Asthma Management Handbook

Considering triggers and comorbidities


Ask the person or parents/carers about what triggers asthma symptoms or flare-ups, so you can identify those that are clinically relevant to the individual and whether they are potentially avoidable.

Table. Summary of asthma triggers Opens in a new window Please view and print this figure separately:

How this recommendation was developed


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

Last reviewed version 2.0

Ask about exposure to cigarette smoke.

How this recommendation was developed


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

Last reviewed version 2.0

Ask the person about their other health conditions and consider whether comorbid medical conditions may be affecting asthma control, e.g.:

  • uncontrolled allergic rhinitis/rhinosinusitis
  • gastro-oesophageal reflux disease
  • nasal polyposis
  • obesity
  • upper airway dysfunction
  • cardiovascular disease.
How this recommendation was developed


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

Last reviewed version 2.0

Ask the person about all the medicines (including complementary medicines) they take for other health conditions, and consider if these may be affecting asthma.

How this recommendation was developed


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

Last reviewed version 2.0

Ask about the person’s current main health concerns and main general concerns, in order to understand whether other health or life priorities may be affecting asthma self-management.

How this recommendation was developed


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

Last reviewed version 2.0

Ask the person about possible contact with new allergens (e.g. pets, moulds).

How this recommendation was developed


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

Last reviewed version 2.0

Ask about possible exposure to irritants or allergens in the workplace or due to a new activity or hobby.

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



Low molecular weight agents

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

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


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


  • 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


  • 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:

Asset ID: 45


Table. Questions to consider for patients with suspected work-related asthma

Was there any unusual exposure to any substance at work within the 24 hours before symptoms began?

Did the person’s co-workers experience respiratory symptoms?

Does the person’s asthma symptoms improve when away from work (e.g. weekends, holidays)?

Are symptoms of rhinitis or conjunctivitis worse at work?

Source: Adapted from Tarlo SM, Balmes J, Balkissoon R et al. Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest 2008; 134(3 Suppl): 1S-41S. Available from:

Asset ID: 46


Table. Features of history in work-related asthma


Work-exacerbated asthma

Occupational asthma

Sensitiser-induced occupational asthma Irritant-induced occupational asthma

Onset of asthma symptoms

Before or during working life

Typically weeks to months after first exposure to sensitiser

Typically within 24 hours of major exposure to respiratory irritant

Pattern of asthma symptoms

Worse on workdays

Worse during or after work shift and improve when away from work

Persist for at least 12 weeks with no previous chronic lung disease

Other factors

Exposure to dust, smoke, fumes, cold

Exposure to known sensitiser

Exposure to large amount of respiratory irritant

Adapted from:

Hoy R, Abramson MJ, Sim MR. Work related asthma. Aust Fam Physician 2010; 39: 39-42. Available from:

Tarlo SM, Liss GM. Occupational asthma: an approach to diagnosis and management. Can Med Assoc J 2003; 168: 867-71. Available from:

Asset ID: 47

How this recommendation was developed


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

Last reviewed version 2.0

More information

Investigation of work-related asthma symptoms

Asking all workers with asthma whether their asthma symptoms improve when away from work is a useful screening tool. Those who answer 'yes' need investigation for work-related asthma.1

Investigation of suspected work-related asthma is complex. It involves confirming the diagnosis of asthma, identifying the workplace as the cause of asthma symptoms, and identifying the specific causal agents. This involves taking a detailed history, further investigations (e.g. serial peak expiratory flow measurement, skin prick tests, bronchial provocation [challenge] testing) and sometimes worksite visits.23

People with suspected work-related asthma should ask their employer to provide a safety data sheet containing information about the constituents and properties of substances used at the workplace. Information about safety data sheets (previously called Material Safety Data Sheets) is available from Safe Work Australia.

Accurate diagnosis and documentation are essential to support a potential Workers Compensation claim. This normally requires a report from a specialist with experience investigating work-related asthma.

Effects of smoking on asthma control and medicines

Smoking reduces the probability of achieving good asthma control.4 Among adults with asthma, exposure to cigarette smoke (smoking or regular exposure to environmental tobacco smoke within the previous 12 months) has been associated with a significantly increased risk of needing acute asthma care within the next 2–3 years.5

Smoking reduces response to inhaled corticosteroids and oral corticosteroids in people with asthma.678, 9, 10 People who smoke may need higher doses of inhaled corticosteroids to receive the same benefits (improvement in lung function and reduction in flare-ups) as non-smokers.10

Therapeutic response to montelukast appears to be unchanged by smoking.8 Therefore, montelukast may be useful in smokers with mild asthma.11, 12

Note: PBS status as at March 2019: Montelukast treatment is not subsidised by the PBS for people aged 15 years or over. Special Authority is available for DVA gold card holders, or white card holders with approval for asthma treatments.

Effects of exposure to environmental tobacco smoke on asthma

Among adults with asthma, exposure to cigarette smoke (smoking or regular exposure to environmental tobacco smoke within the previous 12 months) has been associated with a significantly increased risk of needing acute asthma care within the next 2–3 years.5

Gastro-oesophageal reflux disease links with asthma

The majority of patients with asthma report symptoms of gastro-oesophageal reflux disease or an abnormal result on the 24-hour oesophageal pH test.13 Among children treated in referral clinics, the prevalence of gastro-oesophageal reflux disease is higher among those with asthma than those without asthma,14 but the causal link is unclear.14

Asthma may contribute to gastro-oesophageal reflux disease via changes in intrathoracic pressure or the effects of asthma medicines on the gastro-oesophageal sphincter.13

Gastro-oesophageal reflux disease may contribute to bronchoconstriction through various mechanisms (e.g. vagally mediated reflexes, increased airway hyperresponsiveness, chronic microaspiration of gastric fluid into the airways, or airway neurogenic inflammatory responses).13

Although the presence of gastro-oesophageal reflux disease is generally thought to worsen asthma control, the precise effect of gastro-oesophageal reflux disease on asthma is unclear.13

Hyperventilation and asthma

Attacks of hyperventilation can be confused with asthma symptoms in people with asthma and in those without asthma.15 Some patients with asthma who experience hyperventilation attacks cannot readily distinguish the sensation of dyspnoea associated with hyperventilation from that associated with their asthma.15

Obesity links with asthma

Prevalence and mechanisms

Obesity (defined as BMI ≥ 30 kg/m2) is associated with an increased prevalence of asthma.13

Obesity could contribute to asthma development or worsening via mechanical, inflammatory and genetic/developmental factors.13 Increased rates of obstructive sleep apnoea or gastro-oesophageal reflux disease among obese people do not entirely explain the higher rates of symptoms and morbidity seen in obese people with asthma, compared people with asthma who have a normal BMI.16

Asthma in obese patients appears to be a specific phenotype1317 associated with changes in lung function caused by breathing at low lung volumes, a systemic inflammatory process, and a reduced response to asthma medicines.13 Obesity reduces chest wall compliance, which results in reduced lung volumes, increased work of breathing and increased energy and oxygen costs of breathing.18

Considerations for diagnosis and assessment

Obese people with asthma report more dyspnoea and asthma-like symptoms than non-obese patients.18

Respiratory symptoms associated with obesity can mimic asthma.18

In obese patients it is especially important to confirm a previous diagnosis of asthma by objective measures of variable airflow limitation.19

Last reviewed version 2.0

Upper airway dysfunction

Upper airway dysfunction is intermittent, abnormal adduction of the vocal cords during respiration, resulting in variable upper airway obstruction. It often mimics asthma2021 and is commonly misdiagnosed as asthma.1522 It can cause severe acute episodes of dyspnoea that occur either unpredictably or due to exercise.15 Inspiratory stridor associated with vocal cord dysfunction is often described as ‘wheezing’,15 but symptoms do not respond to asthma treatment.2123

Upper airway dysfunction can coexist with asthma.20 People with asthma who also have upper airway dysfunction experience more symptoms than those with asthma alone and this can result in over-treatment if vocal cord dysfunction is not identified and managed appropriately.20

Upper airway dysfunction probably has multiple causes.20 In some people it is probably due to hyperresponsiveness of the larynx in response to intrinsic and extrinsic triggers.2024 Triggers can include exercise, psychological conditions, airborne irritants, rhinosinusitis, gastro-esophageal reflux disease, and medicines.2122

Upper airway dysfunction should be considered when spirometry shows normal FEV1/FVC ratio in a patient with suspected asthma22 or symptoms do not respond to short-acting beta2 agonist reliever. The shape of the maximal respiratory flow loop obtained by spirometry may suggest the diagnosis.15 Direct observation of the vocal cords is the best method to confirm the diagnosis of upper airway dysfunction.20

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.25 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.26

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.27

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.19, 28, 29, 30, 31 However, the use of antihistamines in children has not been shown to prevent them developing asthma.25

The presence of allergic rhinitis is associated with worse asthma control in children and adults.32, 33, 34, 35 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.36

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.37 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.38

Last reviewed version 2.0

Aspirin and nonsteroidal anti-inflammatory drugs as asthma triggers

Most people with asthma can tolerate aspirin (acetylsalicylic acid) and NSAIDs.

Aspirin-exacerbated respiratory disease is a syndrome of airway inflammation that includes asthma, nasal polyposis, chronic rhinosinusitis and reaction to NSAIDs. It can present with severe sudden-onset asthma.

Known aspirin sensitivity occurs in an estimated:3940

  • 0.5–2.5% of the general population
  • 4–11% of adults with asthma
  • 30% of patients with asthma and nasal polyposis.

In addition, a substantial proportion may be unaware that they are sensitive to aspirin. Aspirin challenge studies have identified aspirin sensitivity in approximately 5% of children with asthma, 21% of  adults with asthma, and 30–42% of people with both asthma and nasal polyposis.

People with aspirin-exacerbated respiratory disease may react to one or more anti-inflammatory agents. In a study of 659 patients with skin or airway reactions to NSAIDs challenged with paracetamol, aspirin and a range of nonselective NSAIDs (COX-1 and COX-2 inhibitors) that included piroxicam, diclofenac, ibuprofen and indomethacin), 76%  showed cross-reaction to chemically distinct or unrelated COX-1 inhibitors and 24% reacted only to a single cyclo-oxygenase inhibitor.41 Nonselective NSAIDS available in Australia also include ketoprofen, naproxen and piroxicam. People with NSAID intolerance are unlikely to react to ‘coxib’-type COX-2-selective NSAIDs (celecoxib, etoricoxib, parecoxib).42 Meloxicam has been reported to cause bronchoconstriction at higher doses.42

People with aspirin-exacerbated respiratory disease could be at risk if they use complementary medicines that contain salicylates (e.g. willowbark) or salicin (e.g. meadowsweet).

Challenge testing is sometimes necessary to confirm the diagnosis in people who have not reported a clear association between aspirin and symptoms.

Management of aspirin-exacerbated respiratory disease involves avoidance of aspirin and NSAIDs.43 Aspirin desensitisation is available.4344

Other medicines that can trigger asthma

Beta blockers

Beta-adrenergic blocking agents (beta blockers) may cause bronchoconstriction and reduce lung function and should be used with caution in people with asthma.

Risk may be reduced with cardioselective systemic beta blockers (i.e. those that primarily block beta1-adrenergic receptors in the heart rather than beta2-receptors in the airways), such as atenolol, bisoprolol, metoprolol and nebivolol. However, selective beta blockers are not risk-free. A meta-analysis of randomised, blinded, placebo-controlled clinical trials evaluating acute beta blocker exposure in patients with asthma found hat selective beta blockers caused a fall in FEV1 of >20% in one in eight patients, and respiratory symptoms in one in 33 patients.45

Nonselective systemic beta blockers (including carvedilol, labetolol, oxprenolol, pindolol and propranolol) should not be used in people with asthma.

Ocular beta blocker preparations (e.g. timolol) may also impair respiratory function,4647 and asthma deaths have been reported.4849 Changing from timolol (nonselective) to betaxolol (selective) might improve respiratory function.47 Blocking the tear duct for 2–3 minutes after administering drops (punctual occlusion) may reduce risk of respiratory effects by minimising systemic absorption.50

Prostaglandin analogues (e.g. bimatoprost, latanoprost, travoprost), alpha2-agonists, carbonic acid inhibitors and cholinergic agents are alternative agents for managing intraocular pressure and have minimal effect on airways.46 Note that some preparations are combined with a beta blocker.

Anticholinesterases and cholinergic agents

Cholinesterase inhibitors (e.g. pyridostygmine, neostigmine, donepezil, rivastigmine, galantamine) should be used with caution in people with asthma: they may reduce lung function and theoretically could cause bronchoconstriction.

Cholinergic agents (e.g. carbachol, pilocarpine) might also cause bronchoconstriction.

Complementary medicines

Some complementary and alternative medicines may trigger asthma:

  • Echinacea51
  • bee products (pollen, propolis, royal jelly).525354
  • complementary medicines that contain salicylates (e.g. willowbark) or salicin (e.g. meadowsweet) – could present a risk to people with aspirin-exacerbated respiratory disease


  1. Aasen TB, Burge PS, Henneberger PK, et al. Diagnostic approach in cases with suspected work-related asthma. J Occup Med Toxicol. 2013; 8: 17. Available from:
  2. Hoy RF, Abramson MJ, Sim MR. Work related asthma - diagnosis and management. Aust Fam Physician. 2010; 39: 39-42. Available from:
  3. Tarlo SM, Balmes J, Balkissoon R, et al. Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest. 2008; 134(3 Suppl): 1S-41S. Available from:
  4. Pedersen SE, Bateman ED, Bousquet J, et al. Determinants of response to fluticasone propionate and salmeterol/fluticasone propionate combination in the Gaining Optimal Asthma controL study. J Allergy Clin Immunol. 2007; 120: 1036-42. Available from:
  5. Osborne ML, Pedula KL, O'Hollaren M, et al. Assessing future need for acute care in adult asthmatics: the Profile of Asthma Risk Study: a prospective health maintenance organization-based study. Chest. 2007; 132: 1151-61. Available from:
  6. Chaudhuri R, Livingston E, McMahon AD, et al. Cigarette smoking impairs the therapeutic response to oral corticosteroids in chronic asthma. Am J Respir Crit Care Med. 2003; 168: 1308-1311. Available from:
  7. Chaudhuri R, Livingston E, McMahon AD, et al. Effects of Smoking Cessation on Lung Function and Airway Inflammation in Smokers with Asthma. Am J Respir Crit Care Med. 2006; 174: 127-133. Available from:
  8. Lazarus SC, Chinchilli VM, Rollings NJ, et al. Smoking affects response to inhaled corticosteroids or leukotriene receptor antagonists in asthma. Am J Respir Crit Care Med. 2007; 175: 783-790. Available from:
  9. Pedersen B, Dahl R, Karlström R, et al. Eosinophil and neutrophil activity in asthma in a one-year trial with inhaled budesonide. The impact of smoking. Am J Respir Crit Care Med. 1996; 153: 1519-29. Available from:
  10. Tomlinson JE, McMahon AD, Chaudhuri R, et al. Efficacy of low and high dose inhaled corticosteroid in smokers versus non-smokers with mild asthma. Thorax. 2005; 60: 282-287. Available from:
  11. Tamimi A, Serdarevic D, Hanania NA. The effects of cigarette smoke on airway inflammation in asthma and COPD: therapeutic implications. Respir Med. 2012; 106: 319-28. Available from:
  12. Thomson NC, Chaudhuri R. Asthma in smokers: challenges and opportunities. Curr Opin Pulm Med. 2009; 15: 39-45. Available from:
  13. Boulet LP. Influence of comorbid conditions on asthma. Eur Respir J. 2009; 33: 897-906. Available from:
  14. Thakkar K, Boatright RO, Gilger MA, El-Serag HB. Gastroesophageal Reflux and Asthma in Children: A Systematic Review. Pediatrics. 2010; 125: e925-e930. Available from:
  15. Weinberger M, Abu-Hasan M. Pseudo-asthma: when cough, wheezing, and dyspnea are not asthma. Pediatrics. 2007; 120: 855-864. Available from:
  16. Farah CS, Salome CM. Asthma and obesity: a known association but unknown mechanism. Respirology. 2012; 17: 412-21. Available from:
  17. Dixon A. The treatment of asthma in obesity. Expert Rev Respir Med. 2012; 6: 331-40. Available from:
  18. Aaron SD, Vandemheen KL, Boulet LP, et al. Overdiagnosis of asthma in obese and nonobese adults. CMAJ. 2008; 179: 1121-1131. Available from:
  19. Chong J, Haran C, Chauhan BF, Asher I. Intermittent inhaled corticosteroid therapy versus placebo for persistent asthma in children and adults. Cochrane Database Syst Rev. 2015; : Cd011032. Available from:
  20. Benninger C, Parsons JP, Mastronarde JG. Vocal cord dysfunction and asthma. Curr Opin Pulm Med. 2011; 17: 45-49. Available from:
  21. Deckert J, Deckert L. Vocal cord dysfunction. Am Fam Physician. 2010; 81: 156-159. Available from:
  22. Morris MJ, Christopher KL. Diagnostic criteria for the classification of vocal cord dysfunction. Chest. 2010; 138: 1213-23. Available from:
  23. Kenn K, Balkissoon R. Vocal cord dysfunction: what do we know?. Eur Respir J. 2011; 37: 194-200. Available from:
  24. Gimenez LM, Zafra H. Vocal cord dysfunction: an update. Ann Allergy Asthma Immunol. 2011; 106: 267-274. Available from:
  25. 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:
  26. Rank, M. A., Johnson, R., Branda, M., et al. Long-term outcomes after stepping down asthma controller medications: a claims-based, time-to-event analysis. Chest. 2015; 148: 630-639. Available from:
  27. 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:
  28. 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.
  29. 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.
  30. 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.
  31. 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:
  32. 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:
  33. 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:
  34. Watts, K, Chavasse, R J P G. Leukotriene receptor antagonists in addition to usual care for acute asthma in adults and children. Cochrane Database Syst Rev. 2012; Issue 5: . Available from:
  35. 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:
  36. Szefler, SJ, Phillips, BR, Martinez, FD, et al. Characterization of within-subject responses to fluticasone and montelukast in childhood asthma. J Allergy Clin Immunol. 2005; 115: 233-242. Available from:
  37. Australasian Society of Clinical Immunology and Allergy,, Pollen calendar - guide to common allergenic pollen. **, . Available from:
  38. National Asthma Council Australia,. Monoclonal antibody therapy for severe asthma. An information paper for health professionals.. NACA, Melbourne, 2018.
  39. Chang JE, White A, Simon RA, Stevenson DD. Aspirin-exacerbated respiratory disease: burden of disease. Allergy Asthma Proc. 2012; 33: 117-21. Available from:
  40. Pfaar O, Klimek L. Aspirin desensitization in aspirin intolerance: update on current standards and recent improvements. Curr Opin Allergy Clin Immunol. 2006; 6: 161-6. Available from:
  41. Dona I, Blanca-Lopez N, Cornejo-Garcia JA, et al. Characteristics of subjects experiencing hypersensitivity to non-steroidal anti-inflammatory drugs: patterns of response. Clin Exp Allergy. 2011; 41: 86-95. Available from:
  42. Szczeklik A, Sanak M. The broken balance in aspirin hypersensitivity. Eur J Pharmacol. 2006; 533: 145-55. Available from:
  43. White AA, Stevenson DD. Aspirin-exacerbated respiratory disease: update on pathogenesis and desensitization. Semin Respir Crit Care Med. 2012; 33: 588-94. Available from:
  44. Klimek L, Pfaar O. Aspirin intolerance: does desensitization alter the course of the disease?. Immunol Allergy Clin North Am. 2009; 29: 669-75. Available from:
  45. Morales, D. R., Jackson, C., Lipworth, B. J., et al. Adverse respiratory effect of acute beta-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials. Chest. 2014; 145: 779-86. Available from:
  46. Waldock A, Snape J, Graham CM. Effects of glaucoma medications on the cardiorespiratory and intraocular pressure status of newly diagnosed glaucoma patients. Br J Ophthalmol. 2000; 84: 710-3. Available from:
  47. Diggory P, Heyworth P, Chau G, et al. Unsuspected bronchospasm in association with topical timolol--a common problem in elderly people: can we easily identify those affected and do cardioselective agents lead to improvement?. Age Ageing. 1994; 23: 17-21. Available from:
  48. Odeh, M., Oliven, A., Bassan, H.. Timolol eyedrop-induced fatal bronchospasm in an asthmatic patient. The Journal of family practice. 1991; 32: 97-8. Available from:
  49. Taniguchi, M., Kino, H., Mori, M., Nakahama, M.. A case of fatal asthma induced by timolol eye-drop. Nihon Kyobu Shikkan Gakkai zasshi. 1990; 28: 156-9. Available from:
  50. Hepsen IF, Yildirim Z, Yilmaz H, Kotuk M. Preventive effect of lacrimal occlusion on topical timolol-induced bronchoconstriction in asthmatics. Clin Experiment Ophthalmol. 2004; 32: 597-602. Available from:
  51. Mullins RJ, Heddle R. Adverse reactions associated with echinacea: the Australian experience. Ann Allergy Asthma Immunol. 2002; 88: 42-51. Available from:
  52. Bullock RJ, Rohan A, Straatmans JA. Fatal royal jelly-induced asthma. Med J Aust. 1994; 160: 44. Available from:
  53. Leung R, Thien FC, Baldo B, Czarny D. Royal jelly-induced asthma and anaphylaxis: clinical characteristics and immunologic correlations. J Allergy Clin Immunol. 1995; 96: 1004-7. Available from:
  54. Thien FC, Leung R, Plomley R, et al. Royal jelly-induced asthma. Med J Aust. 1993; 159: 639. Available from: