Asthma Management Handbook

Assessing allergies to guide asthma management

Recommendations

When taking a history in a patient with suspected asthma, ask about allergies, and the circumstances and timing of symptoms.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

Assess and manage the risk of thunderstorm asthma.

How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • NACA, 20171

When performing a physical examination in a patient with suspected asthma, inspect the upper airway for signs of allergic rhinitis (e.g. swollen turbinates, transverse nasal crease, reduced nasal airflow, mouth breathing, darkness and swelling under eyes caused by sinus congestion).

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

Consider allergy testing as part of diagnostic investigations if you suspect allergic triggers, or to guide management.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

Consider allergy tests (skin prick test or specific IgE assay) for common aeroallergens for children with recurrent wheezing when the results might guide you in (either of):

  • assessing the prognosis (the presence of allergies in preschool children increases the probability that the child will have asthma at primary school age)
  • managing symptoms (e.g. advising parents/carers about management if avoidable allergic triggers are identified).

Notes: Allergy tests are not essential in the diagnostic investigation of asthma in children. The finding of allergic sensitisation on skin-prick testing or specific IgE does not necessarily mean that it is clinically important.

Blood test (immunoassay for allergen-specific immunoglobulin E) can be used if skin prick testing is unavailable, impractical or inappropriate.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

Last reviewed version 2.0

If allergy testing is needed, refer to an appropriate provider for skin prick testing for common aeroallergens.

Notes

If staff are trained in the skin prick test procedure and its interpretation, skin prick testing can be performed in primary care. If not, refer to an appropriate provider.

When performing skin prick testing, follow Australasian Society of Clinical Immunology and Allergy (ASCIA) guidance: Skin prick testing for the diagnosis of allergic disease. A manual for practitioners

How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • Australasian Society of Clinical Immunology and Allergy, 20132

Blood test (immunoassay for allergen-specific immunoglobulin E) can be used if skin prick testing is (any of):

  • unavailable
  • impractical (e.g. a patient who is unable to cooperate with test procedure, a patient taking antihistamines when these cannot be withdrawn, or a patient taking tricyclic antidepressants or pizotifen)
  • contraindicated (e.g. patients with severe dermatographism, extensive skin rash, or those at risk of anaphylaxis including patients with occupational asthma due to latex sensitivity).
How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • Australasian Society of Clinical Immunology and Allergy, 20132

To investigate allergies in a person with severe or unstable asthma, or a history of anaphylaxis, refer to a specialist allergist for investigation to minimise risk.

How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • Australasian Society of Clinical Immunology and Allergy, 20132

Consider offering referral to an appropriate specialist (e.g. respiratory physician, occupational physician or allergist) for patients with:

  • suspected or confirmed work-related asthma
  • other significant allergic disease (e.g. suspected food allergies or severe eczema).
How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available).

If patients are likely to visit practitioners who offer alternative diagnostic tests, explain that none of the following alternative diagnostic practices should be used in the diagnosis of asthma or allergies:

  • cytotoxic testing (Bryans’ or Alcat testing)
  • hair analysis
  • iridology
  • kinesiology
  • oral provocation and neutralisation
  • pulse testing
  • radionics (psionic medicine, dowsing)
  • tests for ‘dysbiosis’
  • vega testing (electrodermal testing)
  • VoiceBio.
How this recommendation was developed

Adapted from existing guidance

Based on reliable clinical practice guideline(s) or position statement(s):

  • Australasian Society of Clinical Immunology and Allergy, 20073

More information

Allergies and asthma: links

There is a strong link between asthma and allergies:4, 5

  • The majority of people with asthma have allergies.
  • Immunoglobulin E-mediated sensitisation to inhalant allergens is an important risk factor for developing asthma, particularly in childhood.
  • In individuals with asthma, exposure to relevant allergens can worsen asthma symptoms and trigger flare-ups, including severe acute asthma.
  • Allergens are a common cause of occupational asthma.

Although atopic sensitisation increases the risk of developing asthma, most people who are allergic to inhalant allergens or food allergens do not have asthma.5 Among people with food allergies, asthma may be a risk factor for fatal anaphylaxis due to food allergens.67 However, foods are rarely a trigger for asthma symtpoms.

Neither asthma nor allergy is a single disease – each has multiple phenotypes and is a complex of several different diseases with different aetiologies, genetic risk factors and environmental risk factors.4

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Links between allergic rhinitis and asthma

Prevalence, aetiology and symptoms

Asthma and allergic rhinitis frequently coexist. At least 75% of patients with asthma also have rhinitis, although estimates vary widely.8 Patients with asthma may have both allergic and non-allergic rhinitis.

Allergic rhinitis that starts early in life is usually due to a classical IgE hypersensitivity. Adult-onset asthma or inflammatory airway conditions typically have more complex causes. Chronic rhinosinusitis with nasal polyps is not a simple allergic condition and generally needs specialist care.9

Symptoms and signs of allergic rhinitis can be local (e.g. nasal discharge, congestion or itch), regional (e.g. effects on ears, eyes, throat or voice), and systemic (e.g. sleep disturbance and lethargy). Most people with allergic rhinitis experience nasal congestion or obstruction as the predominant symptom. Ocular symptoms (e.g. tearing and itch) in people with allergic rhinitis are usually due to coexisting allergic conjunctivitis.10

Patients may mistake symptoms of allergic rhinitis for asthma and vice versa. Allergic rhinitis is sometimes more easily recognised only after asthma has been stabilised.

Effects on asthma

Allergic rhinitis is an independent risk factor for developing asthma in children and adults.11, 12, 13, 14, 15 However, the use of antihistamines in children has not been shown to prevent them developing asthma.8

The presence of allergic rhinitis is associated with worse asthma control in children and adults.16, 17, 18, 19 The use of intranasal corticosteroids in patients with concommitant allergic rhinitis and asthma may improve asthma control in patients who are not already taking regular inhaled corticosteroids.20

Both rhinitis and asthma can be triggered by the same factors, whether allergic (e.g. house dust mite, pet allergens, pollen, cockroach) or non-specific (e.g. cold air, strong odours, environmental tobacco smoke).

Food allergies do not cause allergic rhinitis. Most people with allergic rhinitis are sensitised to multiple allergens (e.g. both pollens and house dust mite), so symptoms may be present throughout the year.

Pollens (e.g. grasses, weeds, trees) and moulds are typically seasonal allergens in southern regions, but can be perennial in tropical northern regions.21 However, ryegrass is not found in tropical regions (see Thunderstorm asthma).

Pollen calendars provide information on when airborne pollen levels are likely to be highest for particular plants.

Thunderstorm asthma

Seasonal allergic rhinitis, which in Australia is typically associated with sensitisation to perennial ryegrass (Lolium perenne), is an important risk factor for thunderstorm asthma.22

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Treatment of allergic rhinitis in adults and adolescents

 

Table. Overview of efficacy of allergic rhinitis medicines for specific symptoms Opens in a new window Please view and print this figure separately: http://www.asthmahandbook.org.au/table/show/102

Intranasal corticosteroids

If continuous treatment is required, an intranasal corticosteroid is the first-choice treatment unless contraindicated. Intranasal corticosteroids are more effective in the treatment of allergic rhinitis than other drug classes including oral H1-antihistamines, intranasal H1-antihistamines and montelukast.20, 8, 23 Intranasal corticosteroid are most effective when taken continuously.20

Intranasal corticosteroids are effective in reducing congestion, rhinorrhoea, sneezing and itching in adults and adolescents with allergic rhinitis.20, 8 They are also effective for ocular symptoms.24

All available intranasal corticosteroids appear to be equally effective.20

The onset of action is between 3 and 36 hours after first dose and, in practice, the full therapeutic effect takes a few days.25

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.23

Intranasal corticosteroids are well tolerated. Common (>1%) adverse effects include nasal stinging, itching, nosebleed, sneezing, sore throat, dry mouth, cough.26 Nose bleeds are usually due to poor spray technique or crusting. Evidence from studies mainly in adults suggests that intranasal corticosteroids do not cause atrophy of nasal epithelium.27

Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects when given in recommended doses.20, 28 Studies in adults evaluating effects on the hypothalamic-pituitary axis using morning cortisol concentrations, cosyntropin stimulation, and 24-hour urinary free cortisol excretion show no adverse effects with beclomethasone dipropionate, budesonide, ciclesonide, fluticasone propionate, fluticasone furoate, or triamcinolone acetonide.20

In patients with asthma already taking inhaled corticosteroids, both the intranasal corticosteroid dose and the inhaled corticosteroid dose should be taken into account when calculating the total daily corticosteroid dose. Drug–drug interactions (e.g. with CYP3A4 inhibitors such as such as erythromycin, clarithromycin, ritonavir and itraconazole) may change the metabolism or increase absorption of corticosteroids administered by any route, increasing the risk of adrenal suppression.26

Combination intranasal corticosteroid plus intranasal antihistamines

Combined intranasal fluticasone propionate and azelastine hydrochloride in a single device is more effective than fluticasone propionate alone for a range of nasal and ocular symptoms.20, 23, 22

The onset of therapeutic action is approximately 30 minutes after dosing.22

Oral antihistamines

Second-generation (less sedating) antihistamines (e.g. cetirizine, desloratadine, fexofenadine or loratadine) should be used in preference to older, more sedating antihistamines. Cetirizine is the most likely of the less sedating antihistamines to cause sedation, while fexofenadine and loratadine appear to be the least sedating.29

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms.23, 30 They can provide adequate relief for some individuals when taken continuously or intermittently.20 Available agents appear to be equally effective.28

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.20, 31 In adults with allergic rhinitis, oral antihistamines usually produce no further improvement when added to intranasal corticosteroid treatment.20

Common (>1%) adverse effects include drowsiness, fatigue, headache, nausea and dry mouth.26 Oral antihistamines can also cause ocular dryness.32

Intranasal antihistamines

Intranasal antihistamines are at least equally effective as second-generation, less sedating oral H1-antihistamines for the treatment of allergic rhinitis, but are generally less effective than intranasal corticosteroids.8

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.20 They have a rapid onset of action (15–30 minutes).20

The most common (>1%) adverse effect is local irritation.26 Bitter taste is more common intranasal antihistamines than with intranasal corticosteroids.20

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.8, 23 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.20, 8 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.23

Montelukast is approved by TGA for treatment of in adults with asthma or seasonal allergic rhinitis.

It is generally very well tolerated, but has been infrequently associated with neuropsychiatric adverse effects, including suicidal ideation, in children and young people.33, 34, 35, 36, 37 A recent analysis of databases of adults and children taking montelukast suggests it is associated with nightmares, depression, and aggression.37 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.37

Other nasal sprays

Ipratropium bromide spray is effective in managing persistent rhinorrhoea in patients with allergic rhinitis, but not blockage or itch.8 It is indicated for use in adults and adolescents over 12 years old.

Intranasal sodium cromoglycate is less effective than intranasal corticosteroids, but is effective in some patients for prevention and treatment of allergic rhinitis and is associated with minimal adverse effects.28

Specific allergen immunotherapy

Specific allergen immunotherapy (desensitisation) is effective in reducing allergic rhinitis symptoms (see separate topic).

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Treatment of allergic rhinitis in children

 

Table. Overview of efficacy of allergic rhinitis medicines for specific symptoms Opens in a new window Please view and print this figure separately: http://www.asthmahandbook.org.au/table/show/102

Intranasal corticosteroids

Intranasal corticosteroids are effective in reducing congestion, rhinorrhoea, sneezing and itching in school-aged children with allergic rhinitis.20, 8 However, there is weaker evidence to support their efficacy in children than in adults.8 There is limited evidence to guide the treatment of allergic rhinitis in preschool children.23

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.23

TGA-approved indications vary between age groups. Intranasal corticosteroids indicated for children aged under 12 years include fluticasone furoate (age 2 years and over), mometasone furoate (age 3 years and over), and budesonide (age 6 years and over).

Intranasal corticosteroids are well tolerated. Evidence from studies mainly in adults suggests that they do not cause atrophy of nasal epithelium.38 Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects in children when given in recommended doses.2028 Studies in children evaluating effects on the hypothalamic-pituitary axis using morning cortisol concentrations, cosyntropin stimulation, and 24-hour urinary free cortisol excretion showed no adverse effects with ciclesonide, fluticasone propionate, fluticasone furoate, mometasone furoate, or triamcinolone acetonide.20 One knemometry study showed reduced lower leg growth rate in children using intranasal budesonide.20 In studies using stadiometry over 12 months, higher-than-recommended doses of intranasal beclomethasone dipropionate were associated with growth suppression, but fluticasone propionate and mometasone furoate showed no effects on growth compared with placebo.20

In children already taking inhaled corticosteroids, both the intranasal corticosteroid dose and the inhaled corticosteroid dose should be taken into account when calculating the total daily corticosteroid dose.

Oral antihistamines

Second-generation (less sedating) antihistamines (e.g. cetirizine, desloratadine, fexofenadine or loratadine) should be used in preference to older, more sedating antihistamines. Cetirizine is the most likely of the less sedating antihistamines to cause sedation, while fexofenadine and loratadine appear to be the least sedating.29

These antihistamines can be taken long term by children. Eighteen months of treatment with cetirizine was well tolerated in a large, prospective, multi-country, randomised controlled trial in infants with atopic dermatitis aged 12–24 months.20

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms,23, 30 including in preschool children. 23 They can provide adequate relief for some individuals when taken continuously or intermittently.20 Available agents appear to be equally effective.28

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.20, 31 The addition of oral antihistamines to intranasal corticosteroids has not been demonstrated to be an effective strategy in children.39

TGA-approved indications vary between age groups. Less sedating oral antihistamines indicated for children under 12 years include cetirizine (1 year and over), loratatidine (1 year and over), desloratadine (6 months and over), and fexofenadine (6 months and over).

Intranasal antihistamines

Intranasal antihistamines are at least equally effective as second-generation, less sedating oral H1-antihistamines for the treatment of allergic rhinitis, but are generally less effective than intranasal corticosteroids.8

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.20 They have a rapid onset of action (15–30 minutes).20

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.8, 23 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.20, 8 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.23

Montelukast is approved by TGA for the treatment of asthma in children over 2 years, and for the treatment of seasonal allergic rhinitis.

It is generally very well tolerated, but has been infrequently associated with neuropsychiatric adverse effects, including suicidal ideation, in children and young people.33, 34, 35, 36 A recent analysis of databases of adults and children taking montelukast suggests it is associated with nightmares (especially in children), depression, and aggression (especially in children).37 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.37

The potential association of montelukast with behaviour-related adverse events should be mentioned to parents when commencing treatment, and treatment should be stopped if such adverse events are suspected.

Specific allergen immunotherapy

Specific allergen immunotherapy (desensitisation) is effective in reducing allergic rhinitis symptoms (see separate topic).

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Non-recommended medications for allergic rhinitis

Intranasal decongestants have a limited role in the management of allergic rhinitis because they should only be used for very short courses (up to 5 days maximum). Repeated or long-term use can cause rebound swelling of nasal mucosa (rhinitis medicamentosa), which can lead to dose escalation by patients, with a risk of atrophic rhinitis. Intranasal decongestants can be considered for a patient with severe nasal congestion to gain rapid relief of symptoms until the full effect of intranasal corticosteroids is achieved.

Oral decongestants (e.g. pseudoephedrine or phenylephrine) should not generally be used in the management of allergic rhinitis. They are indicated for short-term use only (e.g. acute infectious rhinitis, or during air travel by a patient with symptomatic rhinitis, as a single tablet taken one hour before landing). They are associated with adverse effects including palpitations, tachycardia and insomnia.

Oral corticosteroids should be avoided as a treatment for allergic rhinitis. In exceptional circumstances, their use might be considered in consultation with an allergy specialist.

Topical ocular alpha agonist vasoconstrictors (including in combination with antihistamines) should not be used for allergic conjunctivitis because they can cause conjunctivitis medicamentosa.

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Nasal saline irrigation for allergic rhinitis

Nasal irrigation (via a syringe, rinse bottle, spray or other device) can improve nasal symptoms, mucociliary clearance, and quality of life.40 Saline administered by spray or other devices was used at least twice daily in most studies that showed a benefit.40

Isotonic solution is preferable to hypertonic solution because it supports optimal mucociliary clearance.40 Isotonic saline is solution is inexpensive and has no known adverse effects.40 Patients can use either commercially manufactured saline solutions or home-made normal saline: 1 teaspoon (5 g) rock or sea salt in 500 mL of water (preferably bottled or boiled).

There is not enough evidence to determine:

  • whether solutions should be buffered or non-buffered, sterile or non-sterile
  • whether various additives provide any advantage
  • whether inhaling steam or an irritant decongestant (e.g. eucalyptus, menthol) before saline irrigation provides any extra benefit. However, patients are more likely to adhere to simple and convenient regimens, regardless of theoretical advantages. Caution is required with steam inhalation to avoid burns.

If patients are using both saline irrigation and an intranasal corticosteroid or intranasal H1‑antihistamine, they should perform saline irrigation first. Saline can be used again after waiting at least an hour after using an intranasal corticosteroid.

Young children are unlikely to tolerate nasal irrigation.

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Surgical turbinate reduction

Turbinate reduction surgery can be considered when nasal obstruction is due to turbinate hypertrophy and symptoms do not respond to medical treatment. It should not be performed in young children except after thorough investigation and review.

Inferior turbinate hypertrophy secondary to inflammation is a common cause of nasal obstruction in patients with allergic rhinitis.41 Several surgical procedures are available to correct this problem.42 The ideal surgical reduction should preserve the mucosa and physiological function.41

Short-term adverse outcomes of inferior turbinate reduction include nasal bleeding, scarring and crusting. Rarely, it may worsen symptoms when patients have non-specific rhinitic conditions or sino-nasal somatisation disorders (‘empty nose syndrome’).42 There is no evidence that turbinate surgery creates these conditions, but sino-nasal surgery may exacerbate the symptoms.

 

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Thunderstorm asthma

Certain types of thunderstorms in spring or early summer in regions with high grass pollen concentrations in the air can cause life-threatening allergic asthma flare-ups in individuals sensitised to rye grass, even if they have not had asthma before.3,5,6,8,9

Sensitisation to rye grass allergen is almost universal in patients who have reported flare-ups consistent with thunderstorm asthma in Australia.

People with allergic rhinitis and allergy to ryegrass pollen (i.e. most people with springtime allergic rhinitis symptoms) are at risk of thunderstorm asthma if they live in, or are travelling to, a region with seasonal high grass pollen levels – even if they have never had asthma symptoms before. This includes people with undiagnosed asthma, no previous asthma, known asthma.3, 5 Lack of inhaled corticosteroid preventer treatment has been identified as a risk factor.3

Epidemics of thunderstorm asthma can occur when such a storm travels across a region and triggers asthma in many susceptible individuals. Epidemic thunderstorm asthma events are uncommon, but when they occur can they make a high demand on ambulance and health services.1, 9, 10

Data from thunderstorm asthma epidemics suggest that the risk of asthma flare-ups being triggered by a thunderstorm is highest in adults who are sensitised to grass pollen and have seasonal allergic rhinitis (with or without known asthma).3

The worst outcomes are seen in people with poorly controlled asthma.1 Treatment with an inhaled corticosteroid asthma preventer was significantly protective in a well-conducted Australian case-control study.5

There is insufficient evidence to determine whether intranasal corticosteroids help protect against thunderstorm asthma. Intranasal corticosteroids reduce symptoms of allergic rhinitis and limited indirect evidence suggests they may protect against asthma flare-ups in people not taking inhaled corticosteroids.11

The effectiveness of specific allergen immunotherapy in protecting against thunderstorm asthma has not been evaluated in randomised clinical trials, but data from a small Australian open-label study suggest that short-term treatment with five-grass sublingual immunotherapy may have been protective in individuals.4

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Allergy tests in adults with asthma

Allergy tests have a very limited role in the clinical investigation of asthma. They may be useful to guide management if the patient is sensitised to aeroallergens that are avoidable and avoidance has been shown to be effective, or in the investigation of suspected occupational asthma.

The Australasian Society of Clinical Immunology and Allergy (ASCIA) recommends skin prick testing as the first-choice method for investigating allergies in a person with asthma.2

Patients who need allergy tests are usually referred to a specialist for investigation. GPs with appropriate training and experience can also perform skin prick tests for inhalent allergens, if facilities to treat potential systemic allergic reactions are available, or arrange for allergy tests (skin prick testing or blood tests) to be performed by an appropriate provider. Skin prick testing for food allergens should only be performed in specialist practices.

Asthma, particularly uncontrolled or unstable asthma, may be a risk factor for anaphylaxis during skin prick testing;2 however, anaphylaxis due to skin prick testing is extremely rare. As a precaution, ASCIA advises that skin prick testing in people with severe or unstable asthma should be performed only in specialist practices.2 ASCIA’s manual on skin prick testing lists other risk factors.2

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Allergy tests in children

Skin-prick testing

Allergy tests have a very limited role in the clinical investigation of asthma. They may be useful to guide management if the child is sensitised to aeroallergens that are avoidable (e.g. advise parents  against getting a cat if skin-prick testing has shown that the child is sensitised to cat allergens, or advise parents that there is no need to remove a family pet if the child is not sensitised).

Skin-prick testing is the recommended test for allergies in children.

Risk factors for anaphylaxis during skin prick testing are thought to include asthma (particularly uncontrolled or unstable asthma), age less than 6 months, and widespread atopic dermatitis in children.2 As a precaution, the Australasian Society of Clinical Immunology and Allergy (ASCIA) advises that skin prick testing should be performed only in specialist practices for children under 2 years and children with severe or unstable asthma.2 ASCIA’s manual on skin prick testing lists other risk factors.2

Total serum IgE testing

In children aged 0–5 years, total serum immunoglobulin E measurement is a poor predictor of allergies or asthma.43

Specific serum IgE testing

Among children aged 1–4 years attending primary care, those with raised specific IgE for inhaled allergens (e.g. house dust mite, cat dander) are two-to-three times more likely to have asthma at age 6 than non-sensitised children.43 Sensitisation to hen’s egg at the age of 1 year (specific IgE) is a strong predictor of allergic sensitisation to inhaled allergens at age 3 years.43

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Pet allergens

Contact with pets (e.g. cats, dogs and horses) can trigger asthma, mainly due to sensitisation to allergens in sebum or saliva. Exposure can trigger flare-ups or worsen symptoms.4

The amount of allergen excreted differs between breeds.4 Although some breeders claim that certain breeds of dogs are less likely to trigger asthma (‘hypoallergenic’ breeds), allergen levels have not been shown to be lower in the animal’s hair or coat,44 or in owner’s homes45 with these breeds than other breeds.

Cat allergens easily spread on clothing and are found in places where cats have never been.4

The most effective method of allergen avoidance for people with asthma who are allergic to cats or dogs is to not have these pets in the home. However, the allergen can persist for many months, or even years, after the pet has been removed.4

There is not enough clinical trial evidence to determine whether or not air filtration units are effective to reduce allergen levels in the management of pet-allergic asthma.46

Other strategies for reducing exposure to pet allergens include:

  • washing hands and clothes after handling pets
  • washing clothes and pet bedding in hot water  (> 55°C)
  • frequent vacuuming of the home using a vacuum with a HEPA filter
  • cleaning hard floors with a damp/antistatic cloth or a steam mop, and cleaning air-conditioning or heating ducts
  • grooming pets regularly (where possible, the patient should be absent while this occurs), and washing pets regularly, but no more than the vet recommends.
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House dust mite

Exposure to house dust mite (mainly Dermatophagoides pteronyssinus) is a major asthma trigger in Australia.4 These microscopic mites live indoors, feed on skin scales, and thrive in temperate and humid climates such as coastal Australia.

Strategies that have been proposed for reducing exposure to house dust mites include:4

  • encasing bedding (pillows, mattresses and doonas) in mite-impermeable covers
  • weekly washing bed linen (pillow cases, sheets, doona covers) in a hot wash (> 55°C)
  • using pillows manufactured with anti-microbial treatments that suppress fungal growth and dust mites
  • removing unnecessary bedding such as extra pillows and cushions where dust mites might live and breed
  • removing soft toys, or washing them in a hot wash (> 55°C) every week
  • vacuuming rugs and carpets weekly using a vacuum with a high-efficiency particulate air (HEPA) filter, while allergic person is absent
  • cleaning hard floors weekly with a damp or antistatic cloth, mop or a steam mop and dusting weekly using a damp or antistatic cloth
  • regularly washing curtains or replacing curtains with cleanable blinds
  • spraying the area with chemicals that kill mites (acaricides), such as benzyl benzoate spray or liquid nitrogen. Acaricide sprays are not commonly used in Australia.

Some clinical trials assessing the dust mite avoidance strategies (e.g. the use of allergen-impermeable mattress and pillow covers, acaricide sprays, air filters, or combinations of these) have reported a reduction in levels of house dust mite.474849505152535455565758 However, reduced exposure may not improve symptoms.

Overall, clinical trials assessing dust mite avoidance for patients with asthma do not show that these strategies are effective in improving asthma symptoms, improving lung function or reducing asthma medication requirements in adults or children, compared with sham interventions or no interventions.59 The use of allergen-impermeable mattress covers, as a single mite-reduction intervention in adults, is unlikely to be effective in improving asthma.60

Use of mite allergen-impermeable covers for bedding (e.g. mattress covers, pillow covers, doona covers) was a component of some of the multi-component strategies for reducing house dust mite exposure that have been shown to be effective for improving asthma symptoms or control.

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Pollens

Allergy to airborne pollen grains from certain grasses, weeds and trees is common in people with asthma in Australia.4 The highest pollen counts occur on calm, hot, sunny days in spring or early summer, or during the dry season in tropical regions.

Exposure to pollen:4, 61

  • may worsen asthma symptoms during the pollen season
  • can cause outbreaks of asthma flare-ups after thunderstorms
  • is usually caused by imported grasses, weeds and trees (which are wind pollinated) – the pollen can travel many kilometres from its source
  • is not usually caused by Australian native plants (although there are exceptions, such as Cypress Pine)
  • is not usually caused by highly flowered plants as they produce less pollen (which is transported by bees) than wind pollinated plants.

Completely avoiding pollen can be difficult during the pollen season. Strategies that have been proposed for avoiding exposure to pollens include:4

  • avoiding going outdoors on days with high pollen counts (particularly 7–9 am and 4–6 pm), on windy days or after thunderstorms
  • keeping car windows closed, ensuring the vehicle has a pollen cabin air filter and setting the cabin air to recirculate
  • showering (or washing face and hands thoroughly) after being outside with exposure to pollen
  • drying bed linen indoors during the pollen season
  • holidaying out of the pollen season or at the seaside
  • not mowing the grass, and staying inside when it is being mown
  • wearing a facemask and/or glasses in special situations where pollen can’t be avoided, e.g. if mowing is unavoidable
  • removing any plants the patient is sensitive to from their garden.

Daily pollen indices and forecasts are available from news media websites (e.g. www.weatherzone.com.au).

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Moulds

Building repairs to reduce dampness in homes (e.g. leak repair, improvement of ventilation, removal of water-damaged materials) may reduce asthma symptoms and the use of asthma medicines.62 A systematic review and meta-analysis found that damp remediation of houses reduced asthma-related symptoms including wheezing in adults, and reduced acute care visits in children.62 In children living in mouldy houses, remediation of the home may reduce symptoms and flare-ups, compared with cleaning advice about moulds.63

Other strategies that have been proposed for avoiding exposure to moulds include:4

  • removing visible mould by cleaning with bleach or other mould reduction cleaners (patients should avoid breathing vapours)
  • using high-efficiency air filters
  • removing indoor pot plants
  • drying or removing wet carpets
  • treating rising damp as soon as it is detected
  • avoiding the use of organic mulches and compost.
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Triggers in the workplace

A wide range of occupational allergens has been associated with work-related asthma. Investigation of work-related asthma is complex and typically requires specialist referral.

Table. Examples of common sensitising agents and occupations associated with exposure

Agent

Occupations

Low molecular weight agents

Wood dust (e.g. western red cedar, redwood, oak)

  • Carpenters
  • Builders
  • Model builders
  • Sawmill workers
  • Sanders

Isocyanates

  • Automotive industry workers
  • Adhesive workers
  • Chemical industry
  • Mechanics
  • Painters
  • Polyurethane foam production workers

Formaldehyde

  • Cosmetics industry
  • Embalmers
  • Foundry workers
  • Hairdressers
  • Healthcare workers
  • Laboratory workers
  • Tanners
  • Paper, plastics and rubber industry workers

Platinum salts

  • Chemists
  • Dentists
  • Electronics industry workers
  • Metallurgists
  • Photographers

High molecular weight agents

Latex

  • Food handlers
  • Healthcare workers
  • Textile industry workers
  • Toy manufacturers

Flour and grain dust

  • Bakers
  • Combine harvester drivers
  • Cooks
  • Farmers
  • Grocers
  • Pizza makers

Animal allergens (e.g. urine, dander)

  • Animal breeders
  • Animal care workers
  • Jockeys
  • Laboratory workers
  • Pet shop workers
  • Veterinary surgery workers

Source: Adapted from Hoy R, Abramson MJ, Sim MR. Work related asthma. Aust Fam Physician 2010; 39: 39-42. Available from: http://www.racgp.org.au/afp/201001/35841

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Alternative diagnostic tests for asthma and allergy

The Australasian Society of Clinical Immunology and Allergy (ASCIA) recommends against the following techniques for the diagnosis and treatment of allergy, asthma and immune disorders because they have not been shown to be reliable or accurate:3

  • cytotoxic testing (Bryans’ or Alcat testing)
  • hair analysis
  • iridology
  • kinesiology
  • oral provocation and neutralisation
  • pulse testing
  • radionics (psionic medicine, dowsing)
  • tests for ‘dysbiosis’
  • vega testing (electrodermal testing)
  • VoiceBio.

ASCIA also recommends against the use of conventional tests in the investigation of allergies in inappropriate clinical situations, or where the results are presented in a manner amenable to misinterpretation, e.g:3

  • food-specific IgE (RAST, ImmunoCap testing)
  • food-specific IgG, IgG4
  • lymphocyte subset analysis.
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References

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