Ochratoxin A in cocoa and chocolate sampled in Canada.

In order to determine the levels of ochratoxin A (OTA) in cocoa and cocoa products available in Canada, a previously published analytical method, with minor modifications to the extraction and immunoaffinity clean-up and inclusion of an evaporation step, was initially used (Method I). To improve the low method recoveries (46-61%), 40% methanol was then included in the aqueous sodium bicarbonate extraction solvent (pH 7.8) (Method II). Clean-up was on an Ochratest™ immunoaffinity column and OTA was determined by liquid chromatography (LC) with fluorescence detection. Recoveries of OTA from spiked cocoa powder (0.5 and 5 ng g(-1)) were 75-84%; while recoveries from chocolate were 93-94%. The optimized method was sensitive (limit of quantification (LOQ) = 0.07-0.08 ng g(-1)), accurate (recovery = 75-94%) and precise (coefficient of variation (CV) < 5%). It is applicable to cocoa and chocolate. Analysis of 32 samples of cocoa powder (16 alkalized and 16 natural) for OTA showed an incidence of 100%, with concentrations ranging from 0.25 to 7.8 ng g(-1); in six samples the OTA level exceeded 2 ng g(-1), the previously considered European Union limit for cocoa. The frequency of detection of OTA in 28 chocolate samples (21 dark or baking chocolate and seven milk chocolate) was also 100% with concentrations ranging from 0.05 to 1.4 ng g(-1); one sample had a level higher than the previously considered European Union limit for chocolate (1 ng g(-1)).

Surveys of rice sold in Canada for aflatoxins, ochratoxin A and fumonisins.

Approximately 200 samples of rice (including white, brown, red, black, basmati and jasmine, as well as wild rice) from several different countries, including the United States, Canada, Pakistan, India and Thailand, were analysed for aflatoxins, ochratoxin A (OTA) and fumonisins by separate liquid chromatographic methods in two different years. The mean concentrations for aflatoxin B(1) (AFB(1)) were 0.19 and 0.17 ng g(-1) with respective positive incidences of 56% and 43% (≥ the limit of detection (LOD) of 0.002 ng g(-1)). Twenty-three samples analysed in the second year also contained aflatoxin B(2) (AFB(2)) at levels ≥LOD of 0.002 ng g(-1). The five most contaminated samples in each year contained 1.44-7.14 ng AFB(1) g(-1) (year 1) and 1.45-3.48 ng AFB(1) g(-1) (year 2); they were mostly basmati rice from India and Pakistan and black and red rice from Thailand. The average concentrations of ochratoxin A (OTA) were 0.05 and 0.005 ng g(-1) in year 1 and year 2, respectively; incidences of samples containing ≥LOD of 0.05 ng g(-1) were 43% and 1%, respectively, in the 2 years. All positive OTA results were confirmed by LC-MS/MS. For fumonisins, concentrations of fumonisin B(1) (FB(1)) averaged 4.5 ng g(-1) in 15 positive samples (≥0.7 ng g(-1)) from year 1 (n = 99); fumonisin B(2) (FB(2)) and fumonisin B(3) (FB(3)) were also present (≥1 ng g(-1)). In the second year there was only one positive sample (14 ng g(-1) FB(1)) out of 100 analysed. All positive FB(1) results were confirmed by LC-MS/MS.

Subchronic oral toxicity study of furan in Fischer-344 rats.

Rodent studies have shown that furan is a hepatocarcinogen. Previous studies conducted with high doses showed tumors at nearly 100% incidence at all doses. In this paper, a ninety-day gavage experiment conducted with lower doses (0.0, 0.03, 0.12, 0.5, 2.0, and 8.0 mg/kg bw) to identify a no-observed adverse effect level for hepatotoxicity and to characterize non-neoplastic effects including gross changes and histopathology, clinical biochemistry, hematology, and immunotoxicology is reported. As indicated by changes in serum biomarkers, increased liver weights and gross and histological lesions, the liver is the major target organ affected by furan. There were no changes in body weights, food consumption, or histology in other organs. Some of the serum electrolyte markers, including phosphorus, were altered. There was a significant increase in serum thyroxine and triidothyronine in males. This increase was not accompanied by histological thyroid changes. Immunophenotypic analysis showed that thymic lymphocyte maturation was altered in male rats. Although altered clinical biochemistry and hematological parameters were observed at a dose of > 0.5 mg/kg bw, mild histological lesions in the liver were observed at > 0.12 mg/kg bw. Based on this finding, a furan dose of 0.03 mg/kg bw was proposed as the no-observed adverse effect level for hepatic toxicity.