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International studies report marked increases in the prevalence of food allergy, along with increases in hospital admissions and emergency presentations for severe allergic reactions due to foods. The prevalence of self-reported food allergy is common, but generally exceeds that which can be verified from challenge studies, although nut allergies appear to be an important exception to this rule. Studies examining food allergy deaths suggest that those who die of food allergy usually have co-existent asthma. Adolescents and young adults are at most risk, and adrenaline auto-injectors are sub-optimally used. Food chemical sensitivity is very commonly reported but not usually verified by challenge testing. However, the exception to this is sulphite sensitivity, which can elicit reproducible reactions in some. The increasing prevalence of severe food allergies and awareness of its risk in those with asthma demands an especially rigorous approach to the diagnosis and management of co-existent food allergy and asthma, especially in young people who appear to be at most risk from death from severe food allergy. Cite this as: A. Gillman and Jo A. Douglass, Clinical & Experimental Allergy, 2010 (40) 1295–1302. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented concerning peanut allergies and how people suffering nut allergies can reduce their risks of an allergic reaction.

Background: While the relationship between pollen and respiratory allergies is well‐documented, the role of short‐term pollen exposure in food allergy and eczema flares has not previously been explored. We aimed to investigate these associations in a population‐based sample of children. Methods: We investigated 1‐ (n = 1108) and 6‐year‐old (n = 675) children in the grass pollen season from the HealthNuts cohort. Grass pollen concentrations were considered on the day of testing (lag 0), up to three days before (lag 1‐lag 3) and cumulatively (lag 0–3). Associations between grass pollen and food skin‐prick test reactivity (SPT ≥ 2 mm at age 1 year and ≥ 3 mm at age 6 years), eczema flares, challenge‐confirmed food allergy, reaction threshold to oral food challenges (OFC), and serum food‐specific IgE levels were analyzed using either logistic or quantile regression models. Atopy and family history of allergic disease were considered as potent effect modifiers. Results: Grass pollen at lag 0–3 (every 20 grains/m3 increase) was associated with an up to 1.2‐fold increased odds of food SPT reactivity and eczema flares in 6‐year‐olds. In 1‐year‐olds, the associations were only observed for peanut in those with a family history of food allergy. Increasing grass pollen concentrations were associated with a lower reaction threshold to OFC and higher serum IgE levels in peanut‐allergic 1‐year‐olds only. Conclusion: Increasing grass pollen concentration was associated with increased risk of food SPT reactivity and eczema flares in children. The associations in peanut‐allergic infants may be related to immune activation and/or peanut and grass pollen cross‐reactivity leading to a lower reaction threshold. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Recent Australian and international legislation requires labeling of wines made by using the potentially allergenic food proteins casein, milk, egg white, or isinglass (fish-derived) where “there is a detectable residual processing aid.” We investigated whether wines fined using these proteins or non–grape-derived tannins (tree-nut derived) can provoke significant clinical allergic reactions (anaphylaxis) in patients with confirmed immunoglobulin E–mediated relevant food allergy. Methods: A double-blind, placebo-controlled trial was performed to determine whether allergic reactions followed consumption of Australian commercial wines fined using one or more of the legislation-targeted food proteins. In addition, allergenicity of a larger panel of these wines was evaluated by blood basophil activation. Results: No anaphylaxis was induced by wine consumption. Three mild clinical reactions to protein-fined wine and two mild reactions to unfined wine occurred, but there was no statistically significant difference in reaction parameters between subject groups or between processing aids. No pattern of basophil activation correlated with wine type, processing aid, or subject group. Conclusion: Wines fined with egg white, isinglass, or non–grape-derived tannins present an extremely low risk of anaphylaxis to fish-, egg-, or peanut-allergic consumers. Although consumption of milk protein-fined wine did not induce anaphylaxis, there were insufficient subjects to determine statistically whether wines fined with milk proteins present a risk to the very rare milk-allergic consumers. In summary, the observed lack of anaphylaxis and basophil activation induced by wines made using the legislation-targeted food proteins according to good manufacturing practice suggests negligible residual food allergens in these wines. [Copyright &y& Elsevier]