Oral allergy syndrome (OAS): itchy mouth after apples or nuts with pollen allergy

Sensitisation happens first through the airways. A person with birch pollen allergy produces IgE antibodies against the main allergen of that pollen, the protein Bet v 1. This protein belongs to a family of plant defence proteins (PR-10), and similar molecules are found in many edible plants: apple (Mal d 1), hazelnut (Cor a 1), celery (Api g 1), carrot (Dau c 1), peach or kiwi. To the immune system the differences are small enough that antibodies directed against the pollen also recognise these molecules in food. Hence the name: the reaction starts in the nose and shows itself in the mouth.

Why do symptoms usually end in the oral cavity? PR-10 proteins are unstable. They break down under stomach acid and digestive enzymes before they reach the bloodstream in an amount that would cause a systemic reaction. The sensitised mucosa of the mouth and throat, however, meets them directly, in the first seconds, and a local release of histamine follows: itching, tingling, burning, sometimes slight swelling of the lips or tongue. Symptoms usually appear within a few minutes and subside within several tens of minutes, often after rinsing the mouth or swallowing the bite.

A second important thread is variability over time. In many people symptoms worsen during the birch pollen season (in Poland usually in spring) and fade outside it, because IgE levels and mucosal reactivity change with exposure to pollen. That is why an apple tolerated in November may be a problem in April. This does not mean the allergy 'went away' or 'came back': it is the threshold of reaction that changes.

The common advice is that a baked apple, boiled carrot or roasted nut may be safe. The mechanism is rational, because heat denatures unstable PR-10 proteins and profilin, and IgE antibodies recognise mainly their native three-dimensional structure. It is worth knowing, though, that this rule has limits, and that one of the more important studies on the subject added a significant caveat to it.

What does this mean in practice? First, for OAS itself, that is itching of the mouth, cooking is usually effective and the guidelines confirm it. Second, in a person with atopic dermatitis the reaction may take a different, delayed course: not in the mouth but on the skin, within hours or days. This is the result of a single study in a relatively small group, so it should not be exaggerated. It is, however, a reason for people with AD who notice a flare of eczema after a 'safe' cooked food to tell an allergist, rather than put it down to chance.

The list of foods that trigger symptoms depends on what the patient is allergic to, and that in turn depends on geography. In Central and Northern Europe the commonest pattern is allergy to birch (and the related alder and hazel) with reactions to apple, hazelnut, pear, cherry, peach, carrot, celery and kiwi. In Mediterranean regions other allergens play a role, among them lipid transfer proteins (LTP), discussed below. Data from the European EuroPrevall project, which included adults in several cities including Łódź, show that this variation is real.

The table is indicative: not every person allergic to birch will react to every food listed, and the list of reactions is often very individual. The practical conclusion for the patient is that it is their own history of reactions and test results that decide which foods cause problems, not a list from the internet. Many people needlessly give up foods 'just in case', which we discuss in the part on dietary rules.

The distinction between unstable allergens (PR-10, profilins) and stable ones (lipid transfer proteins, LTP, and seed storage proteins) is key to safety. The former usually cause mild OAS. The latter resist heat and digestion, so they pass into the blood unchanged and can cause urticaria, swelling, gastrointestinal symptoms and even anaphylaxis, including after processed foods.

The 2025 British statement on LTP allergy draws attention to something easy to overlook: in people sensitised to LTP, cofactors such as exercise or alcohol are often present, and reactions can be severe. Tree nuts, peanuts, apples, stone fruits, tomatoes and highly processed dishes were listed among the culprit foods. The authors note that a positive test for an individual LTP allergen confirms the diagnosis only when it agrees with a typical clinical history, and that in people with LTP allergy the need for an adrenaline autoinjector should always be considered.

In a typical patient with birch pollen allergy and an itchy mouth after raw fruit, the diagnosis rests mainly on the history. The allergist asks about the foods, the time from eating to symptoms, the effect of heat treatment, seasonality and any symptoms outside the mouth. In addition, skin prick tests are done or specific IgE is measured for pollen and the suspected foods. Remember, though, that a positive IgE result for a food indicates sensitisation, not clinical allergy: in people sensitised to pollen many such results are positive without symptoms.

The guidelines of the European Academy of Allergy and Clinical Immunology (EAACI) on the diagnosis of IgE-mediated food allergy stress that in pollen-sensitised people measuring IgE specific to allergen components can help, for example Cor a 14 for hazelnut, Ara h 2 for peanut or Ana o 3 for cashew. The gold standard of diagnosis remains the oral food challenge, performed in equivocal situations.

Component diagnostics play a special role with nuts. As the authors of the paper on OAS to tree nuts and peanuts note, exclusive sensitisation to PR-10 proteins and profilins indicates that symptoms are due to PFAS, whereas sensitisation to seed storage proteins, with or without sensitisation to PR-10, may indicate a more severe, primary nut allergy phenotype. This distinction decides whether the patient must avoid the nut in every form and carry adrenaline, or can eat roasted nuts or nuts in processed products. We write about nut allergy in adults separately, in the article on diagnosis and anaphylaxis.

An international expert consensus (Delphi method, 25 institutions from 11 countries) published in 2024 formulated 14 agreed statements. The experts agreed that patients with PFAS should receive counselling on the nature of the syndrome, on the rare chance of more severe systemic reactions and on how to recognise them. They recommended avoiding the raw food that caused the index reaction, but not all potentially cross-reactive fruits and vegetables on that basis. An adrenaline autoinjector was recommended for patients who had severe symptoms (beyond the oropharynx) or who are considered at risk.

The British guideline points out that excluding foods looks simple but becomes difficult when another food allergy coexists or when someone follows a plant-based diet. It is therefore worth agreeing a diet tailored to your own profile with a doctor, rather than copying lists from forums. Antihistamines are sometimes used as needed for mild symptoms confined to the mouth, but their use, dose and scope should be settled with a doctor, and not treated as a way of 'pushing through' foods that cause symptoms.

It seems logical that since the cause of OAS is allergy to pollen, desensitisation to birch pollen should reduce reactions to food. Clinical data are, however, inconclusive. A systematic review that included ten studies with a total of 475 patients assessed the effect of subcutaneous and sublingual birch pollen immunotherapy on birch-related food allergy.

The conclusion is therefore cautious: desensitisation to birch pollen is done because of hay fever and asthma, and any benefit for OAS is a pleasant extra, not the aim. The British guideline states plainly that pollen immunotherapy is not an effective treatment for PFS, and the Delphi consensus judged that the benefit of allergen immunotherapy remains unclear and that PFAS should not be the primary indication for such an intervention. Oral or sublingual immunotherapy with the foods themselves is under investigation but is not a routine method.

What this text does not settle: it does not replace diagnosis and does not let you decide on your own which foods are safe. The guidelines cited above rest largely on expert opinion and observational studies, not on large randomised trials, which means that detailed recommendations (for example on peeling fruit or the exact time of cooking) differ between centres. Data on the frequency of OAS in Poland are limited; we draw on European studies, including the centre in Łódź. Nor do we describe here the treatment of hay fever or the details of desensitisation, as they require separate qualification.

Oral allergy syndrome is a good example of a situation in which understanding the mechanism changes everyday decisions. Knowing that an unstable protein is to blame answers the question of why a baked apple is harmless while a raw one scratches the mouth. The same knowledge teaches caution: since the allergen family decides the risk, symptoms beyond the mouth, or linked to nuts, need separate assessment and not the general rule 'it is only pollen-related'.