Asthma Management Handbook

Asthma prevention in adults

Recommendations

Advise people who work with airborne sensitisers or irritants that many airborne substances can damage respiratory health and may cause asthma.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to the following source(s):

 

Last reviewed version 2.0

If a patient who is exposed to occupational sensitisers or irritants develops new-onset rhinitis and/or respiratory symptoms, offer urgent referral to a specialist (e.g. respiratory physician, occupational physician or allergist) with experience in investigating and managing work-related asthma.

How this recommendation was developed

Consensus

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

Last reviewed version 2.0

Warn sportspeople, particularly elite athletes, that training while exposed to airborne pollutants or cold, dry air may increase the risk of developing asthma.

How this recommendation was developed

Consensus

Based on clinical experience and expert opinion (informed by evidence, where available), with particular reference to named source(s):

  • Parsons et al. 20131
  • Weiler et al. 20102
  • Anderson et al. 20083
  • Sue-Chu et al. 20104
  • Bougault et al. 20105
  • Bougault et al. 20096

Last reviewed version 2.0

More information

Prevention of work-related asthma within the workplace

Work-related asthma is potentially preventable. Preventive measures focus on controlling workers’ exposure to respiratory irritants and sensitisers at the workplace, and must be undertaken by employers.

An Australian report has recommended that employers should minimise exposure to sensitisers and irritants for all workers in high-risk workplaces.7  Actions by employers should be guided by occupational health and safety authorities and specialists with expertise in work-related asthma.

Prevention strategies currently in use include:

  • elimination of the substance from the workplace (e.g. substituting the substance, remote control handling)
  • reducing exposure (e.g safety procedures, training)
  • isolating the substance (e.g. changed work processes, segregation of areas)
  • ventilation
  • wearing personal respirators, protective clothing and masks.

The most effective strategy is to eliminate or minimise exposures at the source or in the environment.89

Avoiding the use of powdered latex gloves (e.g. substituting with low-protein, powder-free natural rubber latex gloves or latex-free gloves) reduces natural rubber latex aeroallergens, natural rubber latex sensitisation and natural rubber latex asthma in healthcare workers.8

There is limited evidence that the use of respirators is effective in preventing occupational asthma.8 Most studies have measured effects of respirators on exposure, not asthma incidence. Limited evidence suggests that the risk of developing asthma among workers using hexahydrophthalic anhydride in epoxy resin manufacture may be reduced by wearing respirators. A combination of information and training, exhaust ventilation, and wearing of respirators while handling of powdered bread improvers may reduce the risk of symptomatic sensitisation to flour and fungal amylase in bakers. Small studies suggest that respirators can reduce exposure to isocyanates among spray painters if they are well designed, fitted and maintained, and workers are trained to use them correctly.

If a face mask is recommended to minimise exposure to a particular sensitiser or irritant, the employer should select the appropriate type, and provide the worker with education and training to use it properly. Personal protection should be part of a comprehensive control program – not the sole strategy for reducing exposure.

If an employee develops work-related asthma, this should be considered as a warning that other workers may be at risk and that control measures at the workplace should be reviewed.

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Aetiology of exercise-induced bronchoconstriction

Both genetics and environment may contribute to exercise-induced bronchoconstriction.10

Exercise-induced bronchoconstriction occurs when a person’s ventilatory rate is high and their airways must heat and humidify a large volume of air in a short time. Dehydration of the airway leads to release of inflammatory mediators within the airway and contraction of airway smooth muscle.10 Dry air is one risk factor.10

Exercise-induced bronchoconstriction in athletes who do not have chronic asthma may have different pathogenesis and presentation than exercise-induced bronchoconstriction in people with asthma.10 Elite athletes often report onset of exercise-induced bronchoconstriction after age 20 years and after many years of high-level training.11

In elite athletes, exercise-induced bronchoconstriction is probably due to chronic injury to airway epithelium associated with long-term frequent prolonged high ventilation rates in the presence of environmental exposure to cold air, dry air, and airborne pollutants such as ozone, particulate matter:

  • The high prevalence of exercise-induced bronchoconstriction in ice-rink athletes has been linked to inhalation of cold dry air in combination with airborne pollutants from fossil-fuelled ice resurfacing machines
  • Exercise-induced bronchoconstriction in skiers and other winter athletes has been linked to injury of airway epithelium due to conditioning large volumes of cold dry air121314
  • The high prevalence of asthma and exercise-induced bronchoconstriction reported among competitive swimmers has been associated with exposure to chlorine in indoor swimming pools1215, 16
  • The increased prevalence of exercise-induced bronchoconstriction among distance runners, compared with the general population, has been attributed to exposure to high levels of airborne allergens and ozone1012
  • Certain airborne viruses inhaled during exercise may also contribute to exercise-induced bronchoconstriction.10
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References

  1. Parsons, J P, Hallstrand, TS, Mastronarde, J G, et al. An official American Thoracic Society clinical practice guideline: exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 2013; 187: 1016-1027. Available from: http://www.thoracic.org/statements/resources/allergy-asthma/exercise-induced-bronchoconstriction.pdf
  2. Weiler, J M, Anderson, S D, Randolph, C, et al. Pathogenesis, prevalence, diagnosis, and management of exercise-induced bronchoconstriction: a practice parameter. Ann Allergy Asthma Immunol. 2010; 105(6 Suppl): S1-S47.
  3. Anderson, S D, Kippelen, P. Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes. J Allergy Clin Immunol. 2008; 122: 225-235.
  4. Sue-Chu, M, Brannan, J D, Anderson, S D, et al,. Airway hyperresponsiveness to methacholine, adenosine5-monophosphate, mannitol, eucapnic voluntary hyperpnoea and field exercise challenge in elite cross country skiers. Brit J Sports Med. 2010; 44: 827-832.
  5. Bougault, V, Boulet, L P, Turmel, J. Bronchial challenges and respiratory symptoms in elite swimmers and winter sport athletes. Chest. 2010; 138: 31S-37S.
  6. Bougault, V, Turmel, J, St-Laurent, J, et al,. Asthma, airway inflammation and epithelial damage in swimmers and cold-air athletes. Eur Respir J. 2009; 33: 734-739.
  7. Sim M, Abramson MJ, LaMontagne T, et al. Occupational asthma – detection, surveillance and prevention of the disease burden. Final report. Monash University Department of Epidemiology and Preventive Medicine, Melbourne, 2005.
  8. Heederik D, Henneberger PK, Redlich CA. Primary prevention: exposure reduction, skin exposure and respiratory protection. Eur Respir J. 2012; 21: 112-124. Available from: http://err.ersjournals.com/content/21/124/112.full
  9. Baur X, Sigsgaard T, Aasen TB, et al. Guidelines for the management of work-related asthma. Eur Respir J Supplement. 2012; 39: 529-45. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22379148
  10. Weiler JM, Anderson SD, Randolph C, et al. Pathogenesis, prevalence, diagnosis, and management of exercise-induced bronchoconstriction: a practice parameter. Ann Allergy Asthma Immunol. 2010; 105: S1-47. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21167465
  11. Fitch KD, Sue-Chu M, Anderson SD, et al. Asthma and the elite athlete: Summary of the International Olympic Committee's Consensus Conference, Lausanne, Switzerland, January 22-24, 2008. J Allergy Clin Immunol. 2008; 122: 254-260. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18678340
  12. Parsons JP, Hallstrand TS, Mastronarde JG, et al. An official American Thoracic Society clinical practice guideline: exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 2013; 187: 1016-27. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23634861
  13. Anderson SD, Kippelen P. Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes. J Allergy Clin Immunol. 2008; 122: 225-235. Available from: http://www.jacionline.org/article/S0091-6749(08)00785-9/fulltext
  14. Sue-Chu M, Brannan JD, Anderson SD, et al. Airway hyperresponsiveness to methacholine, adenosine5-monophosphate, mannitol, eucapnic voluntary hyperpnoea and field exercise challenge in elite cross country skiers. Brit J Sports Med. 2010; 44: 827-832. Available from: http://bjsm.bmj.com/content/44/11/827.long
  15. Bougault V, Boulet LP, Turmel J. Bronchial challenges and respiratory symptoms in elite swimmers and winter sport athletes. Chest. 2010; 138: 31S-37S. Available from: http://journal.publications.chestnet.org/article.aspx?articleid=1086631
  16. Bougault V, Turmel J, St-Laurent J, et al. Asthma, airway inflammation and epithelial damage in swimmers and cold-air athletes. Eur Respir J. 2009; 33: 740-746. Available from: http://erj.ersjournals.com/content/33/4/740.long