While the most common asthma inducing allergen in NZ is dust mite faeces, In Australia, pollen is a major problem.
Pollens are known allergens. The articles that follow indicate just some aspects. To prevent pollen contamination of your home, an air filtration system must be added to the Cleanaire HRV (if allergies are an issue).
It is generally recognised that common Pollen grains measure 2 microns and larger in size.
An EU4 grade Air Filter is often referred to as a “pollen filter”.
Air Filtration is a specialised subject. If you have a particular reason to require air filtration, study this website, then ask your Cleanaire dealer for recommendations.
This article from “THE BULLETIN” (Sept 1996) gives interesting information to those who suffer from pollen allergies…
Gardens for sneezers and wheezers
Allergy-free zone: A new book advises on how to make your garden a haven from hay fever
BY DIANA BAGNALL
THE POLLEN SEASON HAS OPENED, but this won’t be news to those who wheeze, sneeze, sniffle and itch from now through until April, when the season closes. About 1.4 million Australians suffer from asthma and a similar number of people endure hay fever and skin rashes. Many of these find that their health is affected simply by going out in their own backyard.
About half of all asthmatics who have a skin-prick allergy test show up as allergic to grasses or pollens or something in the garden. Medication helps, of course. But Sydney doctor and journalist Mark Ragg offers a supplementary line of defence against the plant kingdom in his new book called The Low Allergy Garden.
Certainly, designing such a garden presents some constraints, but any garden is limited in scope, whether by size, slope of the ground or soil type. What has been lacking until now is easy-to-digest information about which plants do and don’t worsen asthma, hay fever and skin rashes.
Culpable: The main plant allergen, pollen, needs a little understanding. Not all pollens are equally culpable. The major cause of allergies are light, wind-borne pollens that are produced in huge quantities and are small enough to he inhaled, to lodge in the lung and set off an allergic reaction. While most pollen falls only a few metres from the plant that releases it, pollen travels much further on windy days. Many trees and shrubs, all weeds and grasses and some flowers produce wind-borne pollen. The main flowers to avoid, advises Ragg, are from the A.steraceae family, which includes daisies, chrysanthemums, calendulas, asters and marigolds.
Plants that are pollinated by birds and insects, on the other hand, produce sticky, heavy pollen particles which are generally too big to fit into human airways. These plants have large, showy flowers, so the rule, according to Ragg, is, go for show! Most grasses, and consequently most lawns, are highly allergenic. For those starting a lawn from scratch, the most suitable grasses are buffalo, “Greenlees Park” couch, kangaroo and rice grass. An alternative is to pave and plant a low growing perennial among the stones. For those who already have a lawn, Ragg suggests mowing regularly, before the grass goes to seed, and mowing while the grass is damp. In fact, people with allergies should always garden early in the morning before the dew disappears. Most grasses release their pollen a couple of hours after sunrise. The pollen rises and sits in a layer 50 centimetres to 2 metres off the ground.
Herbs, vegetables and ground covers all get the thumbs up in a low-allergy garden. But there is a big swag of shrubs and trees that don’t pass muster. Some are suburban favourites, such as birch, liquidambar, cypress, plane and willow. Olive, mulberry and walnut trees are also dodgy. But the uncontested villain of the piece is the privet, once commonly planted as a hedge but now recognised as a noxious weed. Ragg’s tip: “Be vicious with privet. Have no mercy.”
The experts disagree about whether composting and mulching should be part of a low-allergy garden. Some say the mould spores and pollens harboured by organic mulches may worsen asthma and hay fever. Others argue that if you mulch, you dig the garden less often, use less fertiliser, spend less time working in the garden, and fewer weeds grow. Weeds not only look ugly, they act ugly. Plantain, the ugliest of all, is highly allergenic and flowers for up to nine months of the year in some parts of Australia and New Zealand.
Life-threatening: Apart from the plants that may cause allergies because of their pollens, there are some plants that cause problems on touch. Contact dermatitis may be just a rash, but can produce a fever and is sometimes life-threatening. In general, plants that cause contact dermatitis are hairy or sticky and frequently have soft stems. Some have spikes, and others have milky sap. Among them are such common flowers as the marigold, common ivy and primula. And just in case your chest and nose are not already telling you, there are 16 trees scattering their pollen through September. Here’s hoping for a still spring.
The following are articles from issue 91 of the New Zealand publication “Allergy News”
What is Allergic Rhinitis?
By Dr Vincent St Aubyn Crump Auckland Allergy Clinic
Rhinitis means inflammation of the nasal lining or mucosa. It is characterised by chronic or recurrent sneezing, rhinorrhea (runny nose) itchy and blocked nose, which may he labelled as allergic when an allergen is identified. The most well known form of rhinitis is the common cold, which is infectious rhinitis due to a virus.
The hallmark of allergic rhinitis is the temporal relationship of symptoms on exposure to an allergen. Your nose, is not the only organ that may be affected in allergic rhinitis. You may have itching of your eyes (allergic conjunctivitis), throat and ears.
How common is allergic rhinitis?
Allergic rhinitis is estimated to have a prevalence of up to 40% in the New Zealand and Australian populations.
From the recent ISAAC Study (using a standardised epidemiological method to survey the prevalence of allergic rhinitis in over 460,000 children aged 13-14 years from 155 centres in 56 countries worldwide) the prevalence varies from 1 .4% to 39.7% worldwide. The lowest prevalences are found in parts of Eastern Europe, South and Central Asia. High prevalences are reported from centers in several regions, including Canada, Australia, New Zealand, the United States and the United Kingdom. The overall mean prevalence is 13.9% and nearly half of those studied had concomitant asthma or eczema. Areas with a low prevalence of rhinitis tended also to have a low prevalence of asthma and eczema.
There is mounting evidence of a rise in the prevalence of allergic diseases, including rhinitis, over recent decades. Lifestyle factors may be important given the high prevalence of rhinitis and other allergic diseases found in westernised English speaking countries.
What is the mechanism of allergic rhinitis?
Allergic Rhinitis is a hypersensitivity response to specific allergens, in sensitised patients, that are mediated by IgE antibodies in the blood. Sensitised patients with allergic rhinitis have IgE antibodies for specific allergen(s) hound to receptors on the surface of mast cells. On re-exposure to the specific allergen(s), cross-linking of adjacent IgE molecules occurs, and mast cell degranulation (rupture) takes place, releasing a variety of chemical mediators that may be preformed (histamine) or newly synthesized (leukotrienes, prostaglandins).
Histamine causes the cardinal symptoms of allergic rhinitis including sneezing, nasal itching, and runny nose. The nasal congestion is more due to leukotrienes than to histamines. Hence, antihistamines are not very good at relieving nasal congestion. A large number of patients with allergic rhinitis will have an increase in sensitivity to allergens after repeated daily exposure; an effect called ‘priming’ At the start of the pollen season, comparatively large doses of pollens are needed to trigger an allergic response but toward the middle and end of the season, patients become extremely reactive to even small amounts of pollen.
How is allergic rhinitis diagnosed?
It should be ascertained whether the allergic symptoms are seasonal or perennial. The exact month of the year that symptoms start could give a clue as to the specific type of pollen involved.
The tree pollen season starts in late winter and usually ends before the grass pollen season in spring. ~1’he weed pollen season overlaps with the grass season, usually starting in late spring and extending through to end of summer.
Patients who are allergic to their pets will often deny obvious symptoms related to contact with their own pets. This is due to some sort of tolerance developed due to continuous exposure to the allergen. If they were to go away for a two week vacation, they might notice immediate symptoms upon their return.
The predominance of nasal symptoms on waking may suggest the diagnosis of house dust mite allergic rhinitis.
Pale, bluish, swollen mucosa (lining).
Skin Prick Test
Should be performed to identify the specific allergen(s) involved, so that the correct avoidance measures can be recommended.
The skin prick test is a sensitive, simple and cheap diagnostic technique.
How is allergic rhinitis treated?
Broadly speaking there are three main options in the treatment of allergic rhinitis.
Total eradication of the allergen is usually not possible, but measures to reduce the allergen in the local environment should be encouraged. The measures to be used will differ depending on the nature of the allergen.
Pollen particles are part of the reproductive mechanism of plants and are an environmental contaminant, which are difficult or impossible to eliminate. Measures which can help to reduce the exposure, include:
Keep windows in cars and buildings shut
Wear glasses or sunglasses
Avoid open grassy places, particularly in the evening and at night
Use a car with a pollen filter· Check the pollen count in the media
During the peak season take your holidays by the sea or abroad
House dust mite
House dust mites are found in mattresses, pillows, bedcovers, carpets and soft furnishings throughout the home. Optimal conditions for mite growth is achieved through well-insulated, centrally heated homes!
Mattress/bedding barrier intervention has been shown to reduce mite allergen levels and improve clinical symptoms of both rhinitis and asthma.
The major cat allergen is a salivary protein, which is preened on to the fur where it dries into flakes, which become airborne for many hours and are very respirable.
Families with atopic (allergic) members should be advised against furred animals in the home. Psychological factors may render dogmatic statements about removal of a family pet unwise.
Where removal of a pet is not possible, advice can be given to confine the animal outside the house.
Recent studies have suggested that washing the cat (once weekly) when combined with other cleaning measures may effectively reduce airborne cat allergen levels in the home.
Patients need drugs for allergic rhinitis if avoiding the allergen is impossible or fails to control the symptoms.
In recent years, the mainstay of treatment for allergic rhinitis has been the use of topical corticosteroid nasal sprays, and the newer non-sedating antihistamines. These may be highly effective when used either alone or in combination.
Topical sodium cromoglycate represents an alternative anti-inflammatory agent to corticosteroids, particularly in young children.
Topical anticholinergic drugs (e.g. atrovent) and decongestants may have a part to play in defined circumstances.
Corticosteroids and sodium cromoglycate affect the underlying allergic process and should be used as first line treatment for most patients. Compliance may be a problem with cromoglycates, as they need to be used 3-6 times per day.
Antihistamines and decongestants simply relieve symptoms.
Topical decongestants should not be used for more than 3 days because of rebound congestion.
Immunotherapy is the subcutaneous injection of increasing doses of the identified allergen(s).
Both seasonal and perennial allergic rhinitis may, in general, be effectively managed with a combination of allergen avoidance measures plus topical corticosteroids and oral non-sedating antihistamines. There remains a small group of subjects who, despite regular use of medication, continue to have marked symptoms or unacceptable side-effects from their medication.
These patients should be offered immunotherapy.
Pollen Cross Reactions
By Dr Vincent St Aubyn Crump Auckland Allergy Clinic
In an allergic reaction antibodies are produced that are specific to each individual allergen. In other words the antibody should bind to only one type of antigen (allergen), like a tailor-made glove. Occasionally, gloves designed for one particular hand will fit another person’s hand that is of similar size and shape. Similarly, most grass pollens are of similar size & shape & will have areas that are almost identical. So antibodies produced against the ryegrass pollen will Birch cross-react with timothy grass. Grass pollens are quite different from tree pollens; therefore there is not much cross-reaction between grass and tree pollens. Trees in the Birch family, Berulocene (silver birch, alder & hazel) cross-react Grass with each other, but very little with other trees & not with grasses. In New Zealand the silver birch is probably the commonest tree pollen causing ‘hayfever.
Pollen Cross-Reactions with Foods
There are also some fruit & vegetables that have similar & sometimes identical molecular appearance to pollens, and the antibodies produced against these pollens will cross-react with the fresh fruits & vegetables, mistaking them for pollens.
For the majority of hayfever sufferers, cross-reaction to foods are very mild and affect the mouth only, the so-called Oral Allergy Syndrome (OAS).
|These are some known cross-reactions, with the most commonly implicated fruits & vegetables listed first for each pollen:|
Oral Allergy Syndrome
Symptoms of OAS may include itching or swelling of the lips, tongue, throat, or roof of the mouth. Heating or digestion usually destroys the allergens causing these reactions. Therefore affected individuals can usually eat fruits or vegetables that have been cooked, baked, or canned.
OAS was first described in 1942 for apple & hazelnut, in patients allergic to birch pollen. Since then many other kinds of allergic reactions to various fruits and vegetables have been described in association with pollen allergy.
Allergy to fruits and vegetables occur most frequently in hayfever from birch allergy. In one study 35% of subjects with birch pollen allergy had positive skin prick tests to fresh fruits & vegetables. Another Scandinavian study, based on 2626 hayfever subjects, found 63% of birch allergic patients presented with allergy to one or more fruits or vegetables. A similar finding was reported in Austria, where more than 75% of birch allergic patients complained of allergic symptoms after eating apples.
It is important to differentiate OAS from Food Induced Anaphylaxis. IgE antibodies cause both reactions, but anaphylaxis is a much more severe food allergy. Anaphylaxis is usually a generalised reaction, which could include hives, breathing difficulty, swelling of the face and hands; wheezing or loss of consciousness. The foods commonly causing anaphylaxis include peanut & nuts, fish & shellfish, eggs and milk. However, some foods, particularly celery, seeds, or nuts, can cause either anaphylaxis or DAS.
Diagnosis of Oral Allergy Syndrome
The clinical history of oral symptoms occurring when a patient with hayfever eats fresh fruits or vegetables is almost certainly OAS. The diagnosis is confirmed with a skin prick test, preferably using fresh fruits & vegetables, as the commercial extracts are very unreliable for fruits & vegetables. RAST can also be done.
Treatment of OAS
Antihistamines can reduce the symptoms to some extent.
There are recent reports of immunotherapy given for birch pollen, reducing the symptoms of OAS due to birch pollen.