Pollen Food Syndrome; Mostly Harmless, But Not Always

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Pollen food syndrome (PFS) is not the same thing as oral allergy syndrome (OAS). The latter is an innocuous set of symptoms and the former is a potentially dangerous allergy to plant food. Although most people with pollen food syndrome won’t suffer that badly, a small percentage will suffer from systemic symptoms and those who are allergic to certain foods or enjoy a smoothie are at risk of suffering more serious reactions, including anaphylactic attacks. Understanding the finer points of PFS will enable the almost 1 in 10 people who suffer from more than an itching mouth to take control of their allergy.

And now for the details, which include:

Oral allergy syndrome and pollen food syndrome are not the same thing

The terms oral allergy syndrome and pollen food syndrome are often used—even by most doctors—interchangeably, as if they’re describing the same thing, but they’re not.

The confusion arose in 1987 when a team of researchers coined the term ‘oral allergy syndrome’ to describe someone eating a food, getting a positive skin test for an allergy, and showing symptoms mainly confined to the mouth and throat. But they did not specify whether or not the person also had a pollen allergy.

At the time, the term did not attract much attention, but a year later, another study came out describing the oral symptoms suffered by birch-allergic patients after they ate fruits and vegetables. Since these people’s symptoms were the same as those reported in the first study, the authors of this paper also used the term ‘oral allergy syndrome’, and their report reached many more eyes.

From then on, any patient experiencing oral symptoms was labelled as having OAS, which put some patients with pollen food syndrome in the unfortunate position of being mislabelled as having symptoms which, per definition, do not progress (much) beyond the mouth area, or ‘oral cavity’ in medical-speak.

However, while the majority of people with pollen food syndrome will experience symptoms largely limited to their mouth area, around 1 in 10 sufferers can experience systemic symptoms and even anaphylactic reactions.

Systemic symptoms, by the way, are symptoms which do not simply appear at the site which comes into contact with the allergen, but instead involve parts of the body that are removed from the contact site, like a widespread skin rash after eating food or vomiting after being stung. And anaphylactic reactions are systemic reaction that involve 2 or more of the body’s organ systems (i.e. the skin and/or the respiratory system and/or gastrointestinal tract and/or the cardiovascular system).

In 1996, a pair of researchers proposed the term ‘pollen–food allergy syndrome’—PFAS, also known as pollen food syndrome or PFS—to describe a food allergy due to cross-reactivity between pollen and plant food allergens. Unfortunately, it didn’t really catch on. At least, not as a separate concept. Even though it clearly was, to some people at least.

In 2003, researchers surveyed 122 members of the American Academy of Allergy, Asthma and Immunology and reported a general lack of awareness of pollen-food allergies, as well as inconsistencies in diagnosis and treatment among doctors who were using the terms OAS and PFS interchangeably.

12 years later, researchers surveyed 193 health care professionals in the UK and reported similar findings. 64% of the survey respondents thought that OAS and PFS were the same thing and the vast majority (76%) of them reported that they would not recommend an adrenalin auto-injector for the condition.

In recent years, several reviewers have tried to set the record straight, but many allergists still need to ‘wake up and see the pollen from the trees‘.

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What is oral allergy syndrome (OAS)?

Oral allergy syndrome (OAS) has been recognised as a unique set of food allergy symptoms for over 80 years. It’s a form of a contact allergy that occurs when a person’s mouth and throat is exposed to some kind of food that disagrees with their immune system.

The symptoms tend to be restricted to the lips, tongue, oral cavity and/or throat, and they generally appear within 5 to 30 minutes of eating the offending item before spontaneously disappearing 30 to 60 minutes later. In rare cases, the reaction can occur over an hour after eating.

OAS can manifest with any kind of food, from plant foods to animal-based foods such as chicken, eggs, salami, fish or shellfish.

OAS can also be experienced by people who are not allergic to any foods. For example, people who are allergic to pollen can get OAS while eating honey or food containing honey because grains of pollen can get stuck in the nectar when the bee collects it from the flower, and these grains retain their allergenic properties during the honey-making process, arriving the mouth of a pollen sufferer still ready to cause problems.

Reports have also been made of people experiencing OAS symptoms after eating food cooked over mesquite wood. Those people tested positive for allergy to mesquite pollen and the thinking is that the allergens from the wood transferred to the food during cooking, provoking the allergic reactions. People who are allergic to mesquite pollen are therefore advised not to eat food cooked over mesquite wood.

Importantly, oral allergy symptoms can be the first sign of a more severe allergic reaction to a certain food or foods.

Most people with a primary food allergy do not experience a severe reaction when they eat a small amount of the food they are allergic to. Many will actually just experience OAS to start off with, but will then experience systemic reactions or even anaphylaxis if they eat more of the offending food. This is, in fact, what happened in the original 1987 study which introduced the concept of ‘oral allergy syndrome’ in the first place; almost half of the people who had oral allergy symptoms to peanut went on to experience systemic symptoms and anaphylaxis when exposed to more of the troublesome legume.

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What is pollen food syndrome (PFS)?

Pollen food syndrome—aka pollen-food allergy syndrome (PFAS)—was first described in 1942 by a pair of researchers who linked a limited set of gastrointestinal symptoms in pollen-allergic patients to a heat-sensitive allergen in fresh fruits.

PFS is a secondary allergy, that is, an allergy in which a person is first sensitised to grass, tree and/or weed pollens (the primary allergy) and then, in a second step, they are sensitised to plant foods that contain allergens that structurally resemble those in the pollens that they’re actually allergic to. This is also known as a cross-reactive allergy.

(The primary form of a food allergy typically involves sensitisation via the gastrointestinal tract—i.e. when someone eats the food. However, because of the multiple ways in which people can be sensitised to multiple and often unknown allergens in food and pollen, it’s not always possible to distinguish a primary food allergy from a secondary one.)

What actually happens is that, for some as-yet-unknown reason, pollen proteins that are inhaled through the respiratory tract provoke some people’s immune systems into producing IgE antibodies that bind to the surface of immune system cells (mast cells and basophils) throughout their bodies, including in the lining of the mouth. When these antibodies come into contact with food in (or around) the mouth, they recognise protein (and maybe carbohydrate) molecules in the food with similar structures to those of the pollen proteins that they are allergic to. This causes them to trigger the mast cells and basophils to release inflammatory substances like histamine, which is what causes the symptoms of OAS. In most cases, the proteins causing this response are broken down in the stomach, limiting any further reaction. But in around 1 in 10 cases, those proteins continue to cause problems.

Because PFS is a secondary allergy and the initial sensitisation to the food takes place via pollen allergens as opposed to contact with food, allergic reactions to a food can occur the first time it is eaten and catch people unawares.

Triggering foods include, essentially, any kind of plant food. The most common ones depend on which pollen you are allergic to. These include:

Pollen	Fruits	Veg, herbs & grains	Nuts (& legumes) & seeds
Alder (family Betulaceae, genus Alnus) A spring pollen	apple, cherry, peach, pear, raspberry, strawberry	celery, parsley	almond, hazelnut, walnut
Birch (family Betulaceae, genus Betula) A spring pollen	Fruits in the Rosaceae (rose) family: apple, apricot, cherry, pear, peach, plum, raspberry and strawberry, as well as fig, jackfruit, kiwi, mango, Sharon fruit (aka persimmon/kaki fruit), watermelon	Vegetables and spices in the Apiaceae family: aniseed, caraway, carrot, coriander, celery, cumin, dill, fennel and parsley, as well as beans, lentils, green pepper, parsnip, potato, soybean, tomato*, wheat	Tree nuts in the Rosaceae and Betulaceae (birch) families: almond and hazelnut, as well as peanut, pumpkin seed, walnut
Cedar (family Pinaceae, genus cedrus) A summer pollen	kiwi, melon, pineapple	tomato
Cypress (family Cupressaceae, genus Cupressus) A spring pollen	apricot, cherry, citrus fruit, peach, pomegranate
Grass (over 95% of allergies are caused by the Pooideae, Chloridoideae and Panicoideae sub-families) A summer pollen	Fruit in the Cucurbitaceae (melon) family: cantaloupe, honeydew, watermelon, as well as fig, orange, kiwi, peach	Swiss chard, tomato, white potato	peanut
Mugwort (Artemisia vulgaris) An autumn pollen	banana, grape, lychee, mango, peach	Vegetables and spices in the Apiaceae family: aniseed, caraway, carrot, coriander, celery, cumin, dill, fennel and parsley, and vegetables and spices in the Brassicaceae (crucifer) family: broccoli, cabbage, cauliflower and mustard, as well as bell pepper (paprika), black pepper, garlic, onion	peanut, sunflower seed
Olive (family Oleaceae genus Olea) A spring pollen	apple, kiwi, melon, peach, pear	olive	hazelnut, peanut, walnut
Plane/sycamore (family Platanaceae, genus Platanus) A spring pollen	apple, apricot, kiwi, peach, plum	chickpea, corn, green beans, lettuce	hazelnut, peanut, walnut
Ragweed (Ambrosia artemisiifolia L.) An autumn pollen	Fruit in the Cucurbitaceae (melon) family: cantaloupe, honeydew, watermelon, as well as banana	Vegetables in the Cucurbitaceae family: courgette (zucchini), cucumber and squash, as well as artichoke, chamomile, echinacea, pepper	sunflower seed

* yes, I know that tomatoes are fruit (as are cucumbers, courgettes, green beans, pumpkins and many ‘vegetables’), but they are generally regarded as vegetables and are even legally considered to be vegetables in the US.

Some cross reactions are so common that they have been given names, such as:

• Birch-apple syndrome
• Birch-fruit-vegetable syndrome
• Celery-birch-mugwort-spice syndrome
• Celery-mugwort-spice syndrome
• Cypress-peach syndrome
• Goosefoot-fruit association
• Goosefoot-melon association
• Mugwort-chamomile association
• Mugwort-celery-spice syndrome
• Mugwort-mustard syndrome
• Mugwort-peach association
• Pellitory-pistachio association
• Plantain-melon association
• Ragweed-melon-banana syndrome
• Russian thistle-saffron association

Worth repeating: the fruits and veggies mentioned above are simply the ones most commonly reported. Most people with PFS develop a secondary allergy to more than one food because the pollen proteins that cause the allergy have very similar counterparts in all kinds of plants. Someone who suffers from pollen food syndrome can become allergic to pretty much any fruit or vegetable or herb or spice out there.

Pollen power

The allergen(s) you become allergic to depend in large part on where you live and what grows there, as well as what you normally eat.

Birch pollen (notably its bet v 1 allergen) is highly allergenic—it’s much more likely to sensitise people to foods than any other type of pollen.

Birch trees are commonly found in northern and central Europe. A study of German birch pollen-allergic patients reported that about 70% of them had PFS. And a survey of Swedish patients with pollen allergy discovered that about 70% of individuals with a birch pollen allergy had PFS, versus only 19% of people with other pollen allergies.

Likewise, a study from Spain, where birch trees are much rarer, specifically investigated people living in an area without birch trees (or ragweed) and found that, without the powerful pollen to contend with, only about 21% of pollen sensitised patients had PFS.

Birch pollen also provokes more pronounced OAS symptoms than other pollens, according to a study from Croatia.

Most of the birch-allergic who live in northern and central Europe are allergic to fruits (and nuts) of the Rosaceae family, especially apples, as well as hazelnuts (that belong to the Corylus—hazel—family, which is a member of the birch family) and vegetables of the Apiaceae family like carrots and celery.

Reactions to more exotic fruits are also reported, such as kiwi fruit—which, these days, are widely available and thus more likely to be reported as problematic—guava, pomegranate and Japanese pear.

Birch pollen is also (by far) the most widespread allergen in Russia, and almost all food-allergic Russian children suffer from oral allergy syndrome triggered by food allergens related to birch pollen in hazelnut, apple, peanut, peach, soy, celery and kiwi.

n the US, a similar pattern of sensitisation is seen; a link has been noted between sensitisation to birch and members of the Apiaceae family like carrot and celery, and further research has shown that around three quarters of children who are allergic to hazelnut and almonds are likely to be sensitised to birch, and just under two thirds, to peanut.

Birch is not the only problematic tree in the Fagales order: in fact, many trees in this order—which also includes alder, beech, oak, hazel, hickory and hornbeam—can sensitise people in the same kind of way.

In Mexico, children are predominantly allergic to oak and ash trees, and the foods most commonly associated with PFS are the members of the Rosaceae family—peach, apple pear and almond—as well as pineapple and banana.

In Japan, birch is a common cause of PFS but it’s the widespread distribution of alder trees that causes many people to develop allergies to birch-related allergens even in areas without birch trees. For Japanese PFS-sufferers, the most common food culprits are fruits of the Rosaceae family, soy, melon, pineapple and kiwi fruit.

In Korea, birch, alder and oak are the principal problem pollinators, and apple, peach and kiwi the main irritants. However, as well as the usual suspects, locally eaten fruits like taro, jujube, ginseng, persimmon, Chinese yam, kudzu vine, bellflower root, and deodeok (Codonopsis) also trigger PFS symptoms.

Birch pollen sensitisation is also quite common in China, especially in the north, where apple and soybean are common irritants for people with PFS.

Luckily for the birch-allergic population, the most potent birch allergens are of the more easily destroyable PR-10 (bet v 1) and profilin (bet v 2) varieties, so people with birch-induced pollen food syndrome tend to have milder reactions, often (but not always) limited to OAS.

Mugwort (Artemesia) is another important aeroallergen and, unfortunately for the mugwort allergic, one of the most potent allergens in mugwort—art v 3—is an LTP allergen, a type of allergen more likely to cause serious reactions when involved with food allergies.

Mugwort was originally native to Russia but can now be found on every continent except Antarctica, and LTP proteins are found in just about every type of plant food, so the potential for troublesome pollen food syndrome is enormous.

In Europe, reports of LTP food-related allergies initially came from the southern European countries of Spain and Italy. Peach is by far the biggest cause of—often quite serious—food-related reactions, but peanuts and tree nuts are also frequent offenders, although there is some debate as to whether this is because of sensitisation to pollen or a direct allergy to the food. (see Allergen matters later)

Different eating habits in different European countries mean different troublesome foods. In the UK, for example, the mugwort-allergic also tend to be sensitised to cabbage, lettuce and mustard.

In central Europe, celery, celeriac, carrots and spices have been provoking systemic reactions in the mugwort-allergic Swiss since (at least) the 1980s and, in Germany, a case of anaphylaxis to broccoli has been reported in another mugwort-allergic patient.

In Japan, where most people with mugwort-induced PFS have very serious reactions, broccoli was also a problem for a 73-year old man who was admitted to hospital with facial swelling and difficulty breathing after eating some boiled brassica. He tested strongly positive for allergies to mugwort, broccoli and mustard.

In China, where the level of exposure to mugwort is equivalent to that of birch in northern Europe, systemic reactions are quite common in people who have mugwort-related PFS, and they are often triggered by peach or peanut.

And in Korea, a case of anaphylaxis to Chinese bellflower has been described in someone who was allergic to both mugwort and birch.

Ragweed pollen seems to be less problematic for the food-allergic than birch or mugwort.

Ragweed is indigenous to North America and also a major inhalant allergen—melon and banana are common irritants for Americans with PFS, who tend to suffer from oral allergy syndrome. Lab tests have also shown potential cross-reactivity with members of the squash family (watermelon, melon, courgette/zucchini and cucumber) and banana.

Ragweed is increasingly being found in countries all around Europe and, because it cross-reacts with mugwort, the mugwort-allergic are likely to react to ragweed pollen without needing to actually become allergic to it. People who are sensitised to other pollens or food seem more likely to become sensitised to ragweed.

A number of foods have been linked to ragweed sensitisation, possibly because of the protein profilin, which is a widely-distributed allergen present in ragweed and melon, and probably responsible for cross-reactivity between a wide range of plant foods that do not belong to the same family, such as melon, avocado, banana, kiwi and peach.

However, because people who are allergic to ragweed are often sensitised to other pollen allergens—polysensitised—it’s unclear whether ragweed is actually responsible for PFS symptoms or whether the PFS is due to an allergen in another pollen that they’re are also allergic to. When Italian researchers looked at 137 people who were sensitised to only ragweed, they did not find any evidence of a pollen-associated food allergy.

Grass pollen is a big problem for hay fever sufferers, but whether or not it produces symptoms of pollen food syndrome is controversial

Grass pollen contains two main allergens which might cross-react with food allergens. One of them is the group of Cross-reactive Carbohydrate Determinants (CCDs). They have been shown to react with allergens in cereals, rice and peanuts, but they are thought to be ‘clinically irrelevant’—that is, not to produce any symptoms.

However, some studies have suggested a possible role for CCDs in reactions to fruit and vegetables like persimmon (aka kaki fruit or Sharon fruit if from the Sharon plain in Israel), celery and courgette/zucchini.

The other important group of cross-reactive allergens in grass that could produce (generally, oral allergy) symptoms is profilin. One study found IgE against grass pollen profilin in bakers with occupational asthma, food and pollen allergy.

German lab tests confirmed that profilin was responsible for the cross-reactivity in several grass-allergic patients who were sensitised to tomato. A previous Italian study had reported that some grass-allergic Italians suffered from OAS after eating tomato, melon and watermelon.

Another Italian study made a link between an allergy to Timothy grass and citrus fruit (orange, clementine and lemon) which, in a couple of patients, manifested with rashes, swelling, stomach pain and diarrhoea.

In Turkey, where grass pollen is the primary sensitiser, the most problematic foods associated with a monosensitisation to grass are kiwi and tomato. Other frequently-reported problematic foods in the region include melon, watermelon, peach, aubergine (eggplant) and walnut. Allergic reactions are mostly restricted to OAS and rashes.

In Australia, Timothy grass pollen is the most common sensitiser and tropical fruits—mainly watermelon—provide most of the problems for patients with PFS.

Of course, there are plenty of other types of pollen around to worry about.

Plane pollen is mostly problematic in southern Europe, where it causes allergic reactions to peach, walnut, hazelnut and peanut, apple, maize, chickpea, lettuce, banana and celery.

Cypress pollen is also found mostly in countries in the Mediterranean area, and it has been linked with PFS symptoms to peach and citrus fruit in France, but it seems to have a limited effect as far as PFS is concerned, with one study reporting that only 1 out of 22 people with a cypress allergy reporting any symptoms to food.

Olive pollen is an important cause of respiratory allergy in southern Europe and the Mediterranean region although it is not often linked with food allergy. However, in areas of high pollen exposure, the LTP allergen (Ole 7) in the pollen may act as a sensitiser for pollen-food allergy, notably peach allergy. And when LTP allergens are involved, allergic reactions can be quite serious.

In another study, 40 of 134 (30%) Spanish patients allergic to olive pollen were found to be allergic to fruit (melon, peach, kiwi, pear) and/or nuts and to exhibit symptoms ranging from OAS to anaphylaxis.

Cases of people allergic to olive pollen and exclusively to olive fruit have also been reported in Switzerland, Spain, Turkey and Tunisia, with symptoms ranging from OAS and hives to anaphylactic shock.

Cedar pollen is the main trigger of airborne allergy in Japan and Japanese cedar, in turn, can provoke symptoms on eating kiwi and pineapple, melon and, more commonly, tomato. An allergy to (mountain) cedar pollen is also associated with an allergy to tomato and banana in Texas.

Fig pollen is a surprisingly common cause of food allergies, primarily due to the popularity of the weeping fig (ficus benjamina) as an indoor plant for homes and offices. The plant releases allergens into the air which can lead to the development of food allergies.

Allergy to fig as a result of sensitisation to F. benjamina pollen can lead to anaphylaxis, as was the case of a 35-year-old woman who required urgent treatment after eating a dried fig. In another study, 5 people with an allergy to fig pollen and symptoms ranging from OAS to anaphylaxis were tested for possible cross reactions to other fruit, and positive skin tests were obtained with kiwi, papaya and avocado.

A further study identified both fresh and dried fig as well as kiwi as the most common causes of systemic reactions (hives, swelling and asthma) in people allergic to fig pollen, and identified banana and pineapple as other possible cross-reactive fruit.

An allergy to birch pollen can also provoke reactions to fresh fig (and occasionally to dried fig) in the form of OAS and respiratory symptoms.

The pollen allergic are often sensitised to various pollens (‘polysensitised’).

This can lead to surprise reactions, like the case of a multiple-grass-weed-and-tree-pollen-allergic 22-year-old sailor who, on his first port call to Thailand, suffered from hives, itchy eyes and throat swelling after eating a tropical fruit called rambutan for the first time.

It can also lead to a sensitisation to multiple foods, like the case of a 10-year-old Turkish boy, allergic to tree, grass and cereal pollens, who suffered from itching, facial swelling and stomach aches after meals and turned to be sensitised to several types of fruit, veg, nuts and cereals. Luckily, avoiding the ones that gave the biggest skin and blood test responses seemed resolve most of his problems.

The fact is, PFS is a complicated disease and we’re a long way from having all the pieces of the puzzle, hence the head scratching when the pollen-allergic get oral allergy symptoms when eating jackfruit or anaphylactic attacks after eating oranges without being sensitised to the usual allergenic suspects.

And other sources of plant allergens are often overlooked. For example, a 2022 study from Poland reported that allergies to birch, mugwort or grass pollen made people more likely to be allergic to herbs, especially those belonging to the Lamiaceae and Apiaceae families—basil, sage, lemon balm, mint, rosemary, oregano, thyme, anise and caraway—and mustard. Herbal medicines also have been the cause of more frequent reports of allergic reactions over the past few years, including anaphylactic shock.

The search for answers goes on.

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How common is pollen food syndrome?

It’s difficult to know how common PFS is because of the regional differences in the distribution of the trees, grass and weeds that cause PFS, the different strengths of the different pollens and the resulting wide variability in symptoms.

A general lack of awareness of the syndrome among health professionals and the interchangeable use of the terms ‘oral allergy syndrome’ and ‘pollen food syndrome’ adds to the general confusion.

That said, a 2019 review of (English language) studies worldwide estimated the prevalence of pollen-food allergy in the general population as ranging from around 4.7% to 20% in children and 13% to 58% in adults.

11 years earlier, a review of 36 studies investigating the prevalence of plant food allergies across the world found few that used objective assessments. Only 6 included food challenge tests and they reported prevalences between 0.1% and 4.3% for fruits and tree nuts, between 0.1% and 1.4% for vegetables, and less than 1% for wheat, soy, and sesame.

Birch pollen-associated PFS is the most common food allergy in adults in the UK. A study carried out in 2013 reported a PFS prevalence of 0.8% and 4.1% in urban settings in Scotland and England respectively, with a majority of people experiencing their first symptoms below the age of 20.

A survey of school-age children carried out in Japan in 2020 reported oral symptoms to Rosaceae fruits and/or soybean in between 1% to 3% of the children (but didn’t cover any other plant foods).

Most studies have investigated the prevalence of PFS among people with a known pollen allergy. The numbers tend to vary according to geographic location, depending on the aeroallergens present in that location and their ability to cause a secondary food allergy.

In northern and central Europe, where birch trees—which have highly allergenic pollen—are native, PFS is estimated to affect between 50% and 90% of people with an allergy to its pollen. In fact, pollen food syndrome is considered to b most common type of food allergy among adults.

In 2008 in Denmark, researchers sent questionnaires to 1094 random 22-year-olds and got 843 replies. PFS was defined as reactions to pollen related fruits and vegetables in pollen allergic people. 192 of the young adults reported pollen-related symptoms and 141 (73%) of them reported symptoms to pollen-associated foods, with an allergy to kiwi being the most common complaint, followed by hazelnut, pineapple, apple, orange, tomato, peach and Brazil nut.

A 2012 study in Spain carried out on 233 pollen-allergic patients found that 39.9% were sensitised to foods and 30.9% had a clinical allergy (i.e. showed symptoms) to at least one of the plant foods studied.

In Turkey, prevalence rates amongst adults are reported to vary between 14% and 19.3%.

The prevalence of PFS in the US has not been reported, although experts think that it’s probably the most common food allergy in adults.

In Mexico, a study of 267 children aged between 6 and 14 attending allergy clinics for the first time and diagnosed with PFS using questionnaires and skin prick tests reported a prevalence ranging between 9.6% and 12.2%, depending on the type of pollen in the area. Another study that focused on (29) children aged between 6 and 18 who had also had oral food challenges reported a prevalence of 5.3%.

In China, a 2020 study of 402 pollen-allergic adults and children reported a PFS prevalence of 30%.

In Korea, a nationwide study of 648 pollen-allergic adults and children in 2018 reported that 270 (41.7%) had pollen-food allergy. Of those 270 people, a third showed symptoms to 1 fruit or vegetable and the others to more than one. 82 (30%) were allergic to 5 or more different foods.

In Japan, the proportion of patients who are allergic to cedar pollen and have PFS is estimated to be between 7 and 17%.

And a study carried out in 2014 in Australia reported a PFS prevalence of 12.9% in pollen-allergic children.

Although PFS typically affects adults and adolescents, it’s increasingly affecting younger, pollen-allergic children. A 2011 study carried out in Sweden reported that 25% of 8-year-olds with hay fever had oral allergy syndrome and a 2013 study reported a prevalence of PFS in 23.9% Italian children with hay fever.

A 2015 study investigating the sensitisation to peanut allergens among the general population in Norway noted that the sensitisation to Ara h 8, the peanut allergen responsible for cross-reactions with birch pollen, increased markedly from 23.3 % in the youngest children (aged 0–5 years) to 56.3 % by the age of 6. The researchers noted that the increasing sensitisation to pollen-related food allergens in young children was probably due, at least in part, to the milder climate and longer pollen seasons associated with climate change.

A 2022 study carried out in Japan reported that the prevalence of PFS in young Japanese schoolchildren was getting higher and that the average age of onset was getting lower (between 5 and 7 years of age). Around a third of children with PFS had experienced systemic symptoms including skin symptoms, (21.8%) respiratory symptoms (9.6%) and gastrointestinal symptoms (6.4%), and 5.8% of them had had anaphylactic attacks.

A 2021 study investigating 43 children in Poland sensitised to pollen and plant food reported that 4—almost 1 in 10—of them were under 3 years old, and 16 of them—just over a third—under the age of 6. A quarter of the children had OAS, 7 got eczema after eating plant food, and 3 had systemic symptoms (hives and difficulty breathing).

Pollen food syndrome is probably going to become a more common problem. Reports of food- and pollen-associated allergies have increased over the past few decades due to factors caused by global warming, including longer pollen seasons, and experts expect cases of pollen food syndrome to increase further as plants develop more allergenic defence proteins as a result of stress caused by drought and pollution.

Will it go away?

In two words: probably not. In fact, as time goes on, some people with PFS will experience symptoms to more foods. The only way out, according to anecdotal evidence, is to avoid the offending foods for a couple of years. This can cause some sensitisations to disappear, which is why it can be worth getting retested over time.

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Risk factors for getting pollen food syndrome

Several factors have been identified as putting a person at greater risk from getting pollen food syndrome.

People who have other allergic diseases—especially eczema and asthma—are more likely to develop PFS, according to studies from a wide variety of countries including Italy, France, Spain, Portugal, Croatia, Turkey, Mexico and Japan.

A family history of allergy is also a risk factor for developing pollen food syndrome, according to studies carried out in Italy, Turkey, Japan, and Korea.

However, this is not a 2-way street: people who develop PFS do not necessarily have a history of allergic disease. In this Japanese survey of adolescents in the general population (i.e. not seeing an allergist), for example, a past history of allergy such as atopic dermatitis and asthma was not very common in those who had PFS. And in this study of people getting skin prick tests at a Korean hospital, those who were allergic to birch pollen and had asthma were actually less likely to have PFS.

Older age is another risk factor for PFS. The proportion of pollen-allergic children with pollen food syndrome has been shown to increase with age. In a 2016 study, for example, British researchers split 54 children into 3 age groups—0–5, 6–10, 11–15 years— and reported a clinical diagnosis of PFS of 17%, 50% and 78%, respectively. A study carried out in Croatia the previous year also noted that adolescents were more likely to have PFS than small children, and an Italian study also observed that PFS symptoms started in preschool-aged children and noted that ‘its frequency increased progressively with age’.

Being a woman is a risk factor mentioned by studies carried out in a wide variety of countries, including the UK, Italy, Croatia, Turkey, Canada, Korea and Japan. In studies dealing specifically with the treatment of pollen food syndrome, the majority of patients also tend to be women.

Other risk factors for developing pollen food syndrome include exposure to tobacco smoke and being allergic to tree pollens—most notably to pollen from the birch family.

A Japanese study looking at PFS in the context of atopic march—the typical progression of allergic disease in a person over time—examined the data of 521 children born between March 2004 and August 2006 and subsequently followed them for 13 years. They found that being sensitised to Bet v 1—the major birch pollen allergen—at the age of 5 and/or 9 was associated with the biggest risk of having PFS at the age of 13. (They also found data suggesting that owning a dog, but not a cat, might help to prevent the development of PFS, although more studies are needed to confirm that observation.)

The higher your IgE levels to birch pollen, the bigger your risk of getting PFS, as demonstrated by this study in which follow-up testing of a group of people allergic to birch pollen revealed that those who had developed PFS since the first time they were tested now had much higher birch-specific IgE levels than the people who did not have PFS.

Being sensitised to more than one type of pollen also increases your risk of getting PFS. In 2005, for example, a Danish study reported that the number of birch-allergic people who also had PFS was smaller than that typically found in other northern European countries—24%—but that it rose when they were also allergic to grass pollen—35%—and grass and mugwort—52%. Similarly, an Italian study of grass-allergic children found that only 20% of them had PFS, but that number rose to 46% in children allergic to both grass and birch.

Reacting to pollen is also a risk factor for PFS: the longer you have hay fever, the more likely you are to develop an allergy to food—this according to a study of 283 birch pollen-allergic Italian people that found that 41% of those who had had hay fever symptoms for a year had food allergies, a number that rose to 86% in people who had had birch pollen-induced hay fever for over 15 years. This finding is backed up by another study from Iran that also found that, the longer a person had hay fever symptoms, the more likely they were to develop PFS.

Pollen food syndrome has been linked to other diseases, including Eosinophilic Esophagitis (EoE). An American study that looked at 346 adults with EoE treated in one centre between 2002 and 2016 found that 90 (26%) of them had PFS, many brought on by an allergy to tree and weed pollens and provoked by eating apples, carrots and peaches. A Dutch study of 76 EoE sufferers found that 30 (39%) of them were sensitised to birch pollen and cross-reacting foods. The mechanisms underlying this particular link are unknown so we don’t know whether having EoE puts a person at risk of getting PFS, or whether allergy to pollen and/or food causes EoE or simply maintains the inflammation.

Research has shown that pollen can reach the digestive tract by means of swallowing and that birch pollen itself can actually cause inflammation in the gut. Some conditions like eosinophilic esophagitis can get worse with exposure to pollen which is probably why people with eosinophilic esophagitis tend to be diagnosed during the pollen season.

Some people experience gastrointestinal (GI) symptoms only during the pollen season while others experience a worsening of their usual symptoms during that period. The mechanisms underlying this type of allergic reaction is still unknown, but there is research that suggests that some people’s GI symptoms— abdominal distension, gas, pain, diarrhoea and constipation—could be the result of eating pollen-related food (e.g. apple, peach, hazelnut, peanut) rather than exposure to just the pollen itself.

Perhaps unsurprisingly, then, PFS has also been linked to Irritable Bowel Syndrome (IBS), with a study carried out in the UK repoting that around two thirds of the 35 IBS patients they were investigating had hay fever symptoms and around a third also had oral allergy symptoms triggered by kiwi, stone fruits and hazelnut. These latter patients also had worse IBS symptoms than the people who had IBS without PFS.

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What are the symptoms of pollen food syndrome?

When people are initially sensitised to pollen(s), they tend to develop the usual symptoms of hay fever: allergic rhinoconjunctivitis (itchy red eyes and a runny nose) and/or asthma. The vast majority of those who go on to develop pollen food syndrome will experience mild, OAS symptoms, typically:

• itching/burning lips
• an itching/burning tongue and/or palate
• an itching/burning throat
• subtle swelling (angioedema) of the skin inside of the mouth, the cheeks and lips
• subtle swelling of the tongue
• hay fever-like symptoms: teary eyes, runny nose
• swelling around the eyes
• a raised, itchy rash (hives) on the face and neck
• atopic dermatitis on the face and neck
• sneezing

And more rarely:

• red patches or small, short-lived blisters in the mouth (aka ‘blistering of the oral mucosa’)
• a feeling of tightness in the throat and/or difficulties swallowing
• hoarseness
• itchy ears
• contact rashes & itchiness when handling raw veg

Symptoms occur very quickly; either while or 5 to 15 minutes after eating the culprit fruit, vegetable, nut or seed. They usually resolve quickly after the food is swallowed, generally within 10 to 30 minutes, as the structure of offending allergens in the food is slowly destroyed by digestive enzymes and stomach acid.

After the mouth area, the skin is the organ most often involved in allergic reactions to food, with hives and swelling being the most common symptoms, and sometimes generalised flushing. Some people develop contact urticaria (a weal and flare reaction where the food is touched) around their mouths after eating fruit (like apple, kiwi or strawberry) or on their hands after handling raw vegetables.

These symptoms usually manifest within a 5 minutes to 2 hours after touching or eating the food.

There has also been a report of a 34-year-old man whose symptoms—severe stomach pain—were initially suspected to be due to eosinophilic gastroenteritis (EGE). After a few months of suffering from worse and worse stomach pain, he ended up in hospital. On admission, he was found to have a swollen intestine and abnormal levels of eosinophils in his blood and his intestinal tissues, but he did not have the kind of tissue damage associated with a gastrointestinal disease.

Detailed observation of his symptoms revealed that the stomach pain appeared within half an hour of eating his meals and was accompanied by an irritated mouth. Step by step elimination of the foods that irritated him led to a resolution of his symptoms and, because all of those foods were associated with birch pollen and he was known to suffer from seasonal hay fever and shown to be allergic to birch, he was given a diagnosis of PFS.

Although it is quite common for people with PFS to have respiratory symptoms because of their pollen allergy, not all PFS-sufferers have them.

Sometimes, a person’s initial reaction to food—the oral allergy symptoms—precedes respiratory symptoms, which then develop later on in their lives, as was the case with 12 out of 166 (7%) Italian patients who developed OAS before any respiratory symptoms in this study, and 208 out of 496 (42%) Japanese people in this study.

Sometimes the pollen allergy never causes any symptoms and only the cross-reactive food provokes a reaction, as was the case for 238 out of 734 people—about 1 in 3—in the aforementioned Japanese study who had OAS but no hay fever.

Sometimes the pollen allergy is actually secondary to the food allergy, as in the case of 10 peach-allergic Italians in this study who developed their sensitivity to mugwort because of a cross-reaction between the LTP allergens in peach and mugwort. In their case, they had no hay fever symptoms and also no PFS—what they had was a (more dangerous) primary allergy to peach.

More often, pollen-allergic people can be sensitised to food(s) but show no symptoms.

In one of the first studies to demonstrate this, Swiss researchers tested 274 pollen-allergic people and reported that, though 47% of them tested positive for one or more food allergens, many of them had no clinical symptoms of food allergy. In another Swiss study, of 111 people allergic to pollen and sensitised food, only 67 reported oral allergy symptoms.

A recent investigation of 43 Polish children sensitised to both pollen and food found that 16 (37.21%) of them did not have any signs of a food allergy, noting that those who had hay fever symptoms were more likely to have symptoms of food allergy.

The mechanisms underlying the variations in symptoms in people with pollen food syndrome are unknown.

Pollen food syndrome can cause delayed symptoms

As well as the classic, immediate-type reactions to food, PFS has also been linked to delayed-type reactions.

Some people with pollen-food allergy who also have eczema notice that it gets worse a few hours after they eat fruit and/or veg. This has been demonstrated in several studies.

In one study, 12 children around 5 years old with atopic eczema/dermatitis syndrome (AEDS) and a known sensitisation to birch pollen underwent oral challenges with birch pollen-related foods (e.g. apple, carrot, celery, hazelnut). The children had shown none of the expected immediate reactions to these foods in the past and consumed them on a regular basis. 7 of them showed either an immediate and/or a delayed worsening of their eczema after eating the food, 4 of them 24 hours after the challenge.

In another study, 4 adults with birch pollen allergy and eczema were asked to eat cooked apple, celery and carrot to see what effect cooking would have on their symptoms. Results showed that, though they no longer experienced oral allergy symptoms, their eczema still got worse. The authors of the study concluded, ‘… the view that cooked pollen-related foods can be consumed without allergologic consequences should be reconsidered.’

In a third study, 37 birch pollen-allergic adults with atopic dermatitis and no history of immediate allergic reactions to food underwent a double-blind, placebo-controlled food challenge with fresh, birch pollen-related foods. 17 of them showed a worsening of their skin conditions 48 hours after eating the food.

Skin biopsies taken during the exams showed that this reaction was mediated by a T-cell response—that is, a cell-mediated response rather than an IgE response, which would not show up on the standard blood and skin tests done for food allergies. That specific result was backed up by a separate lab test which showed that birch pollen bet v 1-related allergens in apple, hazelnut and celery were somewhat degraded by digestion but still able to activate T cells.

T cell-mediated mechanisms are also behind other conditions like eosinophilic esophagitis and asthma, so it’s entirely possible that eating pollen-related foods might make those conditions worse, too.

Most recently, German researchers gave 182 children and adults with eczema and suspected PFS oral food challenges with birch pollen-related foods to which 32 responded with a significant worsening of their skin condition, making up about a third of all positive reactions. Although those who responded to the food showed higher levels of IgE antibodies to birch and apple, there was no way of differentiating between those who had immediate-type responses and late eczematous responses.

Further, detailed blood tests of people with eczema and suspected PFS showed a trend for those whose eczema got worse to also suffer from hay fever but, due to the small size of the study, the results were not statistically significant, and no other differences (such as differences in age, disease severity or IgE levels against allergens) were found between those whose skin conditions worsened as a result of eating birch pollen-related foods and those who did not react.

Pollen food syndrome can be dangerous

In the words of the British Society for Allergy & Clinical Immunology (BSACI): ‘The typically mild symptoms of PFS can lead to an erroneous perception that this condition is always easily managed, but severe reactions can occur’.

An oft-quoted 1993 review of studies involving a total of 1361 people with plant food allergy reported that 8.7% of sufferers experienced systemic symptoms, 3% experienced systemic symptoms without any oral symptoms and 1.7% experienced anaphylaxis.

Systemic reactions can include:

• widespread skin rashes (hives)
• general eczema
• swelling
• coughing
• nausea
• vomiting
• stomach aches and/or cramps
• diarrhoea
• difficulty breathing
• wheezing, asthma
• hypotension (low blood pressure)

An increasing number of studies are reporting that pollen food syndrome affects all age groups and that significant numbers of adults, especially, tend to experience systemic and even anaphylactic reactions. A number of things may be making the situation worse, including:

• an increasing number of people eating more fruits and vegetables, and the increases popularity of juices and smoothies and plant-based meat substitutes
• an increasing number of nutritional or body-building supplements containing plant foods
• changes in pollen and pollution levels increasing the number of allergy-sufferers in general

More recent studies find increasing numbers of PFS-sufferers who have more to worry about than itchy mouths. For example, this study including 270 Korean adults and children with PFS that reported that 8.9% of them had suffered anaphylactic attacks, this study including 119 Chinese adults and children with PFS that reported that 33 (28%) of them had experienced food-induced anaphylaxis at least once and this smaller Turkish study including 22 children with PFS that reported that 2 of them (9%) had had anaphylactic attacks.

Pollen food syndrome has also been linked with a few cases of food-dependent exercise-induced anaphylaxis (FDEIA). Most recently in Denmark, where a case of anaphylaxis to almond after exercise was noted in a patient with an allergy to pollen and a secondary food allergy. In Korea, a case of FDEIA involving the ‘celery-mugwort-birch-spice syndrome’ was reported in 2009, and, in the US, 3 cases of celery-induced FDEIA were described in the 1980s in 3 patients who were all allergic to the pollen of trees and/or ragweed and/or grass.

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Allergen matters

How you’ll react to the food you’re allergic to depends in large part on the allergen(s) that you’re sensitised to. There are three types of allergen responsible for most pollen-food allergies:

• Profilins: generally destroyed by digestion and heating, tend to cause mild symptoms (OAS), but can cause severe reactions under certain conditions such as high levels of pollen exposure
• Pathogenesis-Related protein group 10 (PR-10): normally destroyed by digestion and heating, generally responsible for mild symptoms (OAS) but can cause severe reactions, especially when eating in large amounts (see Risk factors for more severe reactions later)
• Lipid Transfer Proteins (LTP’): resistant to both digestion and heating, and more likely to cause systemic and serious reactions

These plant food allergens all share structural and functional similarities with pollen allergens, which is how they trigger allergic symptoms. They are all present in a very wide variety of plants and are therefore also known as ‘panallergens’.

Although these 3 types of allergens are though to cause most pollen food-related allergies, a fourth category of allergen has also been linked to pollen-food allergies—cross-reactive carbohydrate determinants (CCD). These are glycoproteins (protein molecules that have carbohydrate groups attached to them) that are able to bind to IgE antibodies and can cause wide-ranging cross-reactivity with different plant species—they exist, for example, in birch, ragweed, celery, tomato, peanut and potato.

Although some researchers do not believe that they actually cause any symptoms, people, especially those with pollen allergies, do produce antibodies against CCDs and there are cases where reactions to foods such as celeriac, persimmon, courgette and tomato have been reported to be caused by CCDs.

New types of allergen are also being discovered, like the snakin/gibberellin-regulated proteins found in cypress pollens that seem to cause mainly mild oral allergy symptoms when people eat fruit like peaches, oranges and apricots, but can also cause rashes and swelling. Their importance may grow in the future, as the prevalence of pollen-food allergies increases.

Of all the allergens, lipid transfer proteins (LTPs) are the ones you least want to be sensitised to.

LTPs can be found in just about every plant, they are resistant to digestion and they are impervious heating, which means that they can still be found in a wide range of processed foods from apple sauce and tomato paste to beer and wine.

The symptoms caused by LTP proteins range from mild contact rashes to potentially life-threatening anaphylactic reactions, and some people with LTP sensitisation can show no symptoms to food.

As LTP proteins are more likely to provoke severe reactions, it’s only natural that, when looking at allergen-specific test results, many doctors will concentrate on the potential danger of those allergens and dismiss the profilin and PR-10 allergens as being ‘clinically irrelevant’.

But just because certain allergens are described as harmless 99% of the time doesn’t mean that you can assume you’re safe.

Although PR-10 proteins and profilins tend to be vulnerable to heat and digestion, meaning that majority of PFS-sufferers get symptoms limited to the mouth and face and can tolerate plant food after cooking it, that’s not always not the case.

A 2023 review of data from the European Anaphylaxis Registry found 3,427 cases of food-induced reactions registered by 10 specialised allergy centres in Europe and Brazil, and reported that celery and soy were both common triggers for anaphylaxis, notably in Germany, France, and Switzerland. Because nearly all of the patients also suffered from hay fever, the researchers concluded that the birch-pollen related PR-10 protein was probably responsible for the reactions.

Their claim was supported by a 2021 study involving anaphylactic patients registered in Berlin which revealed a high sensitisation rate towards pathogenesis-related-10 protein.

Certain foods are involved more often than others in these, more serious, reactions.

Celery; Celery PR-10 proteins and profilins are not completely vulnerable to digestion and this, coupled with the heat-and-digestion-resistant LTP allergen present in its stalk, helps to explain why raw celery can cause systemic reactions and anaphylaxis in pollen-allergic people and has caused (at least) one case of anaphylaxis in a woman who was undergoing oral immunotherapy treatment to try and cure her allergy to birch and grass pollen.

Additionally, celery’s profilins and CCDs are not completely vulnerable to heat and, although the PR10 protein unravels when it’s heated, it partly regains its structure as it cools. Therefore boiled celeriac can also cause (delayed) reactions.

Carrot; Carrots also cause reactions other than OAS, including throat swelling, bronchospasm (contraction of the airways), contact rashes and anaphylaxis in the pollen-allergic.

In a Swiss study specifically investigating carrot allergy, 26 people with a history of allergic reactions to carrot were given an oral food challenge with a carrot drink. 16 of them reacted with OAS and 4 had systemic reactions. The patients’ medical history, however, revealed that 14 had had systemic reactions in the past. Skin tests showed that all of them were sensitised to the pollen of birch, alder and hazel, 80% to grass pollen and 40% to mugwort. Blood tests showed that 17 (85%) of them were reacting to the PR-10 carrot protein Dau c 1 and 4 (20%) to carrot profilin.

Dau c 1 is also able to withstand digestion and cooking and boiled carrot has been shown to produce delayed reactions (eczema).

Soy; Soy often causes problems for people allergic to birch pollen. Soy-induced symptoms range from skin and gastrointestinal symptoms to breathing problems (1) and anaphylaxis.

A Swiss study specifically investigating soy allergy had 25 pollen-allergic people with a history of soy allergy undergo a food challenge with soy-containing chocolate bars. All of them reacted. 12 with subjective symptoms (like OAS or stomach pain) and 11 with objective symptoms ranging from hives to a decrease in blood pressure. The other two did not react to the chocolate bar but did react to a soy drink, one with OAS and a feeling or tightness in the chest and the other with OAS, facial swelling and itchy, red eyes. Soy-based drinks are particularly problematic for people with PFS. (see Risk factors for more severe reactions later)

Hazelnut; In the Netherlands, researchers recruited 21 people with a history of just mild symptoms to hazelnut and/or apple and 21 people with a history anaphylaxis to those foods to try and determine differences between the two groups. They found that people who suffered from anaphylaxis were more likely to be sensitised to the more ‘benign’ PR10-proteins than the more ‘dangerous’ LTP proteins.

In another study, 161 Dutch adults and children who either had objective symptoms (e.g. hives, vomiting, diarrhoea, wheezing) during a food challenge (DBPCFC) or had a convincing history of hazelnut allergy were given blood tests to try and determine the specific allergens that they were allergic to. 13% of the children and 49% of the adults were found to be exclusively sensitised to the hazelnut PR-10 protein.

This PR-10 protein has been shown to be resistant to heat under 100 °C, and even when hazelnuts are roasted at 140°C, some birch-pollen-and-hazelnut-allergic people still get symptoms, although they are generally mild.

Ultimately, whether you’re allergic to so-called benign allergens like PR-10 proteins, profilins or CCDs, or the more worrisome LTP allergen, all of them are responsible for a spectrum of symptom severity ranging from mild to severe.

You can be sensitised to more than one type of allergen.

Cases of polysensitisation are being reported more often. And, although you may have to worry about a wider range of fruits and vegetables, it does seem to have its benefits; several studies have revealed that being co-sensitised to the more benign allergens—PR10 and profilin—often provides a ‘protective effect’ against the more severe reactions brought on by allergies to LTP proteins or seed storage proteins, with people who are simultaneously sensitised to LTP, PR-10 and/or profilin proteins being much more likely just to suffer from oral allergy syndrome.

This provides a possible explanation for why PFS sufferers in northern and central Europe often seem to have less severe reactions to food than their southern European counterparts. People who live in northern and central European countries, when they are sensitised to LTP allergens, also tend to be co-sensitised to birch pollens, particularly the powerful Bet v 1 allergen, a PR-10 protein, as well as Bet v 2, a profilin protein, which cross react with the corresponding proteins in plant food. People with LTP allergies who live in the Mediterranean region, by contrast, tend to be mono-sensitised to LTP allergens and have no birch pollen around to provide them with a protective blanket.

A protective effect has also been shown for grass pollen against birch pollen-induced symptoms, with people who are allergic to both grass and birch pollen being less likely to show symptoms of food allergy. The thinking is that the grass-specific IgE antibodies bind to immune system (mast) cells and take those spots away from the birch-specific IgE antibodies, effectively blocking the latter from provoking symptoms when they come into contact with food allergens that would otherwise trigger a reaction.

The same kind of thing could be behind the protective effect of birch-related proteins in northern and central Europe, with the potent pollen taking up the resources of the immune systems of PFS-sufferers and hampering a substantial immune response to LTPs.

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Risk factors for more severe reactions

Peach, apple, peanuts, tree nuts and mustard have all been associated with higher rates of systemic reactions in people with PFS.

The following factors have also been identified as risk factors for systemic reactions:

• multiple pollen-related food allergies
• history of a systemic reaction to a plant food
• reactions to cooked forms of the food
• positive skin prick test results with a commercial allergen extract of the food
• strong positive responses on skin tests to pollen

In fact, many of these factors imply an allergy to an LTP allergen. But there are other risk factors which do not.

Pollen season

Symptoms of pollen food syndrome can occur at any time of the year but, as several studies have found, they can be worse during the season of the specific pollen that is causing the allergy.

Danish researchers curious about the effects of the pollen season on birch-pollen allergic patients carried out oral food challenges on people allergic to apple before and during birch pollen season and reported that their patients’ symptoms were worse during the birch pollen season, and that their apple-specific IgE levels were higher. A separate study noted that Danish adults who suffered from hay fever were 4 times more likely to have reactions to pollen-related foods than adults who were sensitised to pollen but free from symptoms.

A Swedish study of birch pollen-allergic people reported that those who were who were also allergic to nuts and apples had more symptoms during the birch and hazel pollen seasons, and another reported that the number of cases of food-related anaphylaxis among pollen-allergic Swedish children increased during the tree pollen season.

A British study revealed that hospital admissions for food-induced anaphylaxis in England tend to peak around June (22% higher than January), especially among children younger than 15 years, and that this seasonal peak was associated with birch, ash, willow and elm pollen. However, it was an allergy to the pollen of ash, oak and ragweed that was associated with the highest risk of severe reactions, with even low-level exposure to ragweed leading to an increase of food-related anaphylaxis hospitalisations.

In France, 2 cases of anaphylaxis were reported in patients who were allergic to the PR-10 allergen in hazelnut. The patients both suffered body rashes and stomach pain, one had asthma and both ended up unconscious. Both had eaten hazelnut without problems before but, at the time of the attacks, one had severe asthma, the other was suffering from stress, and both had been exposed to large amounts of birch pollen.

A Spanish study noted that people who are sensitised to allergens which normally produce mild symptoms are more likely to have severe reactions to pollen-related plant food if they are exposed to large amounts of pollen.

A Japanese study reported that soy-allergic adults were more likely to show symptoms during or after the (birch) pollen season and a study of 273 PFS-suffering Koreans reported that 9.9% of them had had anaphylactic attacks and that the attacks were significantly associated with the strength of the person’s sensitisation to pollen.

And Dutch researchers revealed that people who are allergic to soy can suffer more severe reactions during birch pollen season, even when they are primarily allergic to soy allergens that are not related to pollen. Their report describes the case of a 26-year-old Dutch woman with a primary allergy to soy whose symptoms worsened considerably during birch pollen season when she ate processed soy products (i.e. products containing allergens not connected to birch pollen). Although she could tolerate small amounts of those products outside of the pollen season, if she ate them during the season, she experienced symptoms including PFS, gastrointestinal symptoms and, on two occasions,anaphylaxis.

Worsening allergic reactions to pollen-related foods during the pollen season fits in with the idea of immune system ‘priming’, which was put forwards in the 1960s and was used to describe the phenomenon whereby people who are allergic to pollen tend to experience worse symptoms (and with smaller doses of allergen) at the end of the pollen season than at the start. Basically, during the relevant pollen season, the immune system of a person with pollen food syndrome may be more active and therefore ‘primed’ to produce more immune system chemicals like histamine to smaller amounts of food allergen.

Volume of plant food

The most common problem involving the more ‘benign’ allergens seems to be the consumption of large amounts of plant food all at once.

For example, there is the case of a 16-year-old girl with a known allergy to the peanut allergen Ara h 8, a PR-10 protein that is normally regarded as harmless. When she was initially diagnosed, she passed an oral food challenge to peanut and, for 3 years, she ate regular amounts (30 to 40 g) of peanut without having any symptoms. But one day, she she skipped lunch and had a large amount (300 g) of roasted peanuts instead, which led to her having an anaphylactic attack. Afterwards, she resumed eating small amounts of peanuts without any problems.

Another report describes the case of a 30-year-old woman who suffered from hay fever and asthma and ate a meal containing apple, kiwi, peach, pear and pepper and drank a juice containing carrots, lemon and orange. Too many plant foods all at once led to a serious systemic reaction.

And there is the case of a patient with an allergy to sunflower pollen who had an anaphylactic after eating lychee fruit, which happens to contain lots of profilin.

Supplements can also be a source of too much plant protein, according to this study which investigated the reactions of 20 people to a dietary food product made up of 50% soy protein. 18 of the 20 patients—none of whom had reacted to soy before—had had allergic reactions within 10-30 minutes of having the meal replacement shake. The most common reactions were OAS and facial swelling, but some of them had serious systemic reactions that required medical treatment and, in 4 cases, hospitalisation for further monitoring. The other 2 patients had delayed reactions. Blood tests showed that 18 of them had very high levels of IgE antibodies against the bet v 1 birch pollen allergen and that they were reacting to the equivalent protein (Gly m 4) in the soy.

When it comes to serious reactions to otherwise ‘harmless’ allergens, drinks are a particular problem. There are multiple case reports of people having systemic reactions, including anaphylactic attacks, after drinking apple juice or drinks containing courgette, celery and, notably, soy.

It’s not uncommon for people who react to soy drinks to be able to tolerate other minimally processed soy products, such as tofu or edamame beans. For them, it’s the quantity of soy protein that matters, and the fact that drinking it in allows a rapid intake of large amounts of protein that mostly bypasses digestion before quickly reaching the intestines where it is absorbed into the bloodstream.

Additionally, soy drinks may also raise the stomach’s pH, which decreases the rate of soy digestion meaning that more intact allergen can be absorbed in the gut and cause an allergic reaction.

In a similar vein, fasting is also a risk factor for more serious allergic reactions to food, this time because an empty gastrointestinal tract is thought to encourage the rapid absorption of food allergens into the bloodstream.

People with pollen-food allergies are advised to avoid juices and smoothies that contain fruit and vegetables that they are allergic to. Especially on an empty stomach.

Amount of food processing

Another important consideration is how much processing the food products have undergone; more processing often means less allergen content.

As far as soy is concerned, soy-based drinks, such as soy milk, contain minimally processed soy, and thus a high amount of allergenic soy protein. But food processing often involves heating, and the pollen-related soy allergens— Gly m 4 and Gly m 3—are vulnerable to heat. The soy in other foods such as tofu and soy sauce is hydrolysed (broken down using water) proteins, so there is only a minor amount of protein remaining in many processed foods.

A study investigating the effect of processing on birch-pollen allergic people interviewed 94 people about their reactions to soy in everyday life, and gave 16 people oral food challenges with a soy-based drink. Of the 94 people interviewed, 66 had knowingly consumed soy products and around 1 in 10 had experienced OAS as a result, most to soybean sprouts, soy milk or drinks containing soy protein isolate, a couple to tofu and soy protein–based sausage and a couple more to bakery products containing soy. Of the 16 people who underwent the food challenge, all had OAS and 6 had more serious reactions, including hives, throat tightness or swelling and mouth blisters. Most of those people’s history of reactions to soy included symptoms worse than OAS, including anaphylaxis.

Finally, the researchers also tested a range of soy products bought from various manufacturers and supermarkets and measured their Gly m 4 protein content, finding the most in dietary powders and soy drinks, low amounts in soy flakes, tofu and textured soy protein, a still lower amount in a soy-containing candy bar, and finally nothing in highly fermented soy foods like soy sauce and miso or strongly heated foods like roasted soybeans and beans that had been cooked for 4 hours.

Cofactors

Some people’s reactions are caused or worsened by so-called cofactors. These include things like exercise, alcohol and medications—notably nonsteroidal anti-inflammatory drugs (NSAIDs)—as well as stress and lack of sleep.

Cofactors seem to work by decreasing the amount of food you need to eat—in technical parlance, lowering the threshold of allergen needed—to provoke a reaction, often by speeding up the absorption of the allergens into the bloodstream or inhibiting proper digestion of said allergens.

For example, exercise and alcohol and NSAIDS are thought to increase gut permeability. Not only does this allow more of the allergen to pass through, it also allows it to go through quicker and, since pollen cross-reactive proteins often degrade in the stomach and intestine, anything that speeds up the process will leave the allergen more intact and able to provoke a reaction.

Certain medications taken to treat ulcers—such as H2-receptor antagonists and proton pump inhibitors—can also increase the pH of the stomach which impairs digestion and thus the destruction of the allergen.

Cofactors can work together to worsen reactions, as described in this German case report, where a patient suffered anaphylaxis after doing some exercise and following it with a buffet breakfast containing a lot of fruits and vegetables. Testing later showed that she was strongly allergic to the LTP allergens in peach, apple and mugwort, as well as walnut, hazelnut and wheat.

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How is pollen food syndrome diagnosed?

A diagnosis of PFS—as with all food allergies—will primarily be based on your clinical history, a record of consistent symptoms following the consumption of certain pollen-related foods. This will require you to provide your allergist with answers to questions about your general medical background (including any other allergies you may have—notably, hay fever, eczema—and any relevant illnesses in your family) and your dietary history (what you ate to provoke your symptoms, what those symptoms were, how long they lasted, whether you had exercised or taken painkillers and many other details). Your clinical history will determine which tests your doctor asks for to help come up with a diagnosis.

LINK to CONTROL_Clinical History

Immediate symptoms

Pollen food syndrome is difficult to diagnose. Most people with pollen-food allergies are sensitised to more than one inhalant allergen which makes the range of potential cross-reactions very broad and difficult to trace back to a specific pollen. Geographical variations in likely irritants and different nutritional habits add to the complexity. This makes the clinical history especially important—anything you can tell your doctor to help them narrow down the possibilities will be very helpful.

The first step that will probably be taken to try and confirm any allergies the doctor suspects based on your description of your symptoms is a skin prick test. In the case of PFS, a standard skin prick test using commercially-made allergen extracts may not be viable. When it comes to plant-derived food allergens, commercial skin test extracts tend to have a low sensitivity, which can lead to a high rate of false negative results.

This can be for several reasons:

• most commercially available extracts are not biologically standardised and do not necessarily contain all the relevant allergens—i.e. minor allergens and/or heat-unstable ones that are destroyed during the process of making the extracts (and happen to be those that most commonly cause PFS)
• allergens in the extracts can deteriorate during storage
• not all relevant sources of food allergens are commercially available and those that are can be very expensive

As such, if a skin prick test is done and produces a negative result, if you have a history of allergic reactions to a food, the doctor may try to perform a prick to prick test, which uses the natural food.

This test involves pricking the raw or cooked fruit or vegetable with a lancet and then immediately pricking your skin with the same lancet. It is more sensitive than the skin prick test and tends to produce more reliable results when it comes to testing for allergy to many fruit and veg like apple, orange, peach, cherry, tomato, carrot and celery. It also has excellent negative predictive value —that is, if you get a negative result, you are very likely not allergic.

Prick-plus-prick tests can also be carried out with a meal when the mystery food that is causing the problem is lurking in an original recipe, as in this case where a man suffered intense oral allergy symptoms after eating a certain sandwich at a certain restaurant, but not when eating similar sandwiches at other eateries. A thorough history helped the allergist to determine that it was the mojo sauce on the sandwich that provoked the symptoms, and prick-plus-prick testing with the whole sauce and its constituent ingredients, as well as pollens, followed by food challenges, enabled the culprit food (orange) to be identified.

There are limitations to prick-plus-prick testing, including:

• a high rate of false-positive results without clinical relevance
• its dependence on the availability of the fresh food in question
• the lack of standardisation in terms of allergen content, which can vary according to cultivar used, its ripeness and storage conditions
• possible irritation that can mask the allergic reaction when, for example, a spice is tested

In some cases, skin testing with commercial extracts is actually preferable:

• to test for sensitisation to tree nuts and legumes like hazelnut, peanut and pea, which all contain stable allergens (the processing used to make commercial extracts may inadvertently enrich them with stable allergens)
• to test for sensitisation to foods that might be irritating to the skin, like mustard, or difficult to prepare
• to help assess the risk of systemic reactions—testing positive to a commercial extract suggests that you are sensitised to a potentially dangerous allergen that is resistant to digestion and/or heat
• to confirm a pollen sensitisation—skin prick tests have been shown to be very reliable when it comes to testing for aeroallergens (if you don’t show any sensitisation to pollen, you may be dealing with a primary allergy to a food, which could put you at higher risk for systemic reactions)

Sometimes, a blood test will be ordered. This can happen in the following circumstances:

• the case history and skin tests are not giving clear or consistent results
• the food is not suitable for skin testing (like a hot spice)
• the person with the allergy has had a serious reaction in the past
• skin testing is not possible, for example because of a skin condition like eczema or dermographism, or because the person cannot stop taking antihistamines
• the patient is a very young child

For more specific information, a component blood test—aka Component Resolved Diagnosis (CRD)—can be done. Instead of just testing your blood using an extract of whole foods, this test can also measure the reaction of the IgE antibodies in your blood to specific allergens.

This can be useful in trying to predict the potential severity of reactions—for example, if you’re allergic to peanuts and your blood component test shows that you have a sensitisation to Ara h 2 (the LTP protein), you’re more likely to have a systemic reaction than if you’re just sensitised to Ara h 8 (the PR-10 protein), in which case you’re more likely to suffer from oral allergy symptoms.

Similarly, if you’re allergic to hazelnuts, a sensitisation to the birch cross-reactive Cor a 1 allergen means that you’re more likely to experience mild oral symptoms, but a sensitisation to Cor a 9 and/or Cor a 14 means that you’re more likely to have systemic reactions.

Knowing which allergens you’re sensitised to could determine how to manage your food allergy: being sensitised to an LTP allergen would indicate that you will probable also react to cooked forms of the food, and therefore would be better off avoiding it altogether.

However, CRD is not yet considered a routine diagnostic method and it’s not comprehensive; the most widely used tests neither contain all of the identified allergens, nor are they universally available.

Just because you’re sensitised to a food does not necessarily mean that you are allergic and will have symptoms when you eat it. Sensitisation does not equal allergy. Skin and blood tests have a tendency to reveal sensitisations to cross-reacting allergens that don’t actually produce any symptoms—so-called ‘silent sensitisations’.

Similarly, although a higher level of IgE to birch allergens can mean that you are more likely to have symptoms when you eat related foods, that’s no guarantee that you will. Eliminating foods based on lab tests alone, therefore, will result in unnecessarily restrictive diets.

The only way to know for sure whether you’re allergic to any food is to undergo an oral food challenge. This involves eating a very small amount of the offending food, waiting for a reaction, and then doing it again, gradually increasing the dose until a reaction occurs or a maximum dosage is reached. This can take around 4 hours. Because of the risk of severe reactions, this kind of challenge should only be done by an experienced consultant in a medical setting.

Oral food challenges are generally undertaken either when someone’s history and their test results disagree (i.e. they have negative tests results but their history strongly suggests an allergy, or vice versa).

Practically speaking, most people do not undergo this kind of test since it requires a lot of time and resources, and if you only have mild symptoms like oral allergy syndrome—which is also of a subjective nature and therefore difficult to ‘prove’ during a test—you probably will not be asked to undertake a food challenge. However, if you have systemic and potentially dangerous symptoms, a thorough evaluation will be required, especially if it’s not clear with food(s) provoke them.

Delayed symptoms

It’s also possible that you have a delayed allergy to food, in which case, tests looking for IgE antibodies will often give negative results as IgE antibodies are often not involved in these types of reactions.

Before trying to provoke a reaction with a food challenge, you may first be asked to undergo an atopy patch test (APT). This generally involves carrying a small amount of fresh food, pulped or in a solution, in a tiny aluminium chamber taped to your back for 48 hours, and getting a skin reading at 48 hours and 72 hours.

Patch test have been shown to successfully detect delayed reactions to, for example, apple and celery in people with pollen allergies.

While skin tests may provide an indication of sensitisation, they cannot diagnose a food allergy; that has to be done with an oral food challenge. First, an elimination diet will be needed to see if the symptoms disappear. If so, the first step towards a diagnosis will involve reintroducing the suspect foods one by one into the diet to see if the symptoms return. If they do, the allergy can be provisionally diagnosed and the food can then be eliminated from your diet to see if there is a persistent improvement in your health over the coming months.

If eosinophilic oesophagitis is suspected, an upper GI endoscopy (aka an oesophagogastroduodenoscopy) and biopsies will also be required to look for specific levels of eosinophils in the oesophageal tissue (15 or more eosinophils per high-powered field, to be precise) and make a formal diagnosis.

Ultimately, by the end of your testing period, your doctor should be able to tell you whether you have:

1. a relatively benign form of pollen food syndrome, with mild symptoms brought on by an allergy to allergens that are vulnerable to digestion and/or heat, so can be treated by, for example, heating your food
2. a more serious form of PFS with systemic symptoms provoked by an allergy to more stable allergens in foods that you can best avoid eating
3. a primary allergy to a plant food where OAS have been the predominant or only initial symptoms, but could progress to more severe ones

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The bottom line

Oral allergy syndrome is a set of mild symptoms generally limited to the mouth, throat and face that can be brought on by any type of food and can sometimes be the first step of a more severe reaction.

Pollen food syndrome is a secondary food allergy that can manifest with oral allergy symptoms but can also result in more severe reactions, including anaphylaxis.

***They are not the same thing.***

It’s important to know which type of allergy you have. You can hugely help your doctor to help you by giving them as detailed an account of your clinical history as possible—exactly what you ate and drank, in what circumstances (did you take medications, do exercise, not sleep well etc.), and exactly what your symptoms were and when how long they took to develop.

Ideally, you will have a doctor who is up to date on the subject and who is prepared, on the basis of your clinical history and test results, to have a ‘tailored discussion with [you about the] risks of reaction, severity of reaction, and potentially cross-reactive foods’. And is ready to prescribe an adrenaline auto-injector when it’s appropriate.

Unfortunately, you may find yourself in the dubiously impressive position of knowing more about the difference between OAS and PFS than your doctor.

However, now you know that:

• If you’re allergic to pollen and have symptoms that are not just restricted to your mouth area, you may have a more serious version of PFS and you shouldn’t listen to people who tell you just to cook or peel your fruit and veg and everything will be OK
• If you don’t have hay fever symptoms and/or you get oral allergy symptoms after eating a non-plant food, you know that you might have a potentially more serious type of food allergy, and you should try to avoid the food that provokes the symptoms until you can get a professional diagnosis
• If your doctor tells you that your itchy mouth is nothing to worry about because people with OAS just have a harmless allergy, you know your doctor has not had time to keep up to date on their alleged specialist subject. You might want to get a second opinion

Food allergy is a messy and complicated business. Don’t accept generalised assumptions and statements about what applies to the average person. What applies to one person may not apply to you. Believe your own symptoms. If you suffer from moderately bad or severe symptoms after eating plant food, avoid the food that ails you and try to get a (scientific) diagnosis that’s tailored to you.

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