Steve L. Taylor

Identification of a Brazil-nut allergen in transgenic soybeans

BACKGROUND The nutritional quality of soybeans (Glycine max) is compromised by a relative deficiency of methionine in the protein fraction of the seeds. To improve the nutritional quality, methionine-rich 2S albumin from the Brazil nut (Betholletia excelsa) has been introduced into transgenic soybeans. Since the Brazil nut is a known allergenic food, we assessed the allergenicity of the 2S albumin. METHODS The ability of proteins in transgenic and non-transgenic soybeans, Brazil nuts, and purified 2S albumin to bind to IgE in serum from subjects allergic to Brazil nuts was determined by radioallergosorbent tests (4 subjects) and sodium dodecyl sulfate-polyacrylamide-gel electrophoresis (9 subjects) with immunoblotting and autoradiography. Three subjects also underwent skin-prick testing with extracts of soybean, transgenic soybean, and Brazil nut. RESULTS On radioallergosorbent testing of pooled serum from four subjects allergic to Brazil nuts, protein extracts of transgenic soybean inhibited binding of IgE to Brazil-nut proteins. On immunoblotting, serum IgE from eight of nine subjects bound to purified 2S albumin from the Brazil nut and the transgenic soybean. On skin-prick testing, three subjects had positive reactions to extracts of Brazil nut and transgenic soybean and negative reactions to soybean extract. CONCLUSIONS The 2S albumin is probably a major Brazil-nut allergen, and the transgenic soybeans analyzed in this study contain this protein. Our study show that an allergen from a food known to be allergenic can be transferred into another food by genetic engineering.

Histamine food poisoning: Toxicology and clinical aspects

Histamine poisoning can result from the ingestion of food containing unusually high levels of histamine. Fish are most commonly involved in incidents of histamine poisoning, although cheese has also been implicated on occasion. The historic involvement of tuna and mackerel in histamine poisoning led to the longtime usage of the term, scombroid fish poisoning, to describe this food-borne illness. Histamine poisoning is characterized by a short incubation period, a short duration, and symptoms resembling those associated with allergic reactions. The evidence supporting the role of histamine as the causative agent is compelling. The efficacy of antihistamine therapy, the allergic-like symptomology, and the finding of high levels of histamine in the implicated food suggest strongly that histamine is the causative agent. However, histamine ingested with spoiled fish appears to be much more toxic than histamine ingested in an aqueous solution. The presence of potentiators of histamine toxicity in the spoiled fish may account for this difference in toxicity. Several potentiators including other putrefactive amines such as putrescine and cadaverine have been identified. Pharmacologic potentiators may also exist; aminoguanidine and isoniazid are examples. The mechanism of action of these potentiators appears to be the inhibition of intestinal histamine-metabolizing enzymes. This enzyme inhibition causes a decrease in histamine detoxification in the intestinal mucosa and results in increased intestinal uptake and urinary excretion of unmetabolized histamine.

Biogenic amines in cheese and other fermented foods: a review

The biogenic amine content of various foods has been widely studied because of their potential toxicity. Biogenic amines, such as tyramine and β-phenylethylamine, have been proposed as the initiators of hypertensive crisis in certain patients and of dietary-induced migraine. Another amine, histamine, has been implicated as the causative agent in several outbreaks of food poisoning. Histamine poisoning is a foodborne chemical intoxication resulting from the ingestion of foods containing excessive amounts of histamine. Although commonly associated with the consumption of scombroid-type fish, other foods such as cheese have also been associated with outbreaks of histamine poisoning. Fermented foods such as wine, dry sausage, sauerkraut, miso, and soy sauce can also contain histamine along with other biogenic amines. Microorganisms possessing the enzyme histidine decarboxylase, which converts histidine to histamine, are responsible for the formation of histamine in foods. One organism, Lactobacillus buchneri , may be important to the dairy industry due to its involvement in cheese-related outbreaks of histamine-poisoning. The toxicity of histamine appears to be enhanced by the presence of other biogenic amines found in foods that can inhibit histamine-metabolizing enzymes in the small intestine. Estimating the frequency of histamine poisoning is difficult because most countries do not regulate histamine levels in foods, nor do they require notification when an incident of histamine poisoning occurs. Also, because histamine poisoning closely resembles a food allergy, it may often be misdiagnosed. This review will focus on the importance of histamine and biogenic amines in cheese and other fermented foods.

Assessment of the allergenic potential of foods derived from genetically engineered crop plants

This article provides a science-based, decision tree approach to assess the allergenic concerns associated with the introduction of gene products into new plant varieties. The assessment focuses on the source from which the transferred gene was derived. Sources fall into three general categories: common allergenic food proteins; less common allergenic foods or other known allergen sources; and sources with no history of allergenicity. Information concerning the amino acid sequence identity to known allergenic proteins, in vitro and/or in vivo immunologic assays, and assessment of key physiochemical properties are included in reaching a recommendation on whether food derived from the genetically modified plant variety should be labeled as to the source of the transferred gene. In the end, a balanced judgement of all the available data generated during allergenicity assessment will assure the safety of foods derived from genetically engineered crops. Using the approaches described here, new plant varieties generated by genetic modification should be introduced into the marketplace with the same confidence that new plant varieties developed by traditional breeding have been introduced for decades.

Sulfites in Foods: Uses, Analytical Methods, Residues, Fate, Exposure Assessment, Metabolism, Toxicity, and Hypersensitivity

Publisher Summary Sulfiting agents have a long history of use as food ingredients. Sulfur dioxide and several forms of inorganic sulfites, which liberate sulfur dioxide under the conditions of use, are food additives, collectively known as sulfiting agents. In addition to their use as food additives, the sulfites can also occur naturally in foods. Foods contain a variety of sulfur-containing compounds, including the sulfur amino acids, sulfates, sulfites, and sulfides. The key to the understanding of sulfite toxicity may lie in elucidation of sulfite metabolism. Several researchers have proposed that defects in sulfite metabolism among certain segments of the human population may put them at greater risk to the possible toxic effects of sulfite ingestion. If the current generally recognized as safe (GRAS) review leads to some limitation on the continued use of sulfites, it will be necessary to consider alternatives. Enzymatic browning will be inhibited by any process that destroys or inactivates the enzyme. Blanching would obviously work but is impractical for using on fresh fruits and vegetables. Despite their long history of use as food additives, much remains to be learned about sulfites, which would be helpful to the present concerns about their safety.

An evaluation of the sensitivity of subjects with peanut allergy to very low doses of peanut protein: A randomized, double-blind, placebo-controlled food challenge study☆☆☆★

BACKGROUND The minimum dose of food protein to which subjects with food allergy have reacted in double-blind, placebo-controlled food challenges is between 50 and 100 mg. However, subjects with peanut allergy often report severe reactions after minimal contact with peanuts, even through intact skin. OBJECTIVE We sought to determine whether adults previously proven by challenge to be allergic to peanut react to very low doses of peanut protein. METHODS We used a randomized, double-blind, placebo-controlled food challenge of 14 subjects allergic to peanuts with doses of peanut ranging from 10 microg to 50 mg, administered in the form of a commercially available peanut flour. RESULTS One subject had a systemic reaction to 5 mg of peanut protein, and two subjects had mild objective reactions to 2 mg and 50 mg of peanut protein, respectively. Five subjects had mild subjective reactions (1 to 5 mg and 4 to 50 mg). All subjects with convincing objective reactions had short-lived subjective reactions to preceding doses, as low as 100 microg in two cases. Five subjects did not react to any dose up to 50 mg. CONCLUSION Even in a group of well-characterized, highly sensitive subjects with peanut allergy, the threshold dose of peanut protein varies. As little as 100 microg of peanut protein provokes symptoms in some subjects with peanut allergy.

Evaluation of the health aspects of methyl paraben: a review of the published literature

Methyl paraben (CAS No. 99-76-3) is a methyl ester of p-hydroxybenzoic acid. It is a stable, non-volatile compound used as an antimicrobial preservative in foods, drugs and cosmetics for over 50 years. Methyl paraben is readily and completely absorbed through the skin and from the gastrointestinal tract. It is hydrolyzed to p-hydroxybenzoic acid, conjugated, and the conjugates are rapidly excreted in the urine. There is no evidence of accumulation. Acute toxicity studies in animals indicate that methyl paraben is practically non-toxic by both oral and parenteral routes. In a population with normal skin, methyl paraben is practically non-irritating and non-sensitizing. In chronic administration studies, no-observed-effect levels (NOEL) as high as 1050 mg/kg have been reported and a no-observed-adverse-effect level (NOAEL) in the rat of 5700 mg/kg is posited. Methyl paraben is not carcinogenic or mutagenic. It is not teratogenic or embryotoxic and is negative in the uterotrophic assay. The mechanism of cytotoxic action of parabens may be linked to mitochondrial failure dependent on induction of membrane permeability transition accompanied by the mitochondrial depolarization and depletion of cellular ATP through uncoupling of oxidative phosphorylation. Parabens are reported to cause contact dermatitis reactions in some individuals on cutaneous exposure. Parabens have been implicated in numerous cases of contact sensitivity associated with cutaneous exposure; however, the mechanism of this sensitivity is unknown. Sensitization has occurred when medications containing parabens have been applied to damaged or broken skin. Allergic reactions to ingested parabens have been reported, although rigorous evidence of the allergenicity of ingested paraben is lacking.

Safety assessment of propyl paraben: a review of the published literature

Propyl paraben (CAS no. 94-13-3) is a stable, non-volatile compound used as an antimicrobial preservative in foods, drugs and cosmetics for over 50 years. It is an ester of p-hydroxybenzoate. Propyl paraben is readily absorbed via the gastrointestinal tract and dermis. It is hydrolyzed to p-hydroxybenzoic acid, conjugated and the conjugates are rapidly excreted in the urine. There is no evidence of accumulation. Acute toxicity studies in animals indicate that propyl paraben is relatively non-toxic by both oral and parenteral routes, although it is mildly irritating to the skin. Following chronic administration, no-observed-effect levels (NOEL) as high as 1200-4000 mg/kg have been reported and a no-observed-adverse-effect level (NOAEL) in the rat of 5500 mg/kg is posited. Propyl paraben is not carcinogenic, mutagenic or clastogenic. It is not cytogenic in vitro in the absence of carboxyesterase inhibitors. The mechanism of propyl paraben may be linked to mitochondrial failure dependent on induction of membrane permeability transition accompanied by the mitochondrial depolarization and depletion of cellular ATP through uncoupling of oxidative phosphorylation. Sensitization has occurred when medications containing parabens have been applied to damaged or broken skin. Parabens have been implicated in numerous cases of contact sensitivity associated with cutaneous exposure, but high concentrations of 5-15% in patch testing are needed to elicit reaction in susceptible individuals. Allergic reactions to ingested parabens have been reported, although rigorous evidence of the allergenicity of ingested paraben is lacking.

A consensus protocol for the determination of the threshold doses for allergenic foods: how much is too much?

Background While the ingestion of small amounts of an offending food can elicit adverse reactions in individuals with IgE‐mediated food allergies, little information is known regarding these threshold doses for specific allergenic foods. While low‐dose challenge trials have been conducted on an appreciable number of allergic individuals, a variety of different clinical protocols were used making the estimation of the threshold dose very difficult.

Allergenicity assessment of genetically modified crops—what makes sense?

GM crops have great potential to improve food quality, increase harvest yields and decrease dependency on certain chemical pesticides. Before entering the market their safety needs to be scrutinized. This includes a detailed analysis of allergenic risks, as the safety of allergic consumers has high priority. However, not all tests currently being applied to assessing allergenicity have a sound scientific basis. Recent events with transgenic crops reveal the fallacy of applying such tests to GM crops.