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Biomedical subjects

R Greenhalgh

Publications and source records attributed to R Greenhalgh.

At least 37 records · Page 2Linked to original sources

Effects of feeding white Leghorn hens diets that contain deoxynivalenol (vomitoxin)-contaminated wheat.

A short-term (10 weeks, Experiment 1) and a long-term experiment (24 weeks, Experiment 2) were done to determine effects of incorporating either white winter wheat, naturally contaminated with 1 mg deoxynivalenol (DON)/kg, or spring wheats, containing up to 6.5 mg DON/kg, into the diets of White Leghorn hens. Based on chemical analysis, the diets in Experiment 1 contained less than .05 to .7 mg DON/kg, while those in Experiment 2 contained from .2 to 4.9 mg/kg. Incorporation of winter or spring wheat in the experimental diets had no effect (P greater than .05) on feed intake and efficiency, egg production and yield, the number of soft shell and cracked eggs observed in the laying house, body weight at the completion of the experimental period, fertility, hatchability of fertile eggs, and the proportion of malformed embryos and pips. In addition, presence of DON-contaminated wheat did not influence (P greater than .05) the organ weight to body weight ratio for a randomly selected sample of hens necropsied at the completion of each experiment. There was little evidence of lesions in the oral cavity, esophagus, proventriculus and gizzard, hemorrhaging in the viscera or skeletal muscles, or of changes in the appearance of spleen, heart, and kidney. However, the livers from DON hens were fatty in appearance. Furthermore, vomiting (emesis), diarrhea, or changes in behaviour were not apparent and mortality, normally very low, was not increased during either experiment. Inverse linear relationships were obtained in Experiment 1 between dietary DON concentrations and egg weight (P less than .05), shell weight and thickness (P less than .01), and percent shell (P less than .05). Although egg and shell variables measured in Experiment 2 were not significantly influenced (P greater than .05) by DON treatment, trends towards lower values with higher dietary DON levels were evident. Egg specific gravity, nondestructive deformation, and quasistatic compression fracture strength of the egg's shell were not influenced (P greater than .05) by dietary DON levels. The results from these experiments indicate that laying hens can tolerate diets containing up to 5 mg DON/kg from white winter or spring wheat for extended periods of time without serious adverse effects on health and productivity.

Animal Feed↗

Subacute toxicity of dietary 3-acetyldeoxynivalenol in mice.

3-Acetyldeoxynivalenol was incorporated into a semisynthetic diet at levels of 2.5, 5, 10 or 20 ppm and fed to mice for up to 48 days. Body weights and feed consumption were determined, and blood samples for hematological evaluation were taken. Selected tissues were examined microscopically and the humoral immune response was assessed using the Jerne plaque assay. 3-Acetyldeoxynivalenol caused a dose-related depressed feed consumption within the first seven days and reduced body weight until day 14 when fed at levels up to 10 ppm. When fed at a level of 20 ppm, an initial depression in body weight gain and a general malaise were followed by a return to normal. At necropsy, no macroscopic or microscopic lesions could be found. The immune response was not significantly affected after seven or 14 days, but at 21 days, a dose-dependent enhanced response was observed. The findings indicate that, after an initial period of reduced feed intake, animals are apparently able to overcome the toxic effects of 3-acetyldeoxynivalenol.

Animal Feed↗

Pathology of acute 3-acetyldeoxynivalenol toxicity in mice.

Mice were killed 2, 4, 6, 12, 24, 48 and 96 hours after intragastrical administration of 0, 5, 10, 20, or 40 mg/kg body weight of 3-acetyldeoxynivalenol. The animals became clinically ill after 12 hours and some animals in the highest dose group died. Histological examination of duodenal crypts, thymus and spleen revealed, in all dose groups, presence of the characteristic lesions that are known to be produced by trichothecenes, but the intensity of lesions in the 40 mg group corresponded to lesions known to be caused by 4 mg/kg of T-2 toxin. A rabbit skin bioassay with 3-acetyldeoxynivalenol gave negative results on one occasion and a mild reaction to 100 to 500 micrograms/mL on another. It is concluded that 3-acetyldeoxynivalenol is considerably less toxic than T-2 toxin, but causes acute effects in the dividing cells of the body in a manner characteristic of trichothecenes.

Animals↗

Interaction between co-solvents and algae in the residue dynamics of fenitrothion.

Fresh and estuarine water algae maintained in laboratory microcosms simulating river-lake/estuary-bay systems were exposed to 14C-fenitrothion formulated with Atlox and tank mixed with Aerotex or Dowanol (11.5:1.5:1.5 w/v/v). Generally, the tank mix co-solvents determined the amount of uptake and the array of derivatives formed by the algae. Typically, exposed to an Aerotex mix the ratio of ethyl acetate extractable (NP) fraction: ethyl acetate unextractable (P) fraction was as 3.5:1.0, exposed to a Dowanol mix the ratio was as 1.5:1.0. Within any comparable time period, fresh water algae turned over more of the 14C-ring of fenitrothion than the estuarine genera. Turn-over was enhanced when Aerotex was the tank mix co-solvent.

Biodegradation, Environmental↗

Deoxynivalenol, acetyl deoxynivalenol, and zearalenone formation by Canadian isolates of Fusarium graminearum on solid substrates.

Three isolates of Fusarium graminearum (DAOM 180377, 180378, and 180379) were screened for their ability to produce mycotoxins on the solid substrates corn and rice. They all produced deoxynivalenol and zearalenone on corn. On rice, only DAOM 180378 and 180379 produced significant amounts of these mycotoxins, with levels of deoxynivalenol being much higher than those of zearalenone. The effects of the initial moisture content before autoclaving, incubation temperature, and time were studied with isolate DAOM 180378. At 19.5 degrees C the main product was zearalenone, whereas at 25 degrees C both deoxynivalenol and zearalenone were formed. Higher incubation temperatures (28 degrees C) favored deoxynivalenol formation, the maximum amount being 515 ppm (515 micrograms/g) formed after 24 days at an initial moisture content of 40%. The maximum level of zearalenone produced at the same temperature was 399 ppm, but at an initial moisture content of 35%. Other factors, such as pH, oxygen and carbon dioxide concentrations, and size of the culture flask also appeared to affect the production of mycotoxins.

Food Contamination↗

Persistence of fensulfothion in a sandy-loam soil and uptake by rutabagas, carrots and radishes using microplots.

Field microplots were treated with 141 and 282 ppm fensulfothion and 37.1 and 74.2 ppm fensulfothion sulfone. These concentrations are equivalent to field treatment rates of 8.48 and 16.96 kg AI/ha, fensulfothion, and 2.23 and 4.47 kg AI/ha, fensulfothion sulfone, respectively, for banded application (10 cm wide, rows 80 cm apart). The half-lives in a sandy loam soil were 30-39 and 14-23 days, respectively. Fensulfothion sulfone and sulfide were the main derivatives found in fensulfothion treated soil. The maximum levels of these derivatives were 21.22 and 22.95 ppm, respectively for the 8.48 kg/ha treatment and 33.90 and 42.45 ppm, respectively, for the higher treatment, which occurred between 30-60 days. Carrots appeared to take up more fensulfothion from soil than rutabagas or radishes. The residue levels at harvest decreased in the order carrot peel greater than pulp greater than rutabagas root greater than peel greater than pulp. Residue levels of fensulfothion and sulfone in radishes were similar to those found in rutabagas. The ratio sulfoxide/sulfone in rutabagas ranged from 0.4-1.5 and in carrots from 1.7-7.6. This phenomenon is thought to be due to oxidative enzyme systems present in rutabagas. Dimethyl phosphorothioic acid, but not dimethyl phosphoric acid was detected (max. 1.33 ppm) in some rutabagas samples but not in carrots.

Brassica↗

Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion.

Exposure to and absorption of Guthion 50 W.P. (azinphos-methyl) were estimated in orchardists from the Okanagan Valley in British Columbia who were involved in mixing, loading, and application with ultra-low volume air blast equipment. Air monitoring and patch techniques were used to estimate exposure, and alkyl phosphate excretion and cholinesterase inhibition were measured to estimate absorption. All workers were issued with standardized cotton shirts, trousers, and long-sleeved coveralls. All wore half-face respirators, gloves, boots, and hats. Eight wore rubberized protective clothing in addition. The indirect method of measuring urinary metabolites appeared to be the most sensitive. All workers had quantifiable levels of alkyl phosphates following exposure, and 24-h urine samples provided a more reliable estimate than first morning voids. A high correlation was observed between 48-h alkyl phosphate excretion and amount of active ingredient sprayed. A fluorescent tracer was added to the tank along with the Guthion. The finding of Guthion on patches beneath the clothing was confirmed by the presence of the tracer on the skin. With the ultralow-volume application used in this study, the rubberized clothing did not appear to be significantly more protective than the heavy coverall. There was no significant depression of either red blood cell or serum cholinesterase activity in any workers.

Air Pollutants, Occupational↗

A rapid GC method of monitoring Mesurol (4-(methylthio)-3,5-xylyl-N-methyl carbamate) and its sulfoxide and sulfone metabolites and their persistence in lowbush blueberries.

A facile analytical procedure was developed for determining Mesurol (4-(methylthio)-3,5-xylyl-N-methyl carbamate) and its oxidation products in blueberries. It involved blending with acetone, partition with chloroform and derivatization with trifluoroacetic anhydride and quantitation by gas chromatography/flame photometric detector (GC/FPD). The method showed good recoveries for Mesurol and its sulfoxide at the 0.1 ppm level and Mesurol sulfone at the 0.3 ppm level with a 25 g sample. It was applied to monitor levels of the insecticide and its oxidation products on field-treated blueberries. The sensitivity of the method may be increased 5-fold by the inclusion of a clean-up step. The optimal conditions for the detection of Mesurol TFA by the modified Bendix sulphur/phosphorus emission detector operating in the sulphur mode required an oxygen/hydrogen ratio of 0.38, for a column flow of 60 ml/min. The minimum detectable amounts of the TFA derivatives of Mesurol, its sulfoxide and sulfone were calculated as 1.3, 2.3 and 5.8 X 10(-11) g/sec, respectively.

Chromatography, Gas↗

Gas-liquid chromatographic analysis of ethephon and fenoprop residues in apples and their decline before and after harvest.

Ethephon (2-chloroethylphosphonic acid) and fenoprop (2-(2,4,5-trichlorophenoxy) propionic acid) may be determined in the same apple sample. After extraction with methanol, 2 separate methylation procedures were required to quantitatively convert each compound. Ethephon was esterified with diazomethane and analyzed by a flame photometric detector in the P-mode. Fenoprop was esterified with boron trifluoride/methanol and analyzed by electron capture gas chromatography. Average recoveries were about 95% at 0.05 ppm for both compounds. The limit of detection was 0.05 ppm for ethephon and 0.01 ppm for fenoprop in a 1 g sample. The persistence of both compounds before and after harvest was studied. Ethephon and fenoprop were applied simultaneously to apple trees at the recommended concentrations of 300 and 20 ppm, respectively. Ethephon residues averaged 1.6, 0.75, and 0.4 ppm at 2 hr, 10 days, and after washing at 13 days, respectively. The corresponding fenoprop residues were 0.70, 0.025, and 0.024 ppm.

2,4,5-Trichlorophenoxyacetic Acid↗