Monitoring
Notes on Goal Two
The predisposition to asthma is partly genetically determined.1,2,3,4 Among 7-year old children, 12% experienced asthma or wheeze if neither parent experienced asthma, 30% if one parent and 49% if both parents experienced asthma5. Although the specific genetic mechanism awaits discovery, a familial component to allergy and childhood asthma has long been recognised. There is increasing evidence that allergen exposure (both inhaled and ingested) in early life of genetically susceptible children may lead to the development of asthma6. This process, called allergen sensitisation, may be one of the most important factors in the induction of asthma. Asthma symptoms and sensitisation to house dust mite in later childhood have been associated with exposure in the first months of life7. The ultimate expression of this mechanism depends on the complex interaction between the genetic influences and environmental factors, including allergens, viral infections and pre and post-natal cigarette smoke exposure.
Once sensitisation of the airways occurs, asthma can occur with exposure to trigger factors. Allergy, particularly dust mite allergy, is an important trigger of symptoms, quite apart from its role in the development of asthma as described in the previous paragraph. Patients with asthma who are at risk from an allergy trigger need to be identified. Other triggers include respiratory tract infections, food and food additive sensitivity, certain drugs and both indoor and outdoor pollutants.
Our current knowledge about asthma regarding immunological and allergic mechanisms suggests that research, assessment and intervention to reduce risk factors must become a high priority.
Principal Strategies
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Perform research to define and identify the key risk factors for the development of asthma (genetic, environmental and dietary).
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Encourage strategies to help doctors and their patients define and identify the risk factors for each person (physical, social and psychological), for the triggering of asthma attacks.
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Develop management procedures to reduce or eliminate risk factors for asthma.
Detailed Strategies
S2.1 Evaluate techniques and strategies to communicate with genetically predisposed persons.
2.1.1 Conduct uniform and ongoing research to determine effective preventive measures for people who are genetically disposed.
2.1.2 Provide culturally appropriate education and information so that families with disease can be informed of appropriate preventive measures.
S2.2 Research and implement measures to advise high-risk families about risk factors. High risk: where a first degree family member has clinical evidence of an atopic disease such as asthma, hay fever or eczema.
2.2.1 Develop and implement a national system for recording at-risk families with allergy or asthma.
2.2.2 Provide effective antenatal advice (aero-allergens, diet, passive smoking) to high-risk families.
2.2.3 Provide advice about effective aero-allergen avoidance to all high-risk families.
S2.3 Reduce asthma exacerbations due to allergen exposure.
2.3.1 Develop, evaluate and implement effective allergy management plans.
2.3.2 Ensure that people with current asthma have an allergy assessment including objective measurement of sensitisation by a medical practitioner.
2.3.3. Undertake research to evaluate interventions aimed at reducing allergen exposure.
2.3.4. Educate patients, their families and doctors concerning appropriate measures and interventions to minimise allergen exposure.
S2.4 Reduce asthma exacerbations due to tobacco smoke.
2.4.1 Facilitate continuing reduction in cigarette smoking by lobbying for national and state legislation regarding cigarette smoking in public places and in cars.
2.4.2. Encourage the dissemination of intervention programs likely to change the behaviour of smokers with asthma.
S2.5 Reduce asthma exacerbations due to other identifiable trigger factors.
2.5.1 Educate doctors in order to provide and implement effective management plans for asthma exacerbations.
2.5.2 Educate doctors in order to identify important triggers for asthma initiation and exacerbations and establish effective preventive measures.
2.5.3 Provide educational materials to patients/parents to educate them regarding the risk of asthma exacerbation with infection and to alert them to the need for increased medication at the outset of infection.
2.5.4 Work with the food manufacturing industry so that it is aware of dangers of hidden ingredients in foods and identifies all ingredients on labels.
2.5.5 Provide dietary advice to sensitive patients and educate them about identifying ingredients on labels and observing precautions when eating commercially prepared or complex foods.
2.5.6 Develop educational campaigns to increase public awareness of some medications (NSAIDs, including aspirin, beta-adrenergic blocking agents, including eyedrops, and non-proprietary preparations such Royal Jelly) as possible triggers for asthma.
2.5.7 Ensure effective immunological assessment in patients with long-standing severe asthma.
S2.6 Reduce exposure to pollutants and workplace environmental triggers.
2.6.1 Establish uniform national guidelines for indoor/outdoor air quality.
2.6.2 Provide information on effective screening and monitoring to workers and management in high-risk industries.
2.6.3 Establish a register for occupational asthma which provides data about products causing occupational asthma, patients who have occupational asthma and industries monitoring occupational asthma.
S2.7 Provide education and resources to health professionals.
2.7. 1 Ensure all aspects of allergy and immunology relevant to asthma are covered in undergraduate medical, nursing and pharmacy courses and form part of continuing education.
| Current Situation/Evidence |
Performance Indicators |
| Genetically predisposed children with an affected parent or sibling have approximately six times the risk of developing asthma8. |
Reduction in the development of asthma in genetically predisposed persons by implementation of preventive measures. |
| The effects of allergen avoidance in infancy is to reduce sensitisation9,10 |
A modification of diet and environmental factors to minimise the risk of atopic disease and the risk of sensitisation to allergens, both parentally and in babies and young children in high-risk families. |
| Passive smoking may influence both incidence and severity of asthma11. |
A reduction in asthma exacerbations due to allergen exposure and tobacco smoke. A reduction in the prevalence of wheezing and abnormal lung function in infancy due to parental smoking |
| Up to 50% of wheezing illness and asthma in childhood is due to respiratory tract infections. People with asthma and food allergy have approximately 5 times the risk of severe asthma exacerbation12. Approximately 10% of all severe asthma attacks are linked to drugs13 |
A reduction in the risk of triggering asthma due to respiratory tract infections, food allergens, food additives and certain drugs. |
| The severity of wheezing in pre-school children developing asthma after viral respiratory infections can be modified14. |
A reduction in the risk of triggering asthma due to respiratory tract infections, food allergens, food additives and certain drugs. |
| Certain occupations have a high risk in susceptible individuals15. |
A reduction of indoor, outdoor and workplace environmental factors which trigger asthma. |
| Limited material available to doctors and community concerning the risk of allergen exposure and sensitivity during pregnancy and early life. |
An increase in the number of families with allergic diseases who are alerted to the risk of sensitisation to allergens. An increase in the number of families and pregnant women with allergic diseases who are informed of appropriate preventive measures and warned of inappropriate measures. |
| No national system for recording families with atopy or asthma (at risk or current). |
The establishment of a system to record at birth any history of asthma, eczema and rhinitis in first degree relatives of the newborn. |
| The number of people with current asthma who have had an allergy assessment in the previous 12 months is unknown |
An increase in the number of people with asthma requiring treatment in the previous 12 months who have an allergy assessment by a medical practitioner, including objective measurement of sensitisation. |
| Variable standards in quality assurance in high-risk occupations. |
An increase in the number of workers in high-risk industries and occupations who are offered preventive measures to reduce the risk/potential risk of development of occupational asthma. |
| Poor community perception of risk factors. |
An increase in public awareness of and avoidance of triggers for asthma including tobacco smoke, food allergens, food additives and certain drugs |
| National Food Authority is reviewing readability and understandability of food labelling for consumers. |
An increase in readability and comprehension of all labelling of foods, food supplements and additives. |
| Exposure to allergens is a risk factor for hospital attendees16 and current asthma17. |
A reduction in the risk of acute exacerbations and current asthma by implementation of effective allergy management plans. |
| Limited understanding among GPs concerning optimum management of asthma exacerbations18. |
An increase in the proportion of GPs who identify and manage asthma exacerbations effectively. |
Monitoring
Investigate the feasibility of:
- establishing a central recording system for general practitioners and other medical practitioners to collect:
- causes of particular asthma exacerbations
- number of allergy assessments in people with asthma
- history of asthma, eczema or rhinitis in first degree relatives of newborns.
- establishing a recording system in A & E departments to record asthma exacerbations in which a food or drug trigger is suspected
- conducting asthma audits through General Practice Divisions
- surveying workplace smoking restrictions
- tracking changes in food labelling
- conducting a population-based survey to ascertain public awareness of triggers
- surveying workers in high-risk industries to measure increase in knowledge and awareness
- developing epidemiological tools to measure the long-term health outcomes of optimally managed asthma.
Notes to Goal Two
1. Sibbald B. Genetics of asthma and atopy: an overview. Clin Allergy 1991; 21:178-81.
2. Peat JK, Haby M, Spijker J, Berry G, Woolcock AJ. Prevalence of asthma in adults in Busselton, Western Australia. BMJ 1992;305:1326-9.
3. Dold S, Wjst M, von Mutius E, Reitmeir P, Stiepel E. Genetic risk for asthma, allergic rhinitis and atopic determatitis. Arch Dis Child 1992;67:1018-22.
4. Paoletti P, Viegi G, Carozzi L. Bronchodilator hyperresponsiveness, genetic predisposition and environmental factors: the importance of epidemiological research. Eur Respir J 1992;5:910-12.
5. Jenkins MA, Hopper, JL, Flander LB, Carlin JB, Giles GG. The association between childhood asthma and atopy, and parental asthma, hayfever and smoking. Pediatr Perinatal Epidemiol 1993;7:67-76.
6. Holt PG, McMenamin C, Nelson D. Primary sensitisation to inhaled allergens during infancy. Pediatr Allergy Immunol 1990;1:3-13.
7. Sporik R, Holgate ST, Platts-Mills TAE, Cogswell JJ. Exposure to house mite allergen (Der pl) and the development of asthma in childhood - a prospective study. N Engl J Med 1990;323:502-7.
8. Abramson M, Kutin J, Raven J, et al. Risk factors for asthma in young adults. Allergy Clin Immunol News 1994;2:391.
9. Hide DW, Matthews S, Matthews L, et al. Effects of allergen avoidance in infancy. J Allergy Clin Immunol 1994;93:842-6.
10. Arshad SH, Matthews S, Gant C, Hide DW. Effects of allergen avoidance on development of allergic disorders in infancy. Lancet 1992;339:1493-7.
11. NHMRC. Passive effects of smoking draft report. Commonwealth of Australia, 1995.
12. Ernst P, Habbick B, Suissa S, et al. Is the association between inhaled beta agonist use and life-threating asthma because of confounding by severity. Am Rev Respir Dis 1993;148:75-9.
13. Picado C, Castillo JA, Montserrat JM, Agusti-VidalA. Aspirin-intolerance as a precipitating factor of life-threatening attacks of asthma requiring mechanical ventilation, Eur Respir J 1989, 2(2):127-9.
14. Connet G, Lenney W. Prevention of viral induced asthma attacks using inhaled budesonide. Arch Dis Childhood 1993;68:85-7.
15. Chang Yeung M, Meio JL. Occupational asthma. N Engl J Med 1995;333:107-12.
16. Gelber LE, Seltzer LH, Bouzokis JK, Poliart SM, Chapman MD, Platts Mills TAE. Sensitisation and exposure to indoor allergens as risk factors for asthma among patients presenting to hospital. Am Rev Respir Dis 1993;147:573-8.
17. Peat JK, Dorey E, Toelle BG, et al. House dust mite allergens! A major risk factor for childhood asthma in Australia Am J Respir Crib Care Med 1996;153:141-6.
18. Hawley R, Seale JP, Carroll PR, Comino E, Rose D. An educational intervention to improve general practitioners' (GPs') knowledge of the appropriate use of antibacterials in patients with asthma Aust N Z J Med 1995;24:452
Content Updated 1996
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