Aeroallergens

Allergic Rhinitis (Hay Fever)

Recognition of clinical features and possible co-existent conditions

Allergic rhinitis, or Hay Fever, is the most common allergic disorder in Australia and New Zealand. It is often underdiagnosed and undertreated. Allergic rhinitis can have significant impact on sleep, concentration, learning, and daily function, and affect childhood behaviour and development. The cause of symptoms of hay fever are wind pollinated trees, grasses, and weeds. Symptoms may be confused with recurrent upper respiratory tract infection.

Common aeroallergen triggers of allergic rhinitis:

• House dust mite
• Pollens – grass, tree, rye, or weed
• Animal dander
• Mould (and fungal) spores

Clinical presentation of allergic rhinitis can be defined by timing of allergen exposure:

• Perennial (year round) symptoms are often triggered by indoor allergens (e.g. dust mite, animal dander, moulds).
• Seasonal symptoms worsen usually during spring or summer and are often triggered by the pollens of grasses, weeds or trees as well as moulds.

Note, however, that “seasonal” allergens may also present all year round in certain regions and can therefore cause perennial symptoms with seasonal exacerbations. Some patients may also be sensitised to many different “seasonal” allergens resulting in year round symptoms.

Allergic rhinitis and asthma are upper and lower respiratory tract manifestations of the same inflammatory process, conceptually known as the “united airway disease” because inhalation of aeroallergen via the nose may contribute to inflammation in the lungs. Allergic rhinitis is a risk factor for subsequent asthma development and the effective treatment of allergic rhinitis improves asthma management. Patients with either asthma or allergic rhinitis should be assessed for coexistent disease, because 50-80% of patients with asthma have allergic rhinitis while 20-30% of patients with allergic rhinitis have asthma.

So-called “thunderstorm asthma” is usually due to rapid and large changes in wind, temperature, and humidity. Other allergens such as fungal spores, can also affect some people with asthma and other respiratory diseases during a thunderstorm.

Allergic rhinitis can also coexist with a range of other conditions besides asthma:

• Nasal polyps: this is not usually a single phenomenon but rather the “end-stage” of a coexistent allergic rhinitis, commonly seen in those with aspirin hypersensitivity and asthma (Samter’s triad). Polyps should be considered if patient presents with persistent nasal obstruction and/or anosmia. Large polyps may be seen on anterior rhinoscopy. Referral should be considered to an ear, nose and throat (ENT) surgeon or clinical immunology/allergy specialist with expertise in this area.
• Eustachian tube dysfunction: allergic rhinitis may contribute to ear symptoms of fullness, blockage, and hearing loss due to mucous and oedema in the Eustachian tube. Blockage of the Eustachian tube results in negative middle ear pressure and middle ear effusion (glue ear).
• Oral allergy syndrome: some patients with pollen allergy will complain that certain fresh vegetables and fruits cause oral symptoms of itch and swelling. This is known as oral allergy syndrome (OAS). Serious OAS reactions are rare. OAS is thought to be due to cross-reactions between proteins found both in pollens and fruit and vegetables. In Australia, where sensitisation to plantain weed is relatively common, individuals with plantain allergy may also present with an oral allergy to certain fruits, such as melons, tomato, orange, and kiwi fruit. People suffering from hay fever sometimes develop an itchy mouth, a scratchy throat or swelling in their lips, mouth, tongue or throat after eating raw fruit, vegetables, or certain tree nuts. This can be a sign of oral allergy syndrome—when proteins in these raw foods bear a close-enough immunological resemblance to pollen that they cause an allergic response. Peeling, cooking or canning the fruit or vegetable may prevent symptoms for those with oral allergy syndrome. Apart from plantain weed, birch, grass, and ragweed pollens are common triggers of oral allergy syndrome.
• Conjunctivitis
• Non-Allergic Rhinitis

Aeroallergens and the skin – Eczema and the atopic individual

 Inhalation or cutaneous contact with aeroallergens can trigger a release of proteins in the form of an allergic reaction on the skin and mucous membranes. But airborne particles, such as various chemicals (e.g. volatile organic compounds) but also combustion product irritants (CO₂, CO, NO₂, SO₂, etc.)  can also cause contact irritant reactions, without causing an immunological response. Allergies only affect susceptible individuals, irritant reactions can affect anyone.

Other aeroallergens may include:

• Lilies, daisies, and other perfumed flowers
• Latex allergen in glove powder
• Rodent dander, fur, urine, and saliva (eg, from mice, rats, and guinea pigs)
• Cockroach debris
• Mould and fungal spores
• Cosmetics, including perfume, antiperspirants and deodorants
• Pesticide spray
• Tobacco smoke (a common irritant and a rare allergen)._¹

Role of the primary care physician in the management of allergic rhinitis:

• Diagnosis of allergic rhinitis
• Diagnosis and management of comorbid conditions – e.g. asthma, allergic conjunctivitis
• Initiation of pharmacotherapy (where required)
• Patient Education:
  • Discuss strategies to minimise aeroallergen exposure
  • Demonstrate correct administration of intranasal sprays
  • Discuss potential side effects of medication
• Referral to a specialist (where indicated)

Important signs of allergic rhinitis on physical examination:

• Darkened circles around eyes – allergic “shiners”
• Transverse nasal crease – allergic salute, from upward rubbing of nose
• Examine each nostril with an otoscope for:
  • Pale, swollen inferior turbinate(s)
  • ± Strands of mucus
  • ± Clear watery discharge
  • Exclude presence of larger polyps
• Signs of allergic conjunctivitis:
  • Red, oedematous eyelids
  • Conjunctiva papillae

Pharmacotherapy for allergic rhinitis can be initiated without waiting for diagnostic allergy testing. Testing, however, increases the accuracy of diagnosis and allows for the identification of potential aeroallergen triggers.

Diagnostic allergy testing involves either:

1. Skin prick testing (SPT): involves pricking the individual with commercially available aeroallergen/s into the skin and, after 15-20 minutes, positive reactions are read and wheal size recorded. Patients should avoid antihistamines and drugs with antihistamine activity (e.g. pizotifen and tricyclics) for 3-4 days prior to SPT.
2. Serum specific IgE (ssIgE): testing for aeroallergen sensitisation is a blood test available to detect IgE against dust mite, pollen mixes, mould mixes, and animal dander. However, only certain aeroallergens in mixes may be clinically relevant. Antihistamines do not affect the results of ssIgE testing.

Both SPT and ssIgE testing detect the presence of IgE antibodies to potential allergens. These tests are considered surrogates for nasal allergy, they do not directly assess the response of the nasal mucosa to allergens.

Positive SPT or ssIgE test results do not automatically prove the allergen/s are causing the symptoms. They do, however, confirm the presence of IgE antibodies or sensitisation to that allergen. Further, Positive SPT or ssIgE test results to particular aeroallergens may not be clinically relevant; in a patient with seasonal symptoms but positive SPT or ssIgE test results to dust mite, for instance, as dust mite is unlikely to be clinically important since they are present all year round. Moreover, SPT wheal size or ssIgE level to aeroallergens cannot be used to determine the clinical significance of the trigger – i.e., a “severe” dust mite interpretation on a laboratory report is not necessarily indicative of a clinically severe dust mite allergy. Knowledge of common inhalant allergens relevant to the patient’s geographical location is useful to ensure that tests are initiated for relevant aeroallergens.

Food specific IgE testing (e.g. food mix “RAST”) should not be performed in allergic rhinitis investigation, since food allergy is not a cause of intermittent or persistent allergic rhinitis. Irrelevant positive results may cause unnecessary concern. A full blood count and total IgE is of little clinical use in the investigation of allergic rhinitis. (Unproven testing methods include IgG testing, cytotoxic food testing, kinesiology, Vega testing, electrodermal testing, pulse testing, reflexology and hair analysis. They are not scientifically validated and may lead to unnecessary and costly avoidance strategies.)

Non-allergic and allergic rhinitis can co-exist in the same patient. Non-allergic rhinitis encompasses a range of disorders where the rhinitis (nasal obstruction, rhinorrhoea) is not caused by an IgE mediated allergy to aeroallergen.

Differential diagnosis:

• Chronic rhinosinusitis/polyposis
• Non-allergic rhinitis with eosinophilia
• Hormonal rhinitis: e.g. pregnancy
• Drug induced rhinitis: typically due to aspirin and other NSAIDs but a range of other medications have also been reported
• Granulomatous diseases: external nasal swelling, sinusitis, nose bleeds, septal perforation, collapse of nasal bridge, multi-system involvement
• Idiopathic/vasomotor rhinitis: paroxysmal watery nasal discharge; can be triggered by strong smells or changes in environmental temperature

Distinguishing features:

• Unilateral nasal obstruction:
  • foreign body, in children
  • nasal polyp
  • deviated septum
  • tumour
• Discharge: bloody, muco-purulent discharge or unilateral nasal discharge:
  • chronic rhinosinusitis or
  • super-imposed infection / foreign body (children)
  • CSF leakage
• Negative allergy tests:
  • Incorrect aeroallergens selected
  • Non-allergic rhinitis
• Failure to respond to therapy:
  • Compliance
  • Non-allergic rhinitis

Treatment of Allergic Rhinitis:

1. Minimising exposure to confirmed allergen/s may help reduce symptoms in some people.
2. Preventer treatments: intranasal corticosteroid or combined intranasal corticosteroid/antihistamine sprays
   1. Blow nose before spraying, if blocked by mucus
   1. Tilt head slightly forward and gently insert nozzle into nostril
   1. Spray towards ipsilateral ear – i.e. more-or-less horizontally and away from septum
   1. Sniff gently to procure dose but avoid sniffing hard, during or after spraying – consider using a salt-water gargle afterward as a throat rinse
   1. Onset of benefit may take days, so these sprays must be used regularly and should not be stopped every few weeks
   1. If significant pain or bleeding occurs, contact your doctor.
3. Consider allergen immunotherapy.
4. If patient also has asthma, regular use of asthma preventers

House-dust mite are microscopic arthropods that live indoors and feed on human skin flakes. Two major species exist: Dermatophagoides pteronyssinus (most common); and Dermatophagoides farinae. They thrive in temperate and humid climates. The major human dust mite allergens are digestive enzymes excreted in the mite’s faeces. The life span of a house-dust mite is approximately two months, in which time each mite can produce 2,000 faecal particles.

House-dust mite minimisation is possible, house-dust mite eradication is not:

• Bedding:
  • Wash sheets, pillow cases, and other bedding weekly in hot water (> 60°C).
  • If cold water washing, use a commercial product containing tea tree oil.
  • Hot tumble dry washed items for 10 minutes (will kill dust mite).
  • Use dust-mite impermeable covers on pillows and mattresses.
• Remove soft toys, sheepskins, and woollen underlays or wash in eucalyptus oil. Alternatively, smaller items may be placed in the freezer overnight.
• Other measures to consider:
  • Vacuum carpets weekly using high-efficiency particulate air (HEPA) filter
  • Damp dust, or use electrostatic cloths, for hard surfaces weekly

Pollens that cause allergic rhinitis are usually from grasses, weeds, and trees which are wind pollenated. Allergic rhinitis is not caused by Australian or New Zealand native plants. Allergic rhinitis is not caused by highly flowered plants, which not only produce less pollen, than wind-pollinated species, but their pollen is transported by bees and other insects or birds.

Pollen minimisation:

• Remain indoors on windy days or after thunderstorms: when in contact with water, pollens release starch granules which can trigger allergic rhinitis and asthma symptoms – the so-called “thunderstorm” asthma
• Avoid activities known to cause allergen exposure: e.g. mowing grass
• Shower after outdoor activities where exposure to pollen is high
• Use re-circulated air in car when pollen levels are high
• Wear sunglasses to reduce the amount of pollen that gets into eyes
• Dry bedding and clothing indoors or in a tumble dryer

Domestic pets can be a major source of allergens in the home environment:

• Allergens become airborne for prolonged periods
• Clear demonstration of pet-dander triggering the patients symptoms must occur before recommending removal of the pet
• Amount of allergen released can vary between breeds; although one study found there was no difference in the concentration of a dog allergen protein in homes between hypoallergenic breeds vs other breeds.
• Consider removal of the pet from the home where symptoms are severe; however, it can take a while for allergen levels to decrease, an average of 20 weeks for cat-allergen concentrations to reach levels comparable to a house without a cat.
• If pet dander is only causing minor problems, consider keeping the pet outside.
• The effectiveness of washing pets regularly, and the use of HEPA air filters remain uncertain.

Moulds:

• Exposure to moulds can occur both indoors and outdoors, even in dry climates
• Mould in the home can:
  • Typically be found in damp, warm, poorly-lit areas
  • Cause discoloration of surfaces and/or musty smell
• Outdoor moulds can be present in all conditions, particularly in humid climates, albeit with seasonal peaks

Mould avoidance:

• Remove visible mould – e.g. clean with bleach or other mould reduction cleaners
• Ensure adequate ventilation
• Dry or remove wet carpet
• Fix any leaks
• Remove indoor pot plants, as they promote mould growth
• Do not mow lawns or work with garden compost and mulch

Side-effects of Intranasal corticosteroids (INCS):

• Local side effects are uncommon when correctly administered but can include:
  • Dryness
  • Epistaxis (occasionally)
• Topical corticosteroids such as INCS do not cause nasal mucosal atrophy
• Minimal potential for systemic absorption, when used in recommended doses.

Whilst systemic absorption of INCS is negligible with newer formulations, primary care physicians should monitor growth of children and adolescents taking corticosteroids by any route. INCS must be used with caution in patients with pre-existing glaucoma and/or cataracts, as rare instances of cataracts, glaucoma and raised intraocular pressure have been reported following use of INCS.

Other treatment options

Saline nasal irrigation:

• Clears aeroallergens and inflammatory mucus
• Usually well tolerated and effective in reducing rhinitis symptoms
• Safe and inexpensive
• Large volume (> 60 mL) and positive pressure devices appear to be more effective than simple sprays (< 1 mL)

Intranasal chromones (e.g. sodium cromoglycate):

• Typically used for intermittent rhinitis
• This is more useful for episodic treatment of itch, sneeze, rhinorrhoea, than regular prophylaxis
• Duration of action is approximately 4 hours
• Less effective than intranasal corticosteroids

Intranasal ipratropium:

• Anticholinergic sprays useful in non-allergic rhinitis
• Only decreases watery rhinorrhoea
• May be used in allergic rhinitis as adjunct treatment for rhinorrhoea persisting despite antihistamines or intranasal corticosteroid use

Oral leukotriene antagonists:

• Used in children/adolescents with asthma and allergic rhinitis
• No additional benefit if used in combination with antihistamines for treatment of allergic rhinitis
  • Combination of leukotriene antagonists (e.g. Montelukast) and antihistamines are no more effective than intranasal corticosteroids alone for allergic rhinitis
• no Australian or New Zealand government subsidy for use of leukotriene antagonists for patients with allergic rhinitis alone

Decongestants:

• Oral or nasal decongestants may be used short term (up to 3 days) to reduce nasal congestion if severe, and this can allow more effective administration of intranasal corticosteroids if turbinates are very swollen
• Chronic use of intranasal decongestants may lead to rebound nasal obstruction, called rhinitis medicamentosa
• Decongestants should not be used in pregnancy, hypertension, and in patients with coronary artery disease, prostatism, or glaucoma

Systemic steroids for allergic rhinitis:

• Brief courses of oral corticosteroids (3-7 days) are rarely indicated, but may be considered:
  • If there is severe nasal obstruction
  • As short-term rescue medication if symptoms are severe, despite conventional therapy, but only up to a maximum limit of 2 or 3 short courses in a 12 month period
• Depo-corticosteroids are NOT recommended due to short duration of benefit and potential for local (subdermal and dermal atrophy) and systemic side effects.
• Patients requiring oral corticosteroids for allergic rhinitis should be referred to a clinical immunology/allergy/specialist for assessment

Surgery for rhinitis:

Surgery plays a limited role in the management of rhinitis. Turbinate reduction and re-modelling of the nasal airway can improve medically refractory nasal obstruction. Vidian neurectomy (division of autonomic nasal nerves) is not indicated for allergic rhinitis, but can be considered for severe intractable watery rhinorrhoea of non-allergic (vasomotor) rhinitis.

Rhinitis of Pregnancy:

Up to 20% of pregnant women develop symptoms of rhinitis, typically in the second trimester, and improving 2 weeks after delivery. Reassurance may only be required. Saline nasal irrigation and intranasal chromones are safe in pregnancy. Nasal or oral decongestants are not recommended for use in pregnancy. Currently available intranasal antihistamines have a “B3” category.

Management of allergic rhinitis during lactation:

Rhinitis medications in lactating mothers are best taken after a feed, to minimise any potential infant exposure. Saline nasal treatments, intranasal sodium cromoglycate (chromone), intranasal ipratropium (anti-cholinergic), non-sedating oral antihistamines (2nd generation), and intranasal corticosteroids are all considered safe to use during breastfeeding. Evidence is lacking for the safety of intranasal azelastine hydrochloride (antihistamine) and intranasal lodoxamide trometamol (chromone). Oral or intranasal decongestants and intranasal levocabastine hydrochloride (antihistamine) cross into breast milk and are not recommended for use by lactating mothers.

Seasonal Pollens

The pollen season can last for several months during spring, summer and into early autumn. The pollen-producing grasses in Australia responsible for most allergies are rye, bermuda (couch), meadow and paspalum (bahia). The primary weed allergens are plantain, privet, wall pellitory and Patterson’s Curse. The main allergenic trees in Australia are almost all exotic species, for example, silver birch, maple and olive trees, but the native species acacia (wattle) and tea tree are also commonly allergenic. Flowers are rarely implicated, although highly fragrant flowers may cause irritant symptoms.

Features of allergic vs. non-allergic rhinitis:

• Prominent sneezing
• Prominent rhinorrhoea
• Presence of conjunctival symptoms
• Exacerbation in spring and early summer
• Personal history of atopic disease
• Family history of atopic disease
• Demonstration of allergen-specific IgE

Avoiding pollen exposure:

• Stay indoors in early morning, on windy days and after thunderstorms when airborne pollen levels are high.
• Use air-conditioning in the house and car (with recirculation mode) during pollen season.
• Avoid grass mowing or wear a mask if unavoidable.
• Remove weeds and trees to which you are sensitised from your garden.
• Spin sheets/towels and clothing in a tumble dryer for a few minutes after line drying during pollen season.

Testing:

• For single allergens, request specific IgE or RAST e.g. “rye grass RAST” or “rye grass-IgE”
• For allergen mixes, request allergen mix or code e.g. grass mix RAST or “RAST gx2”
• For regional pollen panel which includes grass mix (gx2), weed mix (wx1),
• and tree mix (tx7), request “RAST pollen panel”
• Requests for ≤ 4 specific allergens or allergen mixes in a single episode of patient
• testing are bulk-billed.

Results of allergy tests should always be considered with a patient’s clinical history. Positive tests do not automatically prove the allergen is causing the symptoms. Minimising exposure to confirmed allergens may assist in reducing symptoms in some people. Intranasal corticosteroids sprays or combined intranasal/antihistamine sprays are recommended preventer treatments. Patients should be instructed on the correct and consistent use of intranasal sprays. Effective treatment of allergic rhinitis is important in the management of asthma. If patients are allergic to pollen, recommend staying indoors during thunderstorms in pollen seasons and use preventer treatments. Referral to a specialist should be considered when severe or inadequately controlled allergic rhinitis persists and consideration is being made for allergen immunotherapy.

Ragweed Allergy:

Predominant allergen in late summer and fall.

• In spring and summer, during tree and grass pollen season, levels are highest in the evening. In late summer and early fall, during ragweed pollen season, levels are highest in the morning.
• Pollen can be tracked into your home via your clothes, your hair, or your pet — so change your clothes after being outside for long periods of time, shower before going to bed, and wash your hands after petting an animal that has been outside.

Allergen Immunotherapy (Desensitisation) for Allergic Rhinitis and Asthma

Individual patients will experience different degrees of benefit, and on average there may be a 50% reduction in symptoms and/or medication need. This is the only treatment that can alter the natural history of the disease.

• Involves the regular administration of commercially available allergen extracts to promote clinical tolerance to the allergen/s.
• Is effective in reducing the frequency and severity of symptoms resulting from subsequent exposure to the allergen/s.
• Treatment is usually for 3-5 years in order to produce durable effects.
• Is administered by two routes: subcutaneous injections or sublingual route (liquid drops, sprays or tablets)

Asthma is an inflammatory disease characterised by the presence of cells such as eosinophils, mast cells, basophils, and CD25+ T-lymphocytes in the airway walls. There is close interaction between these cells, because of the activity of cytokines which have a variety of communication and biological effector properties. Chemokines attract cells to the site of inflammation and cytokines activate them, resulting in inflammation and damage to the mucosa. With chronicity of the process, secondary changes occur, such as thickening of basement membrane and fibrosis.

Absolute contraindications

Concomitant administration of β-blockers and immunotherapy is absolutely contraindicated because patients taking β-blockers are at increased risk of anaphylaxis and respond poorly to resuscitation (note that the use of β-blockers is contraindicated in bronchial asthma). Previous anaphylactic reaction to immunotherapy.

Patient Travel Information – Travelling with allergy, asthma and anaphylaxis: checklist

Download an ASCIA Travel Plan for Anaphylaxis and have it completed by your doctor: www.allergy.org.au/health-professionals/anaphylaxis-resources/ascia-travel-plan-anaphylaxis. This helps when carrying adrenaline autoinjectors (e.g. EpiPen or Anapen) in hand luggage and through Customs. Contact your airline/s to determine their policies regarding food allergy well in advance of travel and before you book tickets. Tell your travel agent and airline/s about your food allergy in advance. Have adequate travel insurance. Ensure the policy covers your medical condition. Special approval may be required. Check if there are any special conditions (e.g. doctor’s report required, an additional fee to cover anaphylaxis). While fumes or dust from inhaled food allergen might cause allergic rhinitis (hay fever) or mild asthma symptoms, the risks of serious reactions is very low unless the food is actually eaten. Consider wiping down tables and armrests to remove possible residual food allergens (contact can sometimes trigger mild allergic symptoms). Keep emergency medication with you in hand luggage. If travelling with an adrenaline autoinjector, keep it with you or under the seat in front of you and not in the overhead locker. You need to be able to access an adrenaline autoinjector with your seatbelt fastened.

References

1. Aeroallergens and the skin | DermNet NZ
2. ASCIA. “Allergic Rhinitis Clinical Update.” Australian Society of Clinical Immunology and Allergy. December 2017.
3. ASCIA. “ASCIA Travelling with allergy, asthma and anaphylaxis: checklist.” Australian Society of Clinical Immunology and Allergy 2013. http://www.allergyfacts.org.au/.
4. ASCIA. “Treatment Plan for Allergic Rhinitis (Hay Fever).” Australian Society of Clinical Immunology and Allergy 2020. www.allergy.org.au.
5. Position Statement: Specific allergen immunotherapy for asthma. A Position Paper of the Thoracic Society of Australia and New Zealand and the Australasian Society of Clinical Immunology and Allergy. MJA 167(17); 1997: S40-4.
6. Wallman, Lucinda. “Hay Fever: Clues to Diagnosis and Management of Pollen Allergy.” Laverty Pathology Newsletter. October 2011. www.laverty.com.au.