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-triggered asthma.

How this recommendation was developed

Adapted from existing guidance

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

  • NACA, 2017[REFERENCE1667]

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 for children with recurrent wheezing when the results might guide you in (either of):

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

Note: Allergy tests are not mandatory in the diagnostic investigation of asthma in children.

How this recommendation was developed

Consensus

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

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, 20131

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, 20131

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, 20131

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, 20072

More information

Allergies and asthma: links

There is a strong link between asthma and allergies:3, 4

  • 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.4 Among people with food allergies, asthma may be a risk factor for fatal anaphylaxis due to food allergens.56 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.3

Close
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.7 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.8

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.9

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.10, 11, 12, 13, 14 However, the use of antihistamines in children has not been shown to prevent them developing asthma.7

The presence of allergic rhinitis is associated with worse asthma control in children and adults.15, 16, 17, 18 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.19

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.8 However, ryegrass is not found in tropical regions (see Thunderstorm-triggered asthma).

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

Thunderstorm-triggered asthma

Seasonal allergic rhinitis, which in Australia is typically associated with sensitisation to perennial ryegrass (Lolium perenne), is an important risk factor for thunderstorm-triggered asthma.20

Close
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: https://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.19, 7, 21 Intranasal corticosteroid are most effective when taken continuously.19

Intranasal corticosteroids are effective in reducing congestion, rhinorrhoea, sneezing and itching in adults and adolescents with allergic rhinitis.19, 7 They are also effective for ocular symptoms.22

All available intranasal corticosteroids appear to be equally effective.19

The onset of action is between 3 and 36 hours after first dose and, in practice, the full therapeutic effect takes a few days.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.21

Intranasal corticosteroids are well tolerated. Common (>1%) adverse effects include nasal stinging, itching, nosebleed, sneezing, sore throat, dry mouth, cough.24 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.25

Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects when given in recommended doses.19, 26 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.19

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.24

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.19, 21, 20

The onset of therapeutic action is approximately 30 minutes after dosing.20

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.27

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms.21, 28 They can provide adequate relief for some individuals when taken continuously or intermittently.19 Available agents appear to be equally effective.26

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.19, 29 In adults with allergic rhinitis, oral antihistamines usually produce no further improvement when added to intranasal corticosteroid treatment.19

Common (>1%) adverse effects include drowsiness, fatigue, headache, nausea and dry mouth.24 Oral antihistamines can also cause ocular dryness.30

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.7

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.19 They have a rapid onset of action (15–30 minutes).19

The most common (>1%) adverse effect is local irritation.24 Bitter taste is more common intranasal antihistamines than with intranasal corticosteroids.19

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.7, 21 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.19, 7 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.21

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.31, 32, 33, 34, 35 A recent analysis of databases of adults and children taking montelukast suggests it is associated with nightmares, depression, and aggression.35 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.35

Other nasal sprays

Ipratropium bromide spray is effective in managing persistent rhinorrhoea in patients with allergic rhinitis, but not blockage or itch.7 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.26

Specific allergen immunotherapy

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

Close
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: https://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.19, 7 However, there is weaker evidence to support their efficacy in children than in adults.7 There is limited evidence to guide the treatment of allergic rhinitis in preschool children.21

The addition of an oral H1-antihistamine or leukotriene receptor antagonist to an intranasal corticosteroid is generally no more effective than intranasal corticosteroid monotherapy.21

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.36 Intranasal corticosteroids are not generally associated with clinically significant systemic adverse effects in children when given in recommended doses.1926 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.19 One knemometry study showed reduced lower leg growth rate in children using intranasal budesonide.19 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.19

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.27

Less sedating oral H1-antihistamines are effective in managing allergic rhinitis symptoms of rhinorrhoea, sneezing, nasal itching and ocular symptoms,21, 28 including in preschool children. 21 They can provide adequate relief for some individuals when taken continuously or intermittently.19 Available agents appear to be equally effective.26

However, oral antihistamines are less effective than continuous intranasal corticosteroids, especially for nasal congestion.19, 29 The addition of oral antihistamines to intranasal corticosteroids has not been demonstrated to be an effective strategy in children.37

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.7

Intranasal antihistamines are more effective than oral antihistamines for reducing nasal congestion.19 They have a rapid onset of action (15–30 minutes).19

Montelukast

Leukotriene receptor antagonists are no more effective than oral H1-antihistamines.7, 21 Montelukast is less effective than intranasal corticosteroid in the treatment of allergic rhinitis.19, 7 In most studies, adding montelukast to an intranasal corticosteroid was not more effective than intranasal corticosteroid alone.21

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.31, 32, 33, 34 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).35 Allergic granulomatous angiitis has also been reported, but a causal relationship has not been established.35

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).

 

Close
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.

Close
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.38 Saline administered by spray or other devices was used at least twice daily in most studies that showed a benefit.38

Isotonic solution is preferable to hypertonic solution because it supports optimal mucociliary clearance.38 Isotonic saline is solution is inexpensive and has no known adverse effects.38 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.

Close
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.39 Several surgical procedures are available to correct this problem.40 The ideal surgical reduction should preserve the mucosa and physiological function.39

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’).40 There is no evidence that turbinate surgery creates these conditions, but sino-nasal surgery may exacerbate the symptoms.

 

Close
Thunderstorm-triggered 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 sensitised individuals, even if they have not had asthma before.41, 20, 42, 43, 21 People at risk of acute asthma flare-ups triggered by a thunderstorm include those with seasonal allergic rhinitis (with or without asthma), those with asthma (or a history of asthma), and those with undiagnosed asthma.20

Epidemics of thunderstorm-triggered asthma can occur when such a storm travels across a region and triggers asthma in many susceptible individuals, causing a high demand on ambulance and health services.42 However, epidemic thunderstorm asthma events are uncommon.

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).20 The worst outcomes are seen in people with poorly controlled asthma. Regular treatment with an inhaled corticosteroid asthma preventer was significantly protective in a well-conducted Australian case-control study.21

Prevention and management are based on:44

  • year-round asthma control, including inhaled corticosteroid-containing preventers where indicated
  • preventive inhaled corticosteroid treatment for adults and adolescents with asthma who have known or suspected allergy to grass pollens (e.g. concomitant allergic rhinitis, a history of spring flare-ups in asthma symptoms) but are not already taking regular medication. Treatment should at least 2 weeks (ideally 6 weeks) before exposure to springtime high pollen concentrations and thunderstorms and continue throughout the local grass pollen season. For children, asthma should be managed according to age group.
  • preventive intranasal corticosteroid treatment for adults and adolescents with seasonal allergic rhinitis, because it can be reasonably assumed that they are allergic to ryegrass pollen. Treatment should start at least 2 weeks (ideally 6 weeks) before exposure to springtime high pollen concentrations and thunderstorms and continue throughout the local grass pollen season. For children, allergic rhinitis should be managed according to age group.
  • advice for at-risk patients to avoid being outdoors just before and during thunderstorms in spring and early summer, especially during wind gusts that precede the rain front
  • advice to ensure appropriate access to relievers during grass pollen season.
Close
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.1

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;1 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.1 ASCIA’s manual on skin prick testing lists other risk factors.1

Close
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.1 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.1 ASCIA’s manual on skin prick testing lists other risk factors.1

Total serum IgE testing

In children aged 0–5 years, total serum immunoglobulin E measurement is a poor predictor of allergies or asthma.45

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.45 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.45

Close
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.3

The amount of allergen excreted differs between breeds.3 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,46 or in owner’s homes47 with these breeds than other breeds.

Cat allergens easily spread on clothing and are found in places where cats have never been.3

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.3

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.48

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.
Close
House dust mite

Exposure to house dust mite (mainly Dermatophagoides pteronyssinus) is a major asthma trigger in Australia.3 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:3

  • 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.495051525354555657585960 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.61 The use of allergen-impermeable mattress covers, as a single mite-reduction intervention in adults, is unlikely to be effective in improving asthma.62

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.

Close
Pollens

Allergy to airborne pollen grains from certain grasses, weeds and trees is common in people with asthma in Australia.3 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:3, 63

  • 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:3

  • 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).

Close
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.64 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.64 In children living in mouldy houses, remediation of the home may reduce symptoms and flare-ups, compared with cleaning advice about moulds.65

Other strategies that have been proposed for avoiding exposure to moulds include:3

  • 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.
Close
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

Asset ID: 45

Close
Close
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:2

  • 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:2

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

References

  1. Australasian Society of Clinical Immunology and Allergy (ASCIA), Skin Prick Testing Working Party. Skin prick testing for the diagnosis of allergic disease: A manual for practitioners. ASCIA, Sydney, 2013. Available from: http://www.allergy.org.au/health-professionals/papers/skin-prick-testing
  2. Australasian Society of Clinical Immunology and Allergy (ASCIA), ASCIA Position Statement. Unorthodox Techniques for the Diagnosis and Treatment of allergy, Asthma and Immune Disorders, ASCIA 2007. Available from: http://www.allergy.org.au/health-professionals/papers/unorthodox-techniques-for-diagnosis-and-treatment
  3. National Asthma Council Australia. Asthma and allergy. National Asthma Council Australia, Melbourne, 2012. Available from: http://www.nationalasthma.org.au/publication/asthma-allergy-hp
  4. Custovic A, Simpson A. The role of inhalant allergens in allergic airways disease. J Investig Allergol Clin Immunol. 2012; 22: 393-401. Available from: http://www.jiaci.org/issues/vol22issue6/vol22issue06-1.htm
  5. Bock SA, Muñoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. 2001; 107: 191-3. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11150011
  6. Bock SA, Muñoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001-2006. J Allergy Clin Immunol. 2007; 119: 1016-1018. Available from: http://www.jacionline.org/article/S0091-6749(06)03814-0/fulltext
  7. Brożek JL, Bousquet J, Baena-Cagnani CE, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines: 2010 Revision. J Allergy Clin Immunol. 2010; 126: 466-476. Available from: http://www.jacionline.org/article/S0091-6749(10)01057-2/fulltext
  8. National Asthma Council Australia. Managing allergic rhinitis in people with asthma. An information paper for health professionals. National Asthma Council Australia, Melbourne, 2012. Available from: http://www.nationalasthma.org.au/publication/allergic-rhinitis-asthma-hp
  9. Spangler DL, Abelson MB, Ober A, Gotnes PJ. Randomized, double-masked comparison of olopatadine ophthalmic solution, mometasone furoate monohydrate nasal spray, and fexofenadine hydrochloride tablets using the conjunctival and nasal allergen challenge models. Clin Ther. 2003; 25: 2245-67. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14512132
  10. Pallasaho, P, Juusela, M, Lindqvist, A, et al. Allergic rhinoconjunctivitis doubles the risk for incident asthma – results from a population study in Helsinki, Finland. Respir Med. 2011; 105: 1449-1456. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21600752
  11. Rochat, M K, Illi, S, Ege, M J, et al. Allergic rhinitis as a predictor for wheezing onset in school-aged children. J Allergy Clin Immunology. 2010; 126: 1170-5.e2.
  12. van den Nieuwenhof, L, Schermer, T, Bosch, Y, et al. Is physician-diagnosed allergic rhinitis a risk factor for the development of asthma?. Allergy. 2010; 65: 1049-1055.
  13. Morais-Almeida, M, Gaspar, A, Pires, G, et al. Risk factors for asthma symptoms at school age: an 8-year prospective study. Allergy Asthma Proc. 2007; 28: 183-189.
  14. Shaaban R, Zureik M, Soussan D, et al. Rhinitis and onset of asthma: a longitudinal population-based study. Lancet. 2008; 372: 1047-1057. Available from: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)61446-4/fulltext
  15. Thomas M, Kocevar VS, Zhang Q, et al. Asthma-related health care resource use among asthmatic children with and without concomitant allergic rhinitis. Pediatrics. 2005; 115: 129-34. Available from: http://pediatrics.aappublications.org/content/115/1/129.long
  16. Price D, Zhang Q, Kocevar VS, et al. Effect of a concomitant diagnosis of allergic rhinitis on asthma-related health care use by adults. Clin Exp Allergy. 2005; 35: 282-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15784104
  17. Oka, A., Matsunaga, K., Kamei, T., et al. Ongoing allergic rhinitis impairs asthma control by enhancing the lower airway inflammation. J Allergy Clin Immunol Pract. 2014; 2: 172-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/24607045
  18. de Groot EP, Nijkamp A, Duiverman EJ, Brand PL. Allergic rhinitis is associated with poor asthma control in children with asthma. Thorax. 2012; 67: 582-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22213738
  19. Seidman MD, Gurgel RK, Lin SY, et al. Clinical practice guideline: Allergic rhinitis. Otolaryngol Head Neck Surg. 2015; 152: S1-43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25644617
  20. Davies J, Queensland University of Technology. Literature review on thunderstorm asthma and its implications for public health advice. Final report. Victorian State Government Department of Health and Human Services, Melbourne, 2017.
  21. Girgis ST, Marks GB, Downs SH, et al. Thunderstorm-associated asthma in an inland town in south-eastern Australia. Who is at risk?. Eur Respir J. 2000; 16: 3-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10933077
  22. Hong J, Bielory B, Rosenberg JL, Bielory L. Efficacy of intranasal corticosteroids for the ocular symptoms of allergic rhinitis: A systematic review. Allergy Asthma Proc. 2011; 32: 22-35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21262095
  23. Bousquet J, Schunemann HJ, Hellings PW, et al. MACVIA clinical decision algorithm in adolescents and adults with allergic rhinitis. J Allergy Clin Immunol Pract. 2016; 138: 367-374.e2. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27260321
  24. . Australian Medicines Handbook. Last modified July 2017. Australian Medicines Handbook Pty Ltd, 2017.
  25. Verkerk, M. M., Bhatia, D., Rimmer, J., et al. Intranasal steroids and the myth of mucosal atrophy: a systematic review of original histological assessments. Am J Rhinol Allergy. 2015; 29: 3-18. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25590306
  26. Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: An updated practice parameter. J Allergy Clin Immunol. 2008; 122: S1-S84. Available from: http://www.jacionline.org/article/S0091-6749(08)01123-8/fulltext
  27. Mann RD, Pearce GL, Dunn N, Shakir S. Sedation with "non-sedating" antihistamines: four prescription-event monitoring studies in general practice. BMJ (Clinical research ed). 2000; 320: 1184-6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10784544
  28. Bachert C, Maspero J. Efficacy of second-generation antihistamines in patients with allergic rhinitis and comorbid asthma. J Asthma. 2011; 48: 965-73. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21970671
  29. Bousquet J, Khaltaev N, Cruz AA, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) 2008. Allergy. 2008; 63: 8-160. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2007.01620.x/full
  30. Ousler GW, Wilcox KA, Gupta G, Abelson MB. An evaluation of the ocular drying effects of 2 systemic antihistamines: loratadine and cetirizine hydrochloride. Ann Allergy Asthma Immunol. 2004; 93: 460-4.
  31. Schumock GT, Stayner LT, Valuck RJ, et al. Risk of suicide attempt in asthmatic children and young adults prescribed leukotriene-modifying agents: a nested case-control study. J Allergy Clin Immunol. 2012; 130: 368-75. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22698520
  32. Wallerstedt SM, Brunlöf G, Sundström A, Eriksson AL. Montelukast and psychiatric disorders in children. Pharmacoepidemiol Drug Saf. 2009; 18: 858-864. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19551697
  33. Philip G, Hustad C, Noonan G, et al. Reports of suicidality in clinical trials of montelukast. J Allergy Clin Immunol. 2009; 124: 691-6.e6. Available from: http://www.jacionline.org/article/S0091-6749(09)01247-0/fulltext
  34. Philip G, Hustad CM, Malice MP, et al. Analysis of behavior-related adverse experiences in clinical trials of montelukast. J Allergy Clin Immunol. 2009; 124: 699-706.e8. Available from: http://www.jacionline.org/article/S0091-6749(09)01248-2/fulltext
  35. Haarman MG, van Hunsel F, de Vries TW. Adverse drug reactions of montelukast in children and adults. Pharmacol Res Perspect. 2017; 5: e00341. Available from: http://onlinelibrary.wiley.com/doi/10.1002/prp2.341/full
  36. Verkerk MM, Bhatia D, Rimmer J, et al. Intranasal steroids and the myth of mucosal atrophy: a systematic review of original histological assessments. Am J Rhinol Allergy. 2015; 29: 3-18. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25590306
  37. Nasser M, Federowicz Z, Aljufairi H, McKerrow W. Antihistamines used in addition to topical nasal steroids for intermittent and persistent allergic rhinitis in children. Cochrane Database Syst Rev. 2010; Issue 7: . Available from: https://www.ncbi.nlm.nih.gov/pubmed/20614452
  38. Hermelingmeier, K. E., Weber, R. K., Hellmich, M., et al. Nasal irrigation as an adjunctive treatment in allergic rhinitis: a systematic review and meta-analysis. Am J Rhinol Allergy. 2012; 26: e119-25. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904042/
  39. Barham, H. P., Thornton, M. A., Knisely, A., et al. Long-term outcomes in medial flap inferior turbinoplasty are superior to submucosal electrocautery and submucosal powered turbinate reduction. Int Forum Allergy Rhinol. 2016; 6: 143-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26681570
  40. Seidman, M. D., Gurgel, R. K., Lin, S. Y., et al. Clinical practice guideline: Allergic rhinitis. Otolaryngol Head Neck Surg. 2015; 152: S1-43. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25644617
  41. D'Amato G, Vitale C, D'Amato M, et al. Thunderstorm-related asthma: what happens and why. Clin Exp Allergy. 2016; 46: 390-6.
  42. Victoria State Government Department of Health and Human Services,. The November 2016 Victorian epidemic thunderstorm asthma event: an assessment of the health impacts. The Chief Health Officer’s Report, 27 April 2017. Victorian Government, Melbourne, 2017.
  43. Marks GB, Colquhoun JR, Girgis ST, et al. Thunderstorm outflows preceding epidemics of asthma during spring and summer. Thorax. 2001; 56: 468-71. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1746065/
  44. National Asthma Council Australia. Thunderstorm asthma. An information paper for health professionals. NACA, Melbourne, 2017.
  45. Brand PL, Baraldi E, Bisgaard H, et al. Definition, assessment and treatment of wheezing disorders in preschool children: an evidence-based approach. Eur Respir J. 2008; 32: 1096-1110. Available from: http://erj.ersjournals.com/content/32/4/1096.full
  46. Vredegoor DW, Willemse T, Chapman MD, et al. Can f 1 levels in hair and homes of different dog breeds: lack of evidence to describe any dog breed as hypoallergenic. J Allergy Clin Immunol. 2012; 130: 904-9.e7. Available from: http://www.jacionline.org/article/S0091-6749(12)00793-2/fulltext
  47. Nicholas CE, Wegienka GR, Havstad SL, et al. Dog allergen levels in homes with hypoallergenic compared with nonhypoallergenic dogs. Am J Rhinol Allergy. 2011; 25: 252-6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680143/
  48. Kilburn S, Lasserson TJ, McKean M. Pet allergen control measures for allergic asthma in children and adults. Cochrane Database Syst Rev. 2001; Issue 1: CD002989. Available from: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD002989/full
  49. de Vries MP, van den Bemt L, Aretz K, et al. House dust mite allergen avoidance and self-management in allergic patients with asthma: randomised controlled trial. Br J Gen Pract. 2007; 57: 184-90. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042544/
  50. Dharmage S, Walters EH, Thien F, et al. Encasement of bedding does not improve asthma in atopic adult asthmatics. Int Arch Allergy Immunol. 2006; 139: 132-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16374022
  51. van den Bemt L, van Knapen L, de Vries MP, et al. Clinical effectiveness of a mite allergen-impermeable bed-covering system in asthmatic mite-sensitive patients. J Allergy Clin Immunol. 2004; 114: 858-62. Available from: http://www.jacionline.org/article/S0091-6749(04)01671-9/fulltext
  52. Cloosterman SG, Schermer TR, Bijl-Hofland ID, et al. Effects of house dust mite avoidance measures on Der p 1 concentrations and clinical condition of mild adult house dust mite-allergic asthmatic patients, using no inhaled steroids. Clin Exp Allergy. 1999; 29: 1336-46. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10520054
  53. van der Heide S, Kauffman HF, Dubois AE, de Monchy JG. Allergen-avoidance measures in homes of house-dust-mite-allergic asthmatic patients: effects of acaricides and mattress encasings. Allergy. 1997; 52: 921-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9298177
  54. Dorward AJ, Colloff MJ, MacKay NS, et al. Effect of house dust mite avoidance measures on adult atopic asthma. Thorax. 1988; 43: 98-102. Available from: http://thorax.bmj.com/content/43/2/98.short
  55. Halken S, Host A, Niklassen U, et al. Effect of mattress and pillow encasings on children with asthma and house dust mite allergy. J Allergy Clin Immunol. 2003; 111: 169-76. Available from: http://www.jacionline.org/article/S0091-6749(02)91267-4/fulltext
  56. Frederick JM, Warner JO, Jessop WJ, et al. Effect of a bed covering system in children with asthma and house dust mite hypersensitivity. Eur Respir J. 1997; 10: 361-6. Available from: http://erj.ersjournals.com/content/10/2/361.short
  57. Warner JA, Marchant JL, Warner JO. Double blind trial of ionisers in children with asthma sensitive to the house dust mite. Thorax. 1993; 48: 330-3. Available from: http://thorax.bmj.com/content/48/4/330.abstract
  58. Thiam DG, Tim CF, Hoon LS, et al. An evaluation of mattress encasings and high efficiency particulate filters on asthma control in the tropics. Asian Pac J Allergy Immunol. 1999; 17: 169-74. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10697255
  59. Rijssenbeek-Nouwens LH, Oosting AJ, de Bruin-Weller MS, et al. Clinical evaluation of the effect of anti-allergic mattress covers in patients with moderate to severe asthma and house dust mite allergy: a randomised double blind placebo controlled study. Thorax. 2002; 57: 784-90. Available from: http://thorax.bmj.com/content/57/9/784.full
  60. Brehler R, Kniest F. Encasing study in mite-allergic patients - One-year, double-blind, placebo and environment-controlled investigation. Allergy & Clin Immunol Inter. 2006; 18: 15-19. Available from: http://acii.net/ezm/index.php?ezm=ACI&la=e&ShowAbstract=16940&IssueID=1622
  61. Gøtzsche PC, Johansen HK. House dust mite control measures for asthma. Cochrane Database Syst Rev. 2008; Issue 2: CD001187. Available from: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD001187.pub3/full
  62. Woodcock A, Forster L, Matthews E, et al. Control of exposure to mite allergen and allergen-impermeable bed covers for adults with asthma. N Engl J Med. 2003; 349: 225-36. Available from: http://www.nejm.org/doi/full/10.1056/NEJMoa023175#t=article
  63. Erbas B, Akram M, Dharmage SC, et al. The role of seasonal grass pollen on childhood asthma emergency department presentations. Clin Exp Allergy. 2012; 42: 799-805. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22515396
  64. Sauni R, Uitti J, Jauhiainen M, et al. Remediating buildings damaged by dampness and mould for preventing or reducing respiratory tract symptoms, infections and asthma. Cochrane Database Syst Rev. 2011; Issue 9: CD007897. Available from: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD007897.pub2/full
  65. Kercsmar CM, Dearborn DG, Schluchter M, et al. Reduction in asthma morbidity in children as a result of home remediation aimed at moisture sources. Environ Health Perspect. 2006; 114: 1574-80. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626393/