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Dive into the research topics where Steve E. Hrudey is active.

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Featured researches published by Steve E. Hrudey.


Risk Analysis | 2001

Socioeconomic Determinants of Health- and Food Safety-Related Risk Perceptions

Donna Dosman; Wiktor L. Adamowicz; Steve E. Hrudey

Individual and societal perceptions of food-related health risks are multidimensional and complex. Social, political, psychological, and economic factors interact with technological factors and affect perceptions in complex ways. Previous research found that the significant determinants of risk perceptions include socioeconomic and behavioral variables. Most of these past results are based on two-way comparisons and factor analysis. The objective of this study was to analyze the significance of socioeconomic determinants of risk perceptions concerning health and food safety. A multivariate approach was used and the results were compared with earlier bivariate results to determine which socioeconomic predictors were robust across methods. There were two major findings in this study. The first was that the results in the multivariate models were generally consistent with earlier bivariate analysis. That is, variables such as household income, number of children, gender, age, and voting preferences were strong predictors of an individuals risk perceptions. The second result was that the gender of the respondent was the only variable found to be robust across all three classes of health and food safety issues across two time periods.


Water Research | 2009

Chlorination disinfection by-products, public health risk tradeoffs and me

Steve E. Hrudey

Since 1974 when trihalomethanes (THMs) were first reported as disinfection by-products (DBPs) in drinking water, there has been an enormous research effort directed at understanding how DBPs are formed in the chlorination or chloramination of drinking water, how these chlorination DBPs can be minimized and whether they pose a public health risk, mainly in the form of cancer or adverse reproductive outcomes. Driven by continuing analytical advances, the original DBPs, the THMs, have been expanded to include over 600 DBPs that have now been reported in drinking water. The historical risk assessment context which presumed cancer could be mainly attributed to exposure to environmental carcinogens played a major role in defining regulatory responses to chlorination DBPs which, in turn, strongly influenced the DBP research agenda. There are now more than 30 years of drinking water quality, treatment and health effects research, including more than 60 epidemiology studies on human populations, directed at the chlorination DBP issue. These provide considerable scope to reflect on what we know now, how our understanding has changed, what those changes mean for public health risk management overall and where we should look to better understand and manage this issue in the future.


Journal of Phycology | 1995

VARIABILITY OF THE HEPATOTOXIN MICROCYSTIN‐LR IN HYPEREUTROPHIC DRINKING WATER LAKES1

Brian G. Kotak; Angeline K-Y. Lam; Ellie E. Prepas; S. L. Kenefick; Steve E. Hrudey

The patterns of occurrence of the peptide hepatotoxin microcystin‐LR (MC‐LR) was studied in three hypereu‐trophic hardwater lakes (Coal, Driedmeat, and Little Beaver) in central Alberta, Canada, over three open‐water seasons. MC‐LR concentration was based on high‐performance liquid chromatography detection and expressed as μg.g−1 of total plankton biomass, ng.L−1 of lake water, and μg.g−1 of Microcystis aeruginosa Kuetz. emend. Elenkin. MC‐LR was highly variable temporally (differences up to 3 orders of magnitude) within each lake over an individual year, between years in an individual lake, and between lakes in any year. Seasonal (within‐year) changes in MC‐LR concentration (expressed in the preceding units) were positively correlated to the abundance and biomass Of the cyanobacterium M. aeruginosa (r =0.60–0.77), total and total dissolved phosphorus concentration (r =0.46–0.59), pH (r=0.38–0.58), and chlorophyll a (r=0.25–0.59). Surprisingly, there was no relationship between MC‐LR concentration and water temperature (range: 7°‐24°C, r =‐0.13 to 0.02) and a negative correlation with nitrate concentration (r =–0.27 to ‐0.34). In two synoptic surveys examining spatial variability, MC‐LR concentrations were quite variable (CV of 185 and 36% between sampling sites for Coal and Little Beaver lakes, respectively). Spatial distribution of MC‐LR on any one day was correlated with the abundance and biomass of M. aeruginosa. Over a 24‐h period, MC‐LR concentration in M. aeruginosa decreased more than 6‐fold at night relative to daytime concentrations. In general, analytical and within‐site variation of MC‐LR was relatively small (CV < 4 and 9%, respectively) but greatest both within and between years in a lake followed by diel and spatial variation.


Water Research | 1984

The effects of phenol and some alkyl phenolics on batch anaerobic methanogenesis

Phillip M. Fedorak; Steve E. Hrudey

Abstract Phenol and seven alkylphenols (o-, m- and p-cresol, 2.5-, 2.6-, 3.4- and 3,5-dimethylphenol) were added at various concentrations to aliquots of domestic anaerobic sludge in Hungate serum bottles and these were incubated at 37°C. The concentration of methane in the headspace gas was monitored to determine if the phenolics were fermented to methane or if they inhibited the anaerobic process. Only phenol and p-cresol were fermented to methane. At 500 mg l−1 (but not at 300 mg l−1) 2,5-, 3,4- and 3,5-dimethylphenol reduced the rate and the amount of methane produced. The cresols were inhibitory at 1000 mg l−1 but not at 400 mg l−1. In cultures supplemented with acetate and propionate (VOA), and in unsupplemented cultures, phenol at concentrations up to 500 mg l−1 was fermented to methane. Between 800 and 1200 mg l−1 phenol, methane production was neither enhanced nor inhibited relative to control cultures containing no phenol. Inhibition of methane production was evident when phenol was present at ⩾ 2000 mg l−1. Thus the methanogens are less susceptible to phenol inhibition than are the phenol-degrading acid formers. In similar experiments with p-cresol: enhanced methane production was observed at concentrations of ⩽ 400 mg l−1; no enhancement or inhibition was observed at 600 mg l−1; and inhibition was noted when p-cresol was present at ⩾ 1000 mg l−1.


Water Research | 1995

Chemical control of hepatotoxic phytoplankton blooms: Implications for human health

Angeline K.-Y. Lam; Ellie E. Prepas; David Spink; Steve E. Hrudey

Chemicals used to control phytoplankton blooms induce the release of phytotoxins that increase the potential health risks in drinking water supplies. To test this hypothesis, the effects of six chemical treatments on the release of the cyanobacterial toxin, microcystin-LR (MCLR; 182–837 μg g−1 dry wt) from freshly collected phytoplankton were examined in laboratory experiments. In addition, the integrity of a chemically-treated culture of Microcystis aeruginosa was examined by both a scanning electron microscope and a transmission electron microscope. Chemicals which control cyanobacterial blooms through inhibition of cell functions (e.g. Reglone A, potassium permanganate, chlorine, and Simazine) appeared to induce cell lysis and subsequently increased dissolved MCLR concentration in the surrounding water. In contrast, both lime and alum treatment (within pH 6–10) controlled the cyanobacterial blooms mainly by cell-coagulation and sedimentation, without any (lime) or only little (alum) increase in dissolved MCLR concentration in the water. The estimated half-life of released MCLR from these dense cyanobacterial blooms ranged from 0.5 (± 0.1) to 1.6 (± 0.0) d. In contrast, × ⩾39% of the MCLR remained in decaying phytoplankton for up to 26 d, therefore it is likely that MCLR would persist and decay inside the lime or alum coagulated Microcystis cells, before being released into the surrounding water phase. For these reasons, lime or to a lesser extent alum, appears to be more suitable than either algicides or chlorine for the control of microcystin-containing cyanobacterial blooms in drinking water.


Water Research | 1993

Occurrence and toxicological evaluation of cyanobacterial toxins in Alberta lakes and farm dugouts

Brian G. Kotak; S. L. Kenefick; David L. Fritz; Colin G. Rousseaux; Ellie E. Prepas; Steve E. Hrudey

Abstract The occurrence of neuro- and hepatotoxins produced by cyanobacteria (blue-green algae) was assessed in eight lakes and six farm dugouts, located in Alberta. Anatoxin-a, an alkaloid neurotoxin produced by Anabaena flos-aquae , was not detected in the lake blooms with gas chromatography-mass spectrometry (GC-MS). Algal blooms which contained Microcystis aeruginosa almost always had detectable concentrations of microcystin-LR, a peptide hepatotoxin, based on high performance liquid chromatography (HPLC) analyses. Bloom samples from the six farm dugouts contained no detectable quantity of either anatoxin-a or microcystin-LR. However, anatoxin-a and microcystin-LR were detected in algae isolated and subsequently cultured from two separate dugouts. Microcystin-RR was not detected in any bloom sample collected. Among three lakes studied in greater detail, the concentration of microcystin-LR present in the blooms was highly variable between lakes and temporally within each lake over the limited sampling period. Fast atom bombardment-mass spectrometry (FAB-MS) performed on a composite of several bloom samples from one lake confirmed the identity of microcystin-LR. Bioassays were performed with a subset of the bloom samples to determine acute toxicity to mice. Intraperitoneal injection of bloom extracts containing microcystin-LR resulted in a massive dose-dependent pooling of blood in the liver, shock and very rapid (as quickly as 50 min post-injection) death of injected mice.


Toxicon | 1996

Hepatic and renal pathology of intraperitoneally administered microcystin-LR in rainbow trout (Oncorhynchus mykiss).

Brian G. Kotak; Souleh Semalulu; David L. Fritz; Ellie E. Prepas; Steve E. Hrudey; Robert W. Coppock

In 26 hr laboratory trials a dose of 1000 micrograms/kg microcystin-LR (MC-LR) caused 100% mortality in rainbow trout, while no mortality was observed at doses of 400 micrograms/kg or less. The liver to body mass ratio increased in fish exposed to the toxin which was likely due to water retention in the liver. In contrast to mammalian studies, hemorrhage of the liver was rare in fish. Exposure to MC-LR caused widespread hepatocellular swelling and lysis of hepatocyte plasma membranes, resulting in liquifactive necrosis (organelles floating in a milieux of cellular debris). Kidney lesions in the fish consisted of coagulative tubular necrosis with a dilation of Bowmans space. Lesions observed in the liver and kidney of fish exposed to MC-LR were considerably different than those previously reported for mammals.


Environmental Technology | 1983

A simple apparatus for measuring gas production by methanogenic cultures in serum bottles

Phillip M. Fedorah; Steve E. Hrudey

Abstract The construction and use of an apparatus for measuring gas production in methanogenic cultures is described. The device consists of two glass syringes and two 3‐way stopcocks assembled and connected to a water manometer. Measurements of known amounts of methane added to serum bottles gave recoveries between 96 and 101%.


Water Research | 1996

Adsorption of microcystin-LR by activated carbon and removal in full scale water treatment

Timothy W. Lambert; Charles F.B. Holmes; Steve E. Hrudey

Abstract Removal of microcystin toxins from drinking water was evaluated at two full scale treatment plants that employed coagulation-sedimentation, dual media filtration and chlorination combined with either granular activated carbon filtration or powdered activated carbon. The influence of natural organic matter on the adsorption of the cyanobacterial toxin, microcystin-LR, by activatedcarbon was also evaluated in laboratory studies over a range of toxin concentrations similar to those typically observed in raw water at these plants. The sensitive protein phosphatase inhibition bioassay was used to quantify microcystin. Conventional treatment processes combined with activated carbon generally removed more than 80% of microcystin from raw water, but a residual concentration of 0.1-0.5 μg equivalents of microcystin-LR per liter was observed considering both (GAC and PAC) treatment facilities. Most values of residual microcystin-LR were at the low end of this range, but the upper end approaches the guidance level being considered by Health Canada for these toxins in drinking water


Water Research | 1995

Physiological toxicity, cell membrane damage and the release of dissolved organic carbon and geosmin by Aphanizomenon flos-aquae after exposure to water treatment chemicals

Hans G. Peterson; Steve E. Hrudey; Ilene A. Cantin; Terrina R. Perley; S. L. Kenefick

Reducing the level of dissolved organic carbon is an increasingly important goal in the treatment of drinking water. Dissolved organic carbon (DOC) compounds react with chemical disinfectants to form undesirable by-products, and DOC provides a substrate for bacterial growth. Chemicals used in water treatment processes and surface water reservoir management can cause the release of dissolved organics from photosynthetic aquatic organisms, and specific organic compounds can impart taste, odour and sometimes toxicity to treated water. Thus, chemical treatment of water may exacerbate the problem of dissolved organic carbon loading. The effects of several chemicals used at different stages of the water treatment process were studied on a nitrogen-fixing strain of the cyanobacterium Aphanizomenon flos-aquae. Chemicals included chlorine, potassium permanganate, aluminum sulphate, ferric chloride, calcium hydroxide, hydrogen peroxide and copper sulphate. Physiological effects on Aphanizomenon, as quantified by its ability to fix nitrogen, were compared with cell membrane damage (manifested as potassium release) and the release of organic cellular components, including DOC and the specific odour compound, geosmin. Aluminum sulphate and ferric chloride did not cause either physiological toxicity, cell membrane damage or the release of DOC at treatment usage concentrations. Calcium hydroxide at low levels and hydrogen peroxide caused physiological toxicity, but only limited membrane damage, DOC and geosmin release. Chlorine, copper sulphate and potassium permanganate caused physiological damage with concomitant release of both DOC and geosmin at concentrations lower than those currently used in water treatment. Consequently, these last three chemicals create potential water treatment problems by releasing DOC and specific problem compounds.

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Samantha Rizak

Cooperative Research Centre

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