inflammation using a retrospective analysis of 2 clinical trial datasets of patients with cancer cachexia. Included patients had gastrointestinal, lung, or pancreatic cancer. Pain was assessed using the pain subscale of the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire C-30. Inflammation was assessed using C-reactive protein (CRP). A regression analysis between pain and logarithmically transformed CRP was run, and Pearson correlation coefficients were calculated. A total of 718 patients entered the trials, of whom 449 had CRP measured. Both trial populations were well matched. Pain positively correlated with CRP. The Pearson correlation coefficients were 0.126 and 0.163 for trials 1 and 2, respectively. This correlation was statistically significant at the P<.05 level. These findings support that pain is related to systemic inflammation in a cohort of cancer patients. Many factors can affect pain and inflammation in cancer, demonstrating that any relationship that exists between pain and inflammation is of interest. This is in keeping with work showing this relationship in nonmalignant pain. Studies targeting inflammation and assessing its effect on pain in cancer would be an important step in the research agenda.

Ozonation of oil sands process-affected water accelerates microbial bioremediation.

Ozonation can degrade toxic naphthenic acids (NAs) in oil sands process-affected water (OSPW), but even after extensive treatment a residual NA fraction remains. Here we hypothesized that mild ozonation would selectively oxidize the most biopersistent NA fraction, thereby accelerating subsequent NA biodegradation and toxicity removal by indigenous microbes. OSPW was ozonated to achieve approximately 50% and 75% NA degradation, and the major ozonation byproducts included oxidized NAs (i.e., hydroxy- or keto-NAs). However, oxidized NAs are already present in untreated OSPW and were shown to be formed during the microbial biodegradation of NAs. Ozonation alone did not affect OSPW toxicity, based on Microtox; however, there was a significant acceleration of toxicity removal in ozonated OSPW following inoculation with native microbes. Furthermore, all residual NAs biodegraded significantly faster in ozonated OSPW. The opposite trend was found for ozonated commercial NAs, which are known to contain no significant biopersistent fraction. Thus, we suggest that ozonation preferentially degraded the most biopersistent OSPW NA fraction, and that ozonation is complementary to the biodegradation capacity of microbial populations in OSPW. The toxicity of ozonated OSPW to higher organisms needs to be assessed, but there is promise that this technique could be applied to accelerate the bioremediation of large volumes of OSPW in Northern Alberta, Canada.

Differential regulation of dendritic plasticity by neurotrophins following deafferentation of the adult spinal cord is independent of p75(NTR).

Spontaneous and/or treatment-evoked re-modeling of the CNS following spinal cord injury is a prerequisite for functional recovery. While there has been considerable interest in the role of endogenous neurotrophins in spontaneous plasticity of several populations of spinal axons, the same cannot be said for morphological changes to dendrites. Here, we examined the responses of dendrites in the mouse lateral spinal nucleus (LSN, a site of sensory integration in the dorsolateral white matter) to exogenous and endogenous neurotrophins. We performed a septuple dorsal rhizotomy, which permanently eliminates sensory input to the spinal cord, and stimulates sprouting of spinal axons. While dendrites showed no change in density following injury alone, they sprouted vigorously (a two-fold increase in density) upon addition of exogenous brain-derived neurotrophic factor (BDNF). On the other hand, endogenous nerve growth factor (NGF) severely restricted dendritic sprouting, as TrkA-Fc treatment also roughly doubled the density of dendritic processes in the LSN. Spontaneous, BDNF- and TrkA-Fc mediated sprouting was unaffected by the absence of p75(NTR). Importantly, TrkA-Fc treatment markedly reduced expression of the truncated BDNF receptor TrkBT1 in both p75(+/+) and p75(-/-) mice, which was robustly-upregulated by deafferentation in both genotypes. We propose that the upregulation of TrkBT1 by NGF results in a reduced availability of endogenous BDNF to dendrites. Accordingly, sprouting of serotonergic axons, a BDNF-dependent consequence of dorsal root injury, was significantly enhanced in TrkA-Fc-treated animals. These results suggest that NGF and BDNF signaling differentially regulates dendritic plasticity in the deafferented spinal cord.

Ozonation of oil sands process water removes naphthenic acids and toxicity.

Naphthenic acids are naturally-occurring, aliphatic or alicyclic carboxylic acids found in petroleum. Water used to extract bitumen from the Athabasca oil sands becomes toxic to various organisms due to the presence of naphthenic acids released from the bitumen. Natural biodegradation was expected to be the most cost-effective method for reducing the toxicity of the oil sands process water (OSPW). However, naphthenic acids are poorly biodegraded in the holding ponds located on properties leased by the oil sands companies. In the present study, chemical oxidation using ozone was investigated as an option for mitigation of this toxicity. Ozonation of sediment-free OSPW was conducted using proprietary technology manufactured by Seair Diffusion Systems Inc. Ozonation for 50min generated a non-toxic effluent (based on the Microtox bioassay) and decreased the naphthenic acids concentration by approximately 70%. After 130min of ozonation, the residual naphthenic acids concentration was 2mgl(-1): <5% of the initial concentration in the filtered OSPW. Total organic carbon did not change with 130min of ozonation, whereas chemical oxygen demand decreased by approximately 50% and 5-d biochemical oxygen demand increased from an initial value of 2mgl(-1) to a final value of 15mgl(-1). GC-MS analysis showed that ozonation resulted in an overall decrease in the proportion of high molecular weight naphthenic acids (n> or = 22).

Naphthenic acids in athabasca oil sands tailings waters are less biodegradable than commercial naphthenic acids.

Naphthenic acids (NAs) are natural constituents in many petroleum sources, including bitumen in the oil sands of Northern Alberta, Canada. Bitumen extraction processes produce tailings waters that cannot be discharged to the environment because NAs are acutely toxic to aquatic species. However, aerobic biodegradation reduces the toxic character of NAs. In this study, four commercial NAs and the NAs in two oil sands tailings waters were characterized by gas chromatography-mass spectrometry. These NAs were also incubated with microorganisms in the tailings waters under aerobic, laboratory conditions. The NAs in the commercial preparations had lower molecular masses than the NAs in the tailings waters. The commercial NAs were biodegraded within 14 days, but only about 25% of the NAs native to the tailings waters were removed after 40-49 days. These results show that low molecular mass NAs (C < or =17) are more readily biodegraded than high molecular mass NAs (C > or =18). Moreover, the results indicate that biodegradation studies using commercial NAs alone will not accurately reflect the potential biodegradability of NAs in the oil sands tailings waters.