Thorax

August 2015

FocusThorax

Adult-onset asthma

Volume 44, No.8, August 2015 Pages 554-557

Jonathan Burdon

Background

Asthma is commonly overlooked or misdiagnosed in adults. Adult-onset asthma differs from asthma that first occurs in childhood as it is less well controlled, more likely to be non-atopic and associated with a faster decline in lung function. Risk factors include exposure to sensitising or irritant substances, obesity, pharmaceutical agents, rhinitis, environmental pollutants, respiratory tract infections and psychological stress.

Objective/s

The aim of this article is to provide an overview of adult-onset asthma.

Discussion

The clinical presentation of adult-onset asthma is similar to that in any age group. Care needs to be taken to differentiate it from chronic obstructive pulmonary disease and other conditions with similar symptoms. Measurement of reversible airflow obstruction, as demonstrated by an increase in forced expiratory volume in 1 second (FEV1) following inhalation of a short-acting beta-2 agonist (eg salbutamol) of more than 200 ml or 12%, or a positive provocation test is needed to confirm the diagnosis. Management of asthma in adults is based on confirming the diagnosis, assessing the symptoms and their control, asthma education and establishing treatment goals.

Asthma may be defined clinically as ‘the combination of variable respiratory symptoms (eg wheeze, shortness of breath, cough and chest tightness) and excessive variation in lung function.1 Asthma is common in Australia, with a prevalence of about 10%.2 Most cases of asthma have their onset during childhood and adolescent years. However, asthma may occur for the first time at any age. It is commonly overlooked or misdiagnosed in adults, particularly in those aged 65 years and older.3–5 Adult-onset asthma differs from asthma that first occurs in childhood as it is less well controlled, more likely to be non-atopic and associated with a faster decline in lung function.6,7 It often occurs in response to an external trigger (eg infection, aeroallergens, exposures to occupational or pharmaceutical agents) or a recurrence of childhood asthma. Adult-onset asthma will become more common because of the increasing longevity of the general population.8

Risk factors and triggers

The cause of asthma at any age is unclear. A number of risk factors for the development of adult-onset asthma have been recognised. These include exposure to sensitising or irritant substances, obesity, pharmaceuticals, rhinitis, environmental pollutants, respiratory tract infections and psychological stress.1 In Australia about 10% of adult-onset asthma cases are caused by occupational exposures.9 Indeed, 20–25% of adults with asthma report that their symptoms are worse at work.10,11 A thorough occupational history is important, especially noting the timing of symptoms and presence in the workplace. Initially, symptoms usually abate when not at work (eg weekends), but become more persistent with continued exposure. The onset of symptoms may also be delayed for a number of hours. Therefore, symptoms experienced after work (eg the evening or at night) may represent a delayed response to an occupational exposure. Common exposures include composite woods (eg chipboard, medium-density fibreboards), western red cedar, baker’s flour, epoxy resins, isocyanates and animal dander.12

Obesity and asthma are common disorders in the Australian community, and the latter has become more prevalent in past 20 years.2 Obesity is a well-recognised cause of breathlessness, but has also been found to be a risk factor in the development of asthma in adults,13 especially those with a body mass index (BMI) 30 kg/m2.13–15 Aspirin and beta-blocker medications are recognised trigger factors for asthma flare-ups and may unmask an underlying bronchial hyper-responsiveness in some individuals. Beta-blocking eye drops (used in the treatment of glaucoma) may cause wheezing, chest tightness or breathlessness in sensitive individuals.

Rhinitis is a risk factor in the development of asthma in non-atopic and atopic adults.16–18 However, the role of nasal polyposis and chronic rhinosinus disease is less clear. Environmental pollutants, and active and passive tobacco smoking have long been recognised as trigger factors in people with asthma. It is less well recognised that cigarette smoking is a risk factor for the development of asthma in individuals aged 7–33 years.18 There is a significant association between lower respiratory tract infections and the occurrence of adult-onset asthma, although its mechanism is unclear.19 Psychological stress has long been recognised as a trigger factor in asthma and is known to alter inflammatory responses in the airways. Stress has also been shown to have a significant association with the occurrence of asthma and hospitalisation in young adults.20

Clinical aspects – history and physical examination

The clinical presentation of asthma in adults is usually straightforward, and complaints of shortness of breath, cough, wheezing and chest tightness are common.

Coughing in isolation is usually associated with an infection, but the diagnosis of asthma should be considered if it is accompanied by wheezing, particularly at night. Recurrent respiratory tract infection should always raise the possibility of poorly controlled asthma. Breathlessness may be ignored or thought to be due to ‘old age’. As with other age groups, exercise-induced asthma needs to be considered in cases of breathlessness on exertion. Shortness of breath on exertion, and complaints of wheezing and coughing in the night should also alert the clinician to the possible alternative diagnosis of ischaemic heart disease, even in the absence of exercise-induced chest pain or discomfort. Enquiries should be made about precipitating and aggravating factors, and any relieving factors (eg use of bronchodilators). A family or past or concurrent history of atopy and a smoking history should be sought.

Asthma that presents for the first time in cigarette smokers with established chronic airflow limitation may be difficult to detect or differentiate from chronic obstructive pulmonary disease (COPD). Other conditions with similar symptoms need to be considered. This includes cardiac disease, pulmonary hypertension, poor cardiopulmonary fitness and other respiratory conditions. Laryngeal disorders (eg vocal cord dysfunction syndrome) should be considered in those who present with normal expiratory spirometry, appear well and who have an upper airway stridor. Symptoms of asthma may be the presenting features in some other conditions. Nocturnal wheeze may be due to gastro-oesophageal reflux, particularly when associated with cough. Churg-Strauss syndrome may present as severe asthma in adults.

In general, asthma is more likely to be the explanation if the presenting symptoms are recurrent or seasonal, worse at night or in the early morning, prompted by recognised triggers and rapidly relieved by short-acting beta-2 agonists. Auscultatory findings of wheezing, unexplained reductions in forced expiratory volume in 1 second (FEV1), peripheral blood eosinophilia and/or total immunoglobulin E (IgE) level are supportive in making the diagnosis.1 Objective lung function response to inhaled beta-2 agonists remains the gold standard for diagnosis.

A reduction in symptoms, and an increase in FEV1 and peak expiratory flow rate (PEFR) should be expected following standard asthma therapy. Slow responses to appropriate therapy may occur in those with longstanding, poorly managed asthma as a consequence of airway remodelling resulting in a degree of fixed airways obstruction. Slow responses and absence of improvement should prompt a careful review for alternative diagnoses.

Special investigations

Clinical recognition of asthma requires the objective measurement of reversible airflow obstruction (spirometry), demonstrated by an increase in FEV1 of at least 200 ml or ≥12% following inhalation of a short-acting beta-2 agonist (eg salbutamol).1,21 The absence of reversibility does not necessarily disprove the diagnosis in some longstanding cases, reversibility is slow and may only be demonstrated by an improvement in lung function over a period of 34 weeks on standard asthma treatment. In those cases where spirometry is normal or relatively so, bronchial provocation testing should be considered but should only be performed in recognised pulmonary function laboratories.

Induced sputum eosinophil counts and the measurement of expired nitric oxide are undertaken in some centres. However, these are not recommended in routine clinical practice. Spirometry and PEFR remain the first-line measurements in most cases.22 Chest X-rays or computed tomography (CT) chest scans are not needed, but may sometimes be advisable if an alternative diagnosis is being considered.

Overview of management

Figure 1. Stepped approach to adjusting asthma medication in adults
ICS, inhaled corticosteroid; SABA, short-acting beta-2 agonist; LABA, long-acting beta-2 agonist
*Reliever: short-acting beta-2 agonist (or low-dose budesonide/eformoterol combination for patients using this combination as both maintenance and reliever)
§In addition, manage flare-ups with extra treatment when they occur, and manage exercise-related asthma symptoms as indicated
†Montelukast can be added to inhaled corticosteroid as an alternative to switching to ICS/LABA, but is less effective
Note: PBS status as at April 2015: 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.
Reproduced with permission from the the National Asthma Council Australia from the Australian Asthma Handbook v1.1

The management of asthma in adults1 is based initially on confirming the diagnosis, assessing the symptoms and their control, providing asthma education about the underlying nature of the condition and establishing treatment goals. Enquiry should always be made about the patient’s expectations, and instruction must be given about asthma self-management, including acute severe asthma, and an appropriate written asthma action plan provided.

In cases of newly diagnosed symptomatic asthma, regular use of low-dose, inhaled corticosteroids, supplemented by the use of inhaled short-acting beta-2 agonists when symptomatic, is appropriate. If symptoms are severe at initial presentation, a short period of high-dose, inhaled steroids and/or a short course of oral steroids may be needed to gain control. Regular review should follow to assess progress. If treatment is effective in achieving good asthma symptom control, then a gradual reduction in dosage should be possible, with the aim of reaching the minimum that controls symptoms. If the asthma is then only partly controlled with low-dose inhaled corticosteroids, stepping up to an inhaled corticosteroid/long-acting beta-2 agonist combination can be considered (Figure 1). Ongoing review at appropriate intervals is important to ensure good asthma control.

Individuals with occupational asthma should avoid the sensitising or triggering agent, but can otherwise be treated in the same way as those with non-work-related asthma. They may be able to continue their job, providing that exposure to triggers is minimised. This is not possible in some cases. It is recommended that the person be referred to a respiratory specialist who is experienced in managing occupational asthma before considering leaving their job.1

Poor treatment responses should prompt re-assessment of inhaler technique and adherence to therapy. The majority of patients do not use their inhaler devices correctly, and clear instructions and regular technique checks are essential.1,23 Patients do forget their regular preventive therapy from time to time. Strategies should be encouraged to improve adherence.

Loss of asthma control may also be associated with respiratory tract infections and exposure to other known irritants and trigger factors. Education and strategies to avoid these situations should be adopted. Worsening asthma control should prompt an increase in preventive medication (inhaled steroids/long-acting beta-2 agonists). In ongoing, severe asthma, or acute flare-ups, oral steroids should be used. Individuals with asthma that is difficult to treat, or in whom control has not been achieved or who present with severe asthma, require objective assessment of lung function, chest imaging and an evaluation of eosinophil response to treatment. Specialist assessment and management, and hospital admission should be considered when this occurs.

Key points

  • Adult-onset asthma is often overlooked or misdiagnosed, especially in older age groups.
  • About 10% of adult-onset asthma cases are caused by occupational exposures.
  • Diagnosis is based on objective lung function testing.
  • Regular preventive therapy is important for those with ongoing symptoms.
  • Poor treatment responses should prompt an assessment of inhaler technique.
  • Worsening asthma not responding to appropriate therapy, ongoing severe asthma or acute flare-ups should prompt specialist assessment.

Author

Jonathan Burdon AM, MBBS, MD, M Hlth & Med Law, FRACP, FCCP, FACLM, FAICD, Consultant Respiratory Physician, Mercy Private Hospital, East Melbourne, VIC; Chairman, National Asthma Council Australia, South Melbourne, VIC. jburdon@bigpond.net.au

Competing interests: None.
Provenance and peer review: Commissioned, externally peer reviewed.

References

  1. National Asthma Council Australia. Australian Asthma Handbook. Version 1.0. Melbourne: National Asthma Council Australia, 2014. Available at www.asthmahandbook.org.au [Accessed 6 March 2015].
  2. Australian Bureau of Statistics. 4338.0 Profiles of Health, Australia, 2011–13. Canberra: ABS, 2014. Available at www.abs.gov.au/AUSSTATS/abs@.nsf/Lookup/4338.0main+features12011-13 [Accessed 18 February 2015].
  3. Gibson PG, McDonald VM, Marks GB. Asthma in older adults. Lancet 2010;376:803–13.
  4. Cousens NE, Goeman DP, Douglass JA, Jenkins CR. The needs of older people with asthma. Aust Fam Physician 2007;36:729–31.
  5. Reed CE. Asthma in the elderly: diagnosis and management. J Allergy Clin Immunol 2010;126:681–17.
  6. Amelink M, de Nijs SB, de Groot JC, et al. Three phenotypes of adult-onset asthma. Allergy 2013;68:674–80.
  7. Ulrik CS, Lange P. Decline of lung function in adults with bronchial asthma. Amer J Respir Crit Care Med 1994;150:629–934.
  8. Australian Bureau of Statistics. 4102.0 – Australian Social trends, Mar 2011. Canberra: ABS, 2012. Available at www.abs.gov.au/AUSSTATS/abs@.nsf/Lookup/4102.0Main+Features10Mar+2011 [Accessed 8 March 2015].
  9. Johnson A, Toelle BG, Yates D, et al. Occupational asthma in New South Wales (NSW): A population-based study. Occup Med 2006;56:258–62.
  10. Abramson MJ, Kutin JJ, Rosier MJ, Bowes G. Morbidity, medication and trigger factors in a community sample of adults with asthma. Med J Aust 1995;162:78–81.
  11. Henneberger PK, Hoffman CD, Magid DJ, Lyons EE. Work-related exacerbation of asthma. Int J Occup Environ Hlth 2002;8:291–96.
  12. Hoy RF, Abramson MJ, Sim MR. Work related asthma. Diagnosis and management. Aust Fam Physician 2010;39:39–42
  13. Beuther DA, Sutherland ER. Overweight, obesity, and incident asthma: A meta-analysis of prospective epidemiologic studies. Amer J Respir Crit Care Med 2007;175:661–66.
  14. Camargo CA, Weiss ST, Zhang S, Willett WC, Speizer FE. Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med 1999;159:2582–88.
  15. Huovinen E, Kaprio J, Koskenvuo M. Factors associated to lifestyle and risk of adult onset asthma. Resp Med 2003;97:273–80.
  16. Guerra S, Sherrill DL, Martinez FD, Barbee RA. Rhinitis as an independent risk factor for adult-onset asthma. J Allergy Clin Immunol 2002;109:419–25.
  17. Toren K, Olin AC, Hellgren J, Hermansson BA. Rhinitis increase the risk for adult-onset asthma – A Swedish population-based case-control study (MAP-study). Respir Med 2002;96:635–41.
  18. Strachan DP, Butland BK, Anderson HR. Incidence and prognosis of asthma and wheezing illness from early childhood to age 33 in a national British cohort. BMJ 1996;312:1195–99.
  19. Rantala A, Jaakkola JJ, Jaakkola MS. Respiratory infections precede adult-onset asthma. PLoS One 2011;6:e27912.
  20. Rod NH, Kristensen TS, Lange P, Prescott E, Diderichsen F. Perceived stress and risk of adult-onset asthma and other atopic disorders: A longitudinal cohort study. Allergy 2012;67:1408–14.
  21. Johns DP, Pierce R. Pocket guide to spirometry. 3rd edn. North Ryde: McGraw Hill, 2011.
  22. Yang IA, Ko FW, Lim TK, Hancox RJ. Year in review: Asthma and chronic obstructive pulmonary disease. Respirology 2013;18:565–72.
  23. Melani AS, Bonavia M, Cilenti C, et al. Inhaler mishandling remains common in real life and is associated with reduced disease control. Respir Med 2011;105:930–38.

Correspondence afp@racgp.org.au

19 September 2015 09:47

Re: Adult-onset asthma

Mike Porter

MBBS, LLB, FRACGP

None

Australian asthma prevalence rates are high by international comparison.(1) As highlighted by Burdon (AFP Aug 2015),(2) prevalence amongst adults is expected to increase as the population ages. While recognising various asthma triggers, Burdon fails to also note the additional asthma burden that will arise as a result of deteriorating air quality secondary to climate change.

Climate change models predict increasing mean temperatures throughout this century in all Australian regions.(3) Australians can anticipate more heatwaves, droughts and bushfires. Individuals will be at heightened risk of asthma onset and poor disease control through increased exposure to climate-sensitive air pollutants. Two of the more studied pollutants are ozone and particulate matter.

We tend to associated climate change with stratospheric ozone depletion. However, ground-level (tropospheric) ozone increases in warmer seasons, reaching very high concentrations during heatwaves. Climate modelling suggests an upward trend in Australian ground-level ozone concentration. Increasing ground-level ozone is significantly associated with increased asthma risk.(4)

Particulate matter can be man-made, such as motor vehicle and industrial emissions, or can arise from natural sources, including bushfires and dust storms. Both man-made and natural pollutants include inhalable particulate matter. Regardless of the source, particulate matter is associated with asthma exacerbation.(5)

The extent of the future impact of man-made particulates on asthmatics is difficult to predict with certainty, as it will depend on emission mitigation efforts in the coming decades. However, even if current emissions are contained, mean global temperatures will continue to rise through to the year 2100. One consequence of this will be greater frequency of bushfires and dust storms, both significant natural contributors to inhalable particulate pollutants.

While endorsing Burdon’s comments about the importance of asthma education,(2) I would add that educating ourselves about the anticipated consequences of climate change is vital. I suggest that this will better equip us to anticipate the effects of deteriorating air quality on health and to optimise care for our asthmatic patients.

1. Australian Centre for Asthma Monitoring 2011. Asthma in Australia 2011. AIHW Asthma Series no. 4. Cat. no. ACM 22. Canberra: AIHW.
2. Burdon J. Adult-onset asthma. Aust Fam Physician 2015; 44(8): 554-57.
3. CSIRO and Bureau of Meteorology 2015, Climate change in Australia: Projections for Australia’s NRM Regions: Technical Report. CSIRO and Bureau of Meteorology, Australia. Available at: http://www.climatechangeinaustralia.gov.au/media/ccia/2.1.5/cms_page_media/168/CCIA_2015_NRM_TechnicalReport_WEB.pdf
4. Li T, Lin G. Examining the role of location-specific associations between ambient air pollutants and adult asthma in the United States. Health & Place 2014; 25: 26-33.
5. Beggs PJ, Bennett CM. Climate change, aeroallergens, natural particulates, and human health in Australia: state of the science and policy. Asia Pac J Public Health 2011; 23: 46S–53.

29 September 2015 04:30

Re: Adult-onset asthma

Jonathan Burdon

Consultant Respiratory Physician

St Vincent's Private Hospital

Dear Editor,

I thank Dr Porter for his letter in which he makes some good points about the expected deterioration in air quality in the future and the subsequent effects of climate change on asthma prevalence and severity.

Dr Porter seems to have overlooked the fact that in my paper (1) I did comment 'exposure to sensitising or irritant substances' as risk factors and triggers in persons suffering from asthma. Most clinicians managing patients with asthma and other airway disorders would accept this and would extrapolate my words to mean that any increase in air pollution in future years will necessarily lead to an increase in asthma prevalence and flare-ups. A detailed examination of the potential increase in asthma prevalence and flare-ups was beyond the brief given for the paper.

In support of Dr Porter's comments, it is fair to say that we have long since recognised that an increase in asthma prevalence and flare-ups occurs in locations were atmospheric pollution is a particular problem and also in places where there has been a temporary increase in air pollutants. Several examples come to mind, such as the severe smog in London in 1952 (2,3) which led to significant morbidity and mortality and, in Australia, the King's Cross underground station fire in 1991 (5) and the list goes on (6). Examples in Australia are the wood smoke in the Tasmania’s Tamar Valley (7) and exposure to bush fire smoke causes an increase in asthma flare-ups locally.

It is also of note that from the medical point of view the health effects of climate change were first reported in the Australian medical literature in 1856!

Yours sincerely,

Jonathan Burdon


References:

1. Burdon J. Adult-onset asthma. Aust Fam Physician 2015; 44(8): 554-57
2. Bell ML, et al. A retrospective assessment of mortality from the London smog episode of 1952: the role of influenza and pollution. Environ Health Perspect 2004;112:6-8
3. Davis DL et al . A look back at the London Smog of 1952 and the half century since. Bell ML, et al. Environ Health Perspect 2002;110:A734-5
4. Castleden WM et al. The mining and burning of coal: effects on health and the environment. Med J Aust 2011;195:333-33
5. Fogarty PW et al. Long-term effects of smoke inhalation in survivors of the King’s Cross underground station fire. Thorax 1991;46:914-918
6. D’Amato G, ST Holgate (editors). The Impact of Air Pollution on respiratory Health. European Respiratory Monograph No 21, 2002, Volume 7
7. Markos J. Submission to the Senate Enquiry into the impacts on health of air quality in Australia. Stranding Committee on Community Affairs (References Committee), Parliament House, Canberra 2013. www.aph.gov.au/DocumentStore.ashx?id=5365c85c-da40-47bb-95c1 accessed 26.09.2015
8. Kilgour J. Effect of the Climate of Australia upon European Constitution in Health and Disease. Aust Med J 1856:1; 53-57

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