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Furan has been found to form in foods during thermal processing. These findings, a classification of furan as a possibly carcinogenic to humans, and a limited amount of data on the concentration of furan in products on the Canadian market prompted the authors to conduct a survey of canned and jarred food products. Methyl analogues of furan, 2-methylfuran and 3-methylfuran, were analysed concurrently with furan via a newly developed isotope dilution method, as these analogues were detected in foods in the authors' earlier work and are likely to undergo a similar metabolic fate as furan itself. The paper reports data on 176 samples, including 17 samples of baby food. The vast majority of samples were packaged in cans or jars. Furan was detected above 1 ng g−1 in all non-baby food samples with a median of 28 ng g−1 and concentrations ranging from 1.1 to 1230 ng g−1. Also, 96% of these samples were found to contain 2-methylfuran above 1 ng g−1 with a median of 12.8 ng g−1 and a maximum concentration of 152 ng g−1, while 81% of samples were found to contain 3-methylfuran above 1 ng g−1 with a median of 6 ng g−1 and a maximum concentration of 151 ng g−1. Similarly, furan was detected above 1 ng g−1 in all baby food samples with a median of 66.2 ng g−1 and concentrations ranging from 8.5 to 331 ng g−1. Also, 100% of these samples were found to contain 2-methylfuran above 1 ng g−1 with a median of 8.7 ng g−1 and a maximum concentration of 50.2 ng g−1, while 65% of samples were found to contain 3-methylfuran above 1 ng g−1 with a median of 1.6 ng g−1 and a maximum concentration of 22.9 ng g−1. Additionally, three coffee samples were analysed 'as is', without brewing, and were found to have high levels of furans, especially 2-methylfuran, at a maximum of 8680 ng g−1. Using this data set, dietary exposures to furan and total furans were calculated. Average furan and total furan intakes by adults (≥20 years) were estimated at approximately 0.37 and 0.71 µg kg−1 of body weight day−1 respectively. [ABSTRACT FROM AUTHOR]

Acrylamide, a known rodent and a probable human carcinogen, is spontaneously formed in foods cooked at high temperature. We studied the role of dietary acrylamide in modulating the early stages of colon carcinogenesis and assessed if dietary fat level was critical in altering the effects of acrylamide. Male F344 rats were subcutaneously injected with azoxymethane and were simultaneously randomized into 8 dietary groups (n=8 rats/group). Diets were based on AIN-93G semi-synthetic formula modified to contain either low fat (7% corn oil) or high fat (23.9% corn oil) and acrylamide at 0, 5, 10 or 50 mg/kg diet (wt/wt). All rats received the experimental diets ad libitum for 8 weeks, after which they were killed and their colons assessed for aberrant crypt foci (ACF), putative precancerous lesions. Irrespective of dietary fat level, rats with the highest tested dose of acrylamide (50 mg/kg diet) had significantly lower total ACF (p<0.05) and lower large ACF (those with 4 or more crypts/focus; p<0.001) compared with their respective controls (0 mg/kg diet). A significantly lower number of large ACF (p=0.046) was noted in rats treated with 10 mg/kg diet acrylamide exclusively in the high fat group, compared to the high fat control. This short-term bio-assay to test carcinogenicity of dietary acrylamide in the colon demonstrates that acrylamide, when administered through the diet at doses known to cause rat tumors, does not increase the risk of developing azoxymethane-induced precancerous lesions of the colon in rats. On the contrary, a high dose of dietary acrylamide decreased the growth of precancerous lesions in both low and high fat diet regimens in this model., (Crown Copyright © 2011. Published by Elsevier Ltd. All rights reserved.)

Celiac disease is an immune-mediated disease, triggered in genetically susceptible individuals by ingested gluten from wheat, rye, barley, and other closely related cereal grains. The only treatment for celiac disease is a strict gluten-free diet for life. This paper presents a systematic review of the scientific literature on the safety of pure oats for individuals with celiac disease, which historically has been subject to debate. Limitations identified within the scientific database include: limited data on long-term consumption, limited numbers of participants in challenge studies, and limited reporting about the reasons for withdrawals from study protocols. Furthermore, some evidence suggests that a small number of individuals with celiac disease may be intolerant to pure oats and some evidence from in vitro studies suggests that an immunological response to oat avenins can occur in the absence of clinical manifestations of celiac disease as well as suggesting that oat cultivars vary in toxicity. Based on the majority of the evidence provided in the scientific database, and despite the limitations, Health Canada and the Canadian Celiac Association (CCA) concluded that the majority of people with celiac disease can tolerate moderate amounts of pure oats. The incorporation of oats into a gluten-free diet provides high fiber and vitamin B content, increased palatability, and beneficial effects on cardiovascular health. However, it is recommended that individuals with celiac disease should have both initial and long-term assessments by a health professional when introducing pure oats into a gluten-free diet.

This report represents the conclusions of a Joint FAO/WHO Expert Committee convened to evaluate the safety of various food additives, including flavouring agents, with a view to recommending acceptable daily intakes (ADIs) and to preparing specifications for identity and purity. The Committee also evaluated the risk posed by two food contaminants, with the aim of advising on risk management options for the purpose of public health protection. The first part of the report contains a general discussion of the principles governing the toxicological evaluation and assessment of intake of food additives (in particular flavouring agents) and contaminants. A summary follows of the Committee's evaluations of technical, toxicological and intake data for certain food additives (acidified sodium chlorite, asparaginase from Aspergillus oryzae expressed in Aspergillus oryzae, carrageenan and processed Eucheuma seaweed, cyclotetraglucose and cyclotetraglucose syrup, isoamylase from Pseudomonas amyloderamosa, magnesium sulfate, phospholipase A1 from Fusarium venenatum expressed in Aspergillus oryzae, sodium iron(III) ethylenediaminetetraacetic acid (EDTA) and steviol glycosides); eight groups of related flavouring agents (linear and branched-chain aliphatic, unsaturated, unconjugated alcohols, aldehydes, acids and related esters; aliphatic acyclic and alicyclic terpenoid tertiary alcohols and structurally related substances; simple aliphatic and aromatic sulfides and thiols; aliphatic acyclic dials, trials and related substances; aliphatic acetals; sulfur-containing heterocyclic compounds; aliphatic and aromatic amines and amides; and aliphatic alicyclic linear alpha, beta -unsaturated di- and trienals and related alcohols, acids and esters); and two food contaminants (aflatoxin and ochratoxin A). Specifications for the following food additives were revised: maltol and ethyl maltol, nisin preparation, pectins, polyvinyl alcohol, and sucrose esters of fatty acids. Specifications for the following flavouring agents were revised: maltol and ethyl maltol, maltyl isobutyrate, 3-acetyl-2,5-dimethylfuran and 2,4,5-trimethyl-delta-oxazoline (Nos 1482, 1506 and 1559), and monomenthyl glutarate (No. 1414), as well as the method of assay for the sodium salts of certain flavouring agents. Annexed to the report are tables summarizing the Committee's recommendations for intakes and toxicological evaluations of the food additives and contaminants considered.

Respiratory allergy and allergy to foods continue to be important health issues. There is evidence to indicate that the incidence of food allergy around the world is on the rise. Current estimates indicate that approximately 5% of young children and 1-2% of adults suffer from true food allergy (Kagan 2003). Although a large number of in vivo and in vitro tests exist for the clinical diagnosis of allergy in humans, we lack validated animal models of allergenicity. This deficiency creates serious problems for regulatory agencies and industries that must define the potential allergenicity of foods before marketing. The emergence of several biotechnologically derived foods and industrial proteins, as well as their potential to sensitize genetically predisposed populations to develop allergy, has prompted health officials and regulatory agencies around the world to seek approaches and methodologies to screen novel proteins for allergenicity.

The radiotracer method of Oldendorf was used to determine if 2450 MHz continuous wave (CW) microwave energy increases blood-brain barrier permeability to [14C]mannitol, which is normally excluded from entering the brain. Anesthetized, adult rats were irradiated singly for 30 min in the quiet zone of an anechoic chamber, at average power densities from 0.1 to 30 mW/sq.cm. Afterwards each rat received an intracarotid bolus injection of [14C]mannitol/[3H]water mixture and was decapitated 15 sec later. Uptake of [14C]mannitol relative to the highly permeable reference substance, [3H]water, was calculated as the brain uptake index (BUI) for 4 brain regions. Mean BUI values for tissues from the microwave-irradiated rats did not differ significantly from sham-irradiated animals, and a microwave influence on barrier permeability was not evident. Irrespective of treatment, BUI values for cerebellum and medulla were much higher and more variable than values for cortex or diencephalon, and were associated with reduced absorbance or retention of [3H]water. Because of a compromising influence of the vertebral arterial supply on the distribution of intracarotid-injected radiotracers, BUI measurements in caudal brain regions are probably unreliable unless accompanied by data on regional radioisotope concentrations. The absence of such data in an earlier BUI study, suggests that increases in BUI for cerebellum and medulla attributed to microwaves were possibly misinterpreted as differences in barrier permeability to [14C]saccharides, when in fact changes in blood flow and [3H]water influx or egress were responsible.