Respiratory disease

What we knowWhat we need to know

Peter N Le Souëf MD, FRACP

What we knowWhat we need to know

Susan M Sawyer MD, FRACP

What we knowWhat we need to know

Mimi LK Tang FRACP, FRCPA

What we knowWhat we need to know

Craig M Mellis MD, MPH

The rates of bronchiectasis for Indigenous children from remote Australian communities are unacceptably high, with one study showing 14.7/1000 Aboriginal children. Children with bronchiectasis need to be identified early for optimisation of medical treatment. Under-reporting of cough is common. Bronchiectasis should be suspected in children with recurrent bronchitis or pneumonia, and when, despite appropriate therapy, pulmonary infiltrates or atelectasis persist 12 weeks beyond the index illness. During acute infective episodes, oral antibiotics and chest physiotherapy to clear the airways should produce prompt resolution; otherwise, hospitalisation is necessary. Management follows the cystic fibrosis model of regular review, encouragement of physical activity, optimising nutrition, maintenance of immunisation and avoidance of environmental toxicants, including passive smoke exposure. Successful management and prevention of bronchiectasis will require improvements in housing, nutrition, and education, as well as access to comprehensive healthcare services, with coordination between primary and hospital-based healthcare providers.

for the Working Group on Indigenous Paediatric Respiratory Health

Re "MJA Practice Essentials – Infectious diseases 3: Community-acquired pneumonia", by Johnson PDR, Irving LB and Turnidge JD, in the 1 April issue of the Journal (Med J Aust 2002; 176: 341-347). The authors would like to clarify an ambiguity in the text, after discussion with Professor Bart Currie (Director of Clinical Research, Tropical Medicine and International Health Unit, Menzies School of Health Research, Darwin, NT). On page 345, the last paragraph should read: "Tropical Australia: Patients in tropical Australia, particularly those with more severe pneumonia, may be infected with B. pseudomallei (melioidosis) or A. baumannii and thus may require different initial empirical therapy. Patients with CAP in risk classes III or IV who also have risk factors for these infections (eg, diabetes, chronic airways disease, high alcohol intake or renal disease) should receive initial therapy with regimens that include intravenous gentamicin plus ceftriaxone (2 g for adults). All patients in risk class V should receive regimens that include intravenous gentamicin plus meropenem, if available. The regimen needs to be further refined if one of these pathogens is identified.26" In addition, the last footnote to Box 6 on page 345 should be replaced with the following: "¶ In tropical Australia, melioidosis and Acinetobacter baumannii infection should be considered in all patients in risk class V and those with risk factors in risk classes III and IV." Antibiotic recommendations are under constant review because of emerging resistance and changes in epidemiology, and we remind clinicians to refer to the latest updates of Australian antibiotic guidelines when prescribing.

Paul DR Johnson PhD, FRACP · Lou B Irving FRACP, FRACGP · John D Turnidge FRACP, FRCPA

The immediate health effects of bushfire smoke are well known to Australia's volunteer firefighters, who willingly fight bushfires each summer with no remuneration and at considerable personal risk. However, the population health impacts of pollution associated with large bushfires or "backburning" operations (prescribed burning to reduce the fuel load and the intensity of future bushfires) are less well defined, but are a matter of concern for emergency, environmental and public health agencies. A study from Darwin, published in this issue of the Journal by Johnston et al (page 535),1 is a welcome addition to this area of research. Johnston and colleagues1 analysed emergency department presentations for asthma in the Darwin region during the "dry" season, April – October (2000), when bushfire activity is high. The authors found that asthma presentations increased significantly (by nearly 2.4 times) on days when PM10 levels (ie, the concentration of respirable particulate matter with an aerodynamic diameter of 10 microns or less) were above 40 µg/m3, compared with days when PM10 levels were less than 10 µg/m3. The Australian National Environment Protection Council's target for maximum mean PM10 concentration is set at 50 µg/m3 in a 24-hour period.2 This level was exceeded on six days, with the maximum being 70 µg/m3. In fact, this value is relatively low in the international context. The Indonesian forest fires in 19973 produced maximum daily PM10 averages of over 1500 µg/m3. During Sydney's Christmas 2001 bushfires, PM10 levels above 150 µg/m3 were sustained for 10 days. In Sydney's 1994 bushfires,4 the peak PM10 was 210 µg/m3, compared with background levels of about 30 µg/m3. Previous Australian studies examined the effects of pollution in Sydney from backburning in May 19915 and bushfires in January 1994.6 Both studies analysed daily numbers of asthma presentations at several metropolitan hospitals for up to a month. The first study provided weak support for a link between particulate air pollution and asthma attendances, but the second found no difference in asthma presentations in the periods before, during and after the high-pollution event. There have been two more detailed studies of the health impacts of the 1994 Sydney bushfires. The first7 extended the period of analysis to six to seven weeks and compared asthma attendances with those in the same period the previous year. The researchers used a more complex analysis strategy, incorporating lag periods of one and two days for independent variables. They found that bushfire-generated particulate air pollution did not result in an increase in asthma presentations to emergency departments in western Sydney. The second study4 measured changes in evening peak expiratory flow rates (PEFR) during the bushfire period in children with wheeze, and used a direct measure of PM10, including pollen and alternaria counts, and meteorological factors (temperature and humidity). Thirty-two children were recruited to the study over a period of one week. Peaks in PM10 levels occurred three days before recruitment and on Days 3 and 8 (PM10 levels of about 70 µg/m3, 150 µg/m3 and 210 µg/m3, respectively, were recorded). Overall, there was no association found between mean PM10 and PEFR. Subgroup analysis of 20 of the children without bronchial hyperreactivity recorded significant falls in PEFR with rising PM10 levels. The remaining 12 children with bronchial hyperreactivity showed no significant association between PM10 and PEFR. The relative timing of exposure and recruitment may have caused changes in respiratory function before the study period, thereby biasing the results. All but one of the previous studies5-7 used indirect measures of particulate pollution, did not account adequately for confounders and did not use appropriate time-series methods. Notwithstanding these shortcomings, the potential for bias is probably low, as most important confounders do not vary on a daily basis. Johnston and colleagues' study1 has the advantage of running for a longer time period, with the episodes of pollution occurring during the study. The findings of the Darwin study should stimulate further research on the health effects of bushfire smoke. Current public health approaches to bushfire or other pollution episodes are to invoke a tiered system of warnings, moving from advice for susceptible subgroups (people with asthma, other chronic respiratory disease, or cardiovascular disease) to whole-population warnings as pollution increases. Applying "backburning" as a fire control measure, in itself an effective public health tool, may be restricted, partly because of the perceived impact of the resultant particulate pollution on urban populations. Better information about these effects will result in more appropriate risk management.

Peter R Lewis DipObsRACOG, MPH, FAFPHM · Stephen J Corbett MPH, MRCGP, FAFPHM

Objective: To examine the relationship between the mean daily concentration of respirable particles arising from bushfire smoke and hospital presentations for asthma. Design and setting: An ecological study conducted in Darwin (Northern Territory, Australia) from 1 April – 31 October 2000, a period characterised by minimal rainfall and almost continuous bushfire activity in the proximate bushland. The exposure variable was the mean atmospheric concentration of particles of 10 microns or less in aerodynamic diameter (PM10) per cubic metre per 24-hour period. Outcome measure: The daily number of presentations for asthma to the Emergency Department of Royal Darwin Hospital. Results: There was a significant increase in asthma presentations with each 10-µg/m3 increase in PM10 concentration, even after adjusting for weekly rates of influenza and for weekend or weekday (adjusted rate ratio, 1.20; 95% CI, 1.09–1.34; P < 0.001). The strongest effect was seen on days when the PM10 was above 40 µg/m3 (adjusted rate ratio, 2.39; 95% CI, 1.46–3.90), compared with days when PM10 levels were less than 10 µg/m3. Conclusion: Airborne particulates from bushfires should be considered as injurious to human health as those from other sources. Thus, the control of smoke pollution from bushfires in urban areas presents an additional challenge for managers of fireprone landscapes.

Fay H Johnston MAppEpi, FAFPHM · Anne M Kavanagh PhD, FAFPHM · David M J S Bowman PhD, DSc · Randall K Scott BAppSci (Biol)

Breathing disorders in sleep. Walter T McNicholas and Eliot A Philipson. London: W B Saunders, 2002 (xii + 339 pp). ISBN 0 7020 2510 0. Sleep disorders are among the most prevalent problems in the Australian community, and compact, reliable sources of information on this topic are hard to find. There are good, large specialist textbooks on sleep medicine but no suitable short texts aimed at non-specialists. This book says that this is its market. Breathing disorders in sleep is, to a sleep specialist, a marvellous book and most sleep specialists will want it (although they might baulk at paying 70 cents a page). The authors are the leading lights in research into sleep-disordered breathing in both North America and the United Kingdom. Several chapters contain valuable new data, some previously unpublished results, and new presentations recalculated from the authors' raw data. Everywhere there are keen insights, some clinical and practical, some theoretical. The book's focus is narrower than its title implies — it is really about adult obstructive sleep apnoea. There are a few pages each on sleep apnoea in children, sleep in chronic obstructive airways disease and chest wall and neuromuscular disease, but specialists expecting a comprehensive reference on breathing during sleep will be disappointed. But is this the book non-specialists have been looking for? No! It looks like a book for non-specialists. A lot of attention has been paid to layout, and there are frequent “key points” boxes. Non-specialists could learn a lot by browsing through these key points boxes, and a good student text on obstructive sleep apnoea could be created from them. However, the book is essentially a collection of research reviews, which are excellent, but of little help to the non-specialist. For example, a reader wanting to know whether obstructive sleep apnoea causes vascular disease will find several detailed discussions of the evidence, but conflicting conclusions reached in different chapters. A lot of knowledge is assumed, and in some cases information is presented in such a technical way that most readers will be unable to make use of it. Clinicians who are used to systematic reviews and to thinking in terms of “absolute risk difference” and “number needed to treat” will be dissatisfied — by the management chapters in particular. Those interested in this book or in the politics of book pricing may like to note that amazon.com sells it new for US$99 or used for US$79, which (even with the shipping cost of US$7) makes it much cheaper than buying locally. Leslie G OlsonDepartment of Respiratory and Sleep Medicine John Hunter Hospital, Newcastle, NSW

Leslie G Olson

Community-acquired pneumonia is caused by a range of organisms, most commonly Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae and respiratory viruses. Chest x-ray is required for diagnosis. A risk score based on patient age, coexisting illness, physical signs and results of investigations can aid management decisions. Patients at low risk can usually be managed with oral antibiotics at home, while those at higher risk should be further assessed, and may need admission to hospital and intravenous therapy. For S. pneumoniae infection, amoxycillin is the recommended oral drug, while benzylpenicillin is recommended for intravenous use; all patients should also receive a tetracycline (eg, doxycycline) or macrolide (eg, roxithromycin) as part of initial therapy. Flucloxacillin or dicloxacillin should be added if staphylococcal pneumonia is suspected, and gentamicin or other specific therapy if gram-negative pneumonia is suspected; a third-generation cephalosporin plus intravenous erythromycin is recommended as initial therapy for severe cases. Infections that require special therapy should be considered (eg, tuberculosis, melioidosis, Legionella, Acinetobacter baumanii and Pneumocystis carinii infection).

Paul D R Johnson PhD, FRACP · Lou B Irving FRACP, FRACGP · John D Turnidge FRACP, FRCPA

Preventive treatment Inhaled corticosteroids are indicated in children with asthma who have more than mild persistent asthma or are unresponsive to non-steroidal medications after 2–4 weeks. Initial administration of 400 µg/day of chlorofluorocarbon-beclomethasone dipropionate, or budesonide, or 200 µg/day of fluticasone propionate or hydrofluoroalkane-beclomethasone dipropionate, is suggested, with subsequent titration of the dose to achieve ongoing control with the lowest dose possible. In situations where asthma control cannot be achieved with the above doses of inhaled corticosteroids, the addition of a long-acting β2-agonist, theophylline or a leukotriene antagonist should be considered. Specialist referral is recommended in children requiring high doses of inhaled steroids, regular oral steroids or in whom there is concern about possible steroid side effects. Treatment of acute asthma Systemic corticosteroid therapy is recommended for children with moderate to severe acute asthma or if there is incomplete response to β2-agonists. Initial administration of 1 mg/kg prednisolone (maximum, 50 mg) orally is suggested, and this may be repeated every 12–24 hours, depending on response. While a course of up to three days is generally sufficient, in more severe cases a prolonged course (with tapering) may occasionally be indicated. The need for recurrent systemic corticosteroid therapy for acute episodes is an indication for reassessment of the child's interval therapy.

Peter P van Asperen MD, FRACP · Craig M Mellis MD, MPH, FRACP · Peter D Sly MD, FRACP

To the Editor: We wish to report the identification of a novel virus causing lower respiratory tract disease in Australian children. The presence of this virus was recently described in Dutch children and tentatively called human metapneumovirus (hMPV).1 Clinical symptoms of infection are reported to resemble those of human respiratory syncytial virus (hRSV) infection. We therefore investigated whether the virus was present in Australian children. Three isolates were identified from a random selection of 200 nasopharyngeal aspirate (NPA) specimens collected throughout 2001 from children presenting to the Royal Children's Hospital, Brisbane, or the Logan Hospital, a public hospital to the south of Brisbane, with clinical respiratory tract disease. All NPA specimens were initially negative for hRSV, influenza A and B, parainfluenza 1, 2 and 3 and adenovirus by direct fluorescent antigen testing and subsequent viral culture. These negative NPA specimens were then screened by polymerase chain reaction (PCR) for hMPV, based on the known sequence of the virus.2 Sequencing of the PCR product in all three positive samples was 100% homologous with the known hMPV sequence. Viral growth was subsequently detected in culture from two of these samples, and confirmed as hMPV, using the method of van den Hoogen et al.1 Co-existent infection with coronavirus, rhinovirus, Bordetella pertussis, Chlamydia pneumoniae and Mycoplasma pneumoniae was excluded by PCR screening of the three hMPV isolates using validated in-house methods based on established protocols. Clinical features of the infected children are summarised in the Box. This is the first report of the presence of hMPV infection in Australian children and describes a new viral respiratory syndrome. It also adds to the clinical spectrum and understanding of respiratory viruses causing acute bronchiolitis in children. Only 25%–33% of NPA specimens collected from our population with suspected respiratory tract disease yield a positive result for a known viral or bacterial pathogen. Clinical features in this small cohort are difficult to separate retrospectively from hRSV. Based on the findings of this limited preliminary study of children presenting to hospital with respiratory tract symptoms, we would predict that hMPV is also relatively common in the Australian community. We are currently undertaking further characterisation of the hMPV isolates, a more detailed study of the epidemiology of hMPV disease, as well as developing improved diagnostic assays to rapidly identify clinical cases and assess seroprevalence of immunity to hMPV. Clinical features of human metapneumovirus in three Australian children Case 1 (Girl, 12 months) Case 2 (Boy, 5 years 11 months) Case 3 (Boy, 20 months) Date of nasopharyngeal aspirate collection 17/2/01 21/3/01 11/5/01 Presenting symptoms Rhinorrhoea, cough, tachypnoea, wheeze, vomiting Rhinorrhoea, cough, pharyngitis, conjunctivitis Rhinorrhoea, cough, fever Symptom duration before presentation (days) 4 3 4 Clinical signs Respiratory distress with hypoxia, rhinorrhoea, pharyngitis, chest wheeze with crackles Pharyngitis, chest wheeze Rhinorrhoea, pharyngitis, chest wheeze, cervical lymphadenopathy Chest X-ray Not performed Bilateral parahilar pneumonic infiltrates Bilateral parahilar pneumonic infiltrates Clinical diagnosis Bronchiolitis Viral lower respiratory tract infection Viral lower respiratory tract infection Outcome Admitted for oxygen therapy and nasal suctioning for three days Symptomatic treatment at home Symptomatic treatment at home

Michael D Nissen · Ian M Mackay · Stephen J Withers · David J Siebert · Theo P Sloots

New advances have reinforced our understanding of respiratory disease as a complex interaction between environment, genetic predisposition and host responses.1 We describe recent advances in diseases that are a major cause of morbidity and mortality. Prevention. Smoking cessation, pollution control, vaccination, medical review and education represent important advances in respiratory disease prevention. Effective interventions for nicotine addiction include replacement therapy (eg, transdermal patches, nasal spray, gum) and antidepressants (bupropion, nortriptyline).2 Both are efficacious when used correctly, but more so in conjunction with behavioural modification.2,3 Epidemiological studies have identified the importance of reducing exposure to occupational dusts and chemicals, air pollution and passive smoking.1,2 Reduction of pollution has required public policy, altered workplace practices and individual protective strategies. The characterisation of the genetic basis of disorders such as cystic fibrosis (CF) and a1-antitrypsin deficiency has made a major impact on their prevention by identifying at-risk individuals.1,2 The emergence of multidrug-resistant strains of Streptococcus pneumoniae has led to the development of a 23-valent pneumococcal vaccine, effective in preventing pneumococcal bacteraemia and pneumonia in high-risk patients.4 Influenza vaccination appears to reduce serious illness and death in chronic obstructive pulmonary disease (COPD).2 Diagnosis. Innovative technologies have enabled the rapid diagnosis of many respiratory disorders.1 Computed tomography (thin-section and spiral) is used to diagnose lung cancer, pulmonary embolus and to assess emphysema.1 The detection of bacterial DNA in clinical samples by polymerase chain reaction (PCR) permits rapid identification of the infection. PCR is also being used to monitor viral load (eg, cytomegalovirus) in immunosuppressed individuals. Invasive surgical techniques include video-assisted thoracoscopy, a procedure with low morbidity, high diagnostic accuracy and short postoperative recovery time.1 Interventions. Treatment of asthma in high risk patients should be aligned to the degree of airway inflammation.4 Inhaled anti-inflammatory drugs are effective maintenance treatment, reducing symptoms and improving quality of life.3,4 Adding a long-acting b2-agonist to inhaled corticosteroids is as effective as increasing the dose of inhaled steroids.4 Combined therapy may have a significant disease-modifying effect on inflammation and remodelling. Leukotriene modulators may be useful for patients when inhaled corticosteroids fail to control asthma.4 Treatment of COPD is still controversial. No current therapy modifies the long-term decline in FEV1.2 Bronchodilators control symptoms,2 and combining a long-acting b2-agonist and an anticholinergic drug or theophylline may produce additional benefits in lung function.2,4 Oxygen therapy and multidisciplinary rehabilitation programs improve survival, symptoms and quality of life.2 Surgical treatments include lung volume reduction surgery (LVRS) for regional emphysema, and bullectomy for giant bullous emphysema. Randomised controlled trials are being conducted to compare LVRS with optimal medical therapy,2 but patients at high risk of death after LVRS have recently been identified. No successful medical therapy has been found to treat interstitial lung disease. However, one study reported significant improvement after 12 months of treatment with interferon-g1b and corticosteroids compared with corticosteroids alone.3 Treatments such as laser methods, endobronchial radiation and airway stents offer palliation for terminal lung cancer.1 The recognition in recent years that mild to moderate obstructive sleep apnoea is a major risk factor in cardiovascular morbidity and mortality represents a major advance. Although S. pneumoniae is the most common pathogen in cases of community acquired pneumonia, other pathogens, such as Legionella species, Staphylococcus aureus, Pseudomonas aeruginosa and Mycoplasma pneumoniae, are also implicated.3 Early therapy with penicillin or third-generation cephalosporin with a macrolide is important.3 Meta-analysis shows that neuraminidase inhibitors are effective in preventing influenza A and B and in shortening the duration of illness.5 The recognition that hyaline membrane disease of the newborn is caused by a surfactant deficiency and subsequent intratracheal administration of surfactant has been estimated to save 2000 neonates per year in the United States.1 Advances in surgical technique and perioperative management have led to improved survival for patients undergoing lung transplantation. In carefully selected patients with advanced lung disease (eg, COPD, CF, ILD or bronchiectasis), lung transplantation has also been reported to improve quality of life and functional capacity.1,2 Ventilatory support includes both non-invasive negative-pressure or positive-pressure ventilation and invasive mechanical ventilation.4 Advances in ventilation have reduced mortality from respiratory failure resulting from acute respiratory distress syndrome, congestive heart failure, asthma and COPD with acute carbon dioxide retention.1 Conclusion. Increasing understanding of the mechanisms of respiratory disease, particularly at the cellular and molecular level, will enable improved diagnosis and treatment. Prevention remains a key strategy.

John H Alpers MB BS, FRACP · Josephine M Cranston BSc(Hons) · Alan J Crockett MPH

Crisis Death in Antarctica Antarctic tourism is flourishing, but Antarctic cruises are often more physically demanding than typical "tropical" cruises. An 82-year-old Antarctic tourist died of probable septic shock secondary to lower respiratory tract infection six days after sustaining a suspected vertebral fracture in a minor fall from an inflatable boat. This case highlights the need for Antarctic cruise ships to be equipped to provide life support and for better screening and education of prospective Antarctic tourists. Paul G Lamberth MJA 2001; 175: 583-584 Clinical record - Discussion - References - Authors' details - - More articles on Travel, aviation and underwater medicine Antarctic tourism has increased rapidly in recent years, possibly because the collapse of the Soviet Union has made available a fleet of icebreakers.1 The combination of cruise ship conditions and the hostile, remote environment portends health risks for travellers. Doctors on scientific expeditions to the Antarctic report dealing with a range of major medical problems, including acute abdomen requiring laparotomy,2 ruptured intracranial aneurysm,3 70% thermal burns,4 and intestinal haemorrhage requiring a multinational rescue operation.5 Although the health needs of workers in Antarctica have been documented, little is known of the requirements of unscreened tourists. I report the death of an Australian tourist on an Antarctic cruise. Clinical record An 82-year-old Australian man boarded a Russian ice-strengthened vessel in Ushuaia, at the southern tip of Argentina, for a two-week cruise to the Antarctic Peninsula. During traverse of the notoriously rough Drake Passage on Day 2, he took dimenhydrinate and hyoscine for motion sickness. On Day 3, he had a minor fall while disembarking from an inflatable boat, leaving him with back pain which he treated with paracetamol and dextropropoxyphene. His only complaint to the ship's doctor (myself) at the time was wheezing induced by the cold air. On Day 5, he missed breakfast and was found lying on the floor of his single cabin. He explained that he had been unable to get up after a fall 12 hours before. I examined him carefully, with the only positive findings being dry mucosae and exquisite localised midline vertebral tenderness elicited at T9. He had a past history of smoking-related chronic airflow limitation, treated with bronchodilators and corticosteroids, and osteoporosis. The working diagnosis was a crush fracture of a lower thoracic vertebra, for which I gave him further analgesia. The following afternoon, subtle disorientation was noted, progressing over four hours to stupor with hypotension, poor peripheral perfusion and tachypnoea. Examination revealed left basal crackles and right-sided wheeze. The right calf had become tender. Intravenous resuscitation with 10% hydroxy-ethyl starch increased his blood pressure to 125/65 mm Hg, and urine output to 40-50 mL/h. Ceftriaxone (1 g) and gentamicin (320 mg) were administered with dexamethasone (4 mg intravenously) in lieu of regular bronchodilator therapy. On Day 8, the stupor persisted. Lung auscultation revealed left basal crackles correlating with a region of dullness to percussion. There was profuse purulent sputum. The patient's insurer agreed to meet the expense of evacuation, but a plan to fly him from the nearby Russian base on King George Island to Punta Arenas in Chile was abandoned when the weather deteriorated. After discussion, the Russian captain's initial plan to leave the patient at the Russian base, which was apparently less well equipped than the ship's hospital, was dropped in favour of returning to Ushuaia at full speed. That evening, the patient developed bilateral ocular deviation to the right, poor peripheral perfusion and periodic respirations. Crystalloid was administered to treat poor perfusion and falling urine output. Lansoprazole, for stress-ulcer prophylaxis, and aspirin, for a probable left leg venous thrombosis, were also given. On Day 9, the patient remained febrile, with normal heart rate and blood pressure. Enteral fluids (2000 mL per day) with sucrose (80 g) and sodium chloride (4 g) were tolerated, with gastric aspirates under 20 mL and normal bowel sounds. That afternoon, his breathing became intermittent, he developed oliguria and bradycardia, and died at 1730 hours. The ship reached Ushuaia 16 hours later. No autopsy was performed, and the body was cremated in Argentina. Discussion The final diagnosis was septic shock secondary to lower respiratory tract infection. The patient may also have had a deep venous thrombosis with possible pulmonary embolism. Contributing factors were chronic airflow limitation, back pain due to a thoracic crush fracture complicating osteoporosis secondary to frequent corticosteroid use, immobilisation and dehydration. Cold air exacerbating bronchospasm probably also contributed, while impairment of balance and cognitive function by anticholinergic medications may have been a factor in the patient's falls. This case illustrates the fundamental principle of incident analysis — a number of seemingly minor factors can combine to produce a disaster that was not predicted from any one precipitant alone.6 The case also raises issues for Antarctic tourism: Medical stocking of ships: As the areas explored can be several days' journey from modern healthcare facilities, there is an argument that ships' hospitals should be able to provide life support for 72 hours. This is not the case on most Antarctic cruise ships, despite travel companies advertising medical supervision as a feature. In contrast, the major "tropical" cruise lines provide advanced medical facilities appropriate to the elderly and infirm nature of many of their clientele. Medical equipment on Antarctic cruises should include intravenous fluids for resuscitation and maintenance and, ideally, a portable ventilator and monitoring device, such as a pulse oximeter. Ships' doctors require a high level of critical care skills to undertake advanced life support at sea. Many ship's doctors now working in Antarctica are Australian emergency physicians. Furthermore, the risks of anticholinergic medications for motion sickness, especially in the elderly, need to be better appreciated. Disturbed balance, sedation and cognitive impairment are a deadly combination in an unfamiliar environment. NASA (the National Aeronautics and Space Administration) advises promethazine for microgravity motion sickness.7 It is believed that promethazine, unlike hyoscine, dimenhydrinate and other common anti-motion-sickness agents, relieves symptoms without impairing adaptation. Therefore, during prolonged exposure, promethazine can be ceased as travellers get their "sea legs". Screening and education of prospective passengers: Factors that increase risk during Antarctic travel include: Moderate to severe reactive airway disease, especially if precipitated by cold air. Caution should be advised for those with chronic airway disease with severe fixed obstruction (FEV1 < 1.0 L/s) or requiring frequent courses of corticosteroids. Decreased mobility or balance problems, because of the need to negotiate steep companionways in heavy seas.8 Conditions with potential complications that would be difficult to treat in a remote environment, such as coronary artery disease, pregnancy and insulin-dependent diabetes. Poorly controlled mental illness. Provision of information on motion sickness, cold environment risks, and hazards such as falls may help passengers look after their own health. Appropriate health and accident insurance should be mandatory. A nihilistic philosophy that requires tourists to accept their own risks does not take into account the impact of illness or injury on other passengers, who may seek legal remedy from the tour operator. Improved surveillance of passengers travelling alone: Passengers in single cabins appear to be at increased risk of adverse events. The failure to detect my patient's predicament until 12 hours had elapsed may have been a crucial factor in his death. A simple system of surveillance would be possible, with passengers on their own reporting to a nominated crew member twice daily. The increase in adventure tourism by the elderly is a significant health challenge. Tour companies should consider developing a standard to equip ships for life support. A well-prepared aeromedical evacuation plan would mitigate this responsibility. Physicians advising prospective passengers should consider the rigorous screening that scientific expeditions apply to participants, and the equipment and training they provide in preparation for medical emergencies.9 Tourists swimming in an active volcano, Deception Island, Antarctic Peninsula. References Prociv P. Health aspects of Antarctic tourism. J Travel Med 1998; 4: 210-212. Priddy RE. An "acute abdomen" in Antarctica. The problems of diagnosis and management. Med J Aust 1985; 143: 108-111. Pardoe RA. A ruptured intracranial aneurysm in Antarctica. Med J Aust 1965; 1: 344-350. Alcorn GB. My Antarctic practice. Med J Aust 1992; 157: 253-258. Poki MT, Semmens K. Intestinal haemorrhage in Antarctica: a multinational rescue operation. Med J Aust 1979; 2: 275-277. Mendick M. What went wrong? Analysis. the little things add up. Flight Safety Aust 2001; 5(4): 14. Cowings PS, Toscano WB, DeRoshia C, et al. Promethazine as a motion sickness treatment: impact on human performance and mood states. Aviat Space Environ Med 2000; 71: 1013-1022. Carter JW. Shipboard medicine on package cruises. BMJ 1972; 1: 553-556. Lugg DJ. Antarctic medicine. JAMA 2000; 283: 2082-2084. Authors' details Department of Emergency Medicine, Canberra Hospital, Canberra, ACT. Paul G Lamberth, FACEM, Emergency Physician, and Consultant, Shock Trauma Service. Reprints will not be available from the author. Correspondence: Dr P G Lamberth, Canberra Hospital, Yamba Drive, Garran, ACT 2606. palamATozemail.com.au Make a comment

Paul G Lamberth

MJA 2001; 175: 141-145 Abstract - Definitions - Prevalence - Severity - Lung function - GP consultation - Hospitalisation - Management - Morbidity and quality of life - Mortality - Discussion - References - Authors' details Make a comment - - - More articles on Psychiatry Abstract In 1997, 27% of Australian children had current wheeze, and this is increasing by 1.4% per year. The prevalence of wheeze among adults is lower and appears to be stable. The prevalence of persistent asthma (wheezing episodes with abnormal airway function between episodes) in children has increased from 5% to 9% in the past 20 years. In adults, the prevalence is 5%-6%. Up to 80% of adults with persistent asthma have abnormal lung function. Asthma deaths in Australia have fallen 28% since peaking in 1989, but the mortality rate is still twice that of England. The Australian Health Ministers' Conference in 1999 acknowledged the importance of asthma as a health issue by making it a National Health Priority Area. In the same year, the Cooperative Research Centre for Asthma (CRCA) was established. The CRCA is a joint venture between two medical research institutes (the Institute of Respiratory Medicine and the Garvan Institute of Medical Research), three universities (the University of Sydney, Monash University, and the University of Western Australia), six pharmaceutical companies, and the New South Wales Department of Health. Its mission is to reduce the burden of asthma on the Australian community. The three research programs of the CRCA are prevention of asthma, treatment of asthma, and diagnostic, delivery and monitoring devices. Here we summarise information on the burden of asthma in Australia and make some international comparisons. We do not attempt to develop a single estimate for the "burden" of asthma, but describe data on prevalence, severity, lung function, general practitioner and hospital attendances, management, morbidity, and mortality as related to asthma. Data on the prevalence of atopy are not presented. Although this is the strongest risk factor for asthma,1 its contribution to the burden of asthma is indirect. Definitions There is no agreed definition of asthma. The terms we use here are defined in Box 1. Asthma prevalence can be measured in terms of self-reported wheeze, doctor-diagnosed asthma, or a combination of symptoms and lung function abnormality.2 Moreover, asthma can be classified as intermittent or persistent, and persistent asthma can be classified into mild, moderate and severe, based on symptoms and degree of airway hyperresponsiveness.3 There are limitations to the use of questionnaires in the measurement of asthma. These arise because of differences between patients, parents, and doctors in the use of the label "asthma" and, to a lesser extent, "wheeze". Furthermore, substantial problems with recall bias may influence the findings. In evaluating questionnaire-based reports of the prevalence of asthma, it is important to be aware of the questions used to define asthma in the particular study. It is also relevant to be aware of assessments of the reliability and validity of the questionnaire. Prevalence Wheeze Children: Over the past 20 years, there have been at least 26 population-based studies measuring self-reported current wheeze in Australian children (Box 2). The prevalence of current wheeze has been increasing at a rate of 1.4% per year.4 The International Study of Asthma and Allergies in Childhood (ISAAC),19 in 38 countries across all continents, found that among children aged 6-7 years Australia had the second-highest prevalence of self-reported current wheeze (24.6%). Approximately a quarter of Australian children have wheezed in the past 12 months, and it seems unlikely that they all have intermittent or persistent asthma that requires treatment or is a burden. At present, there is no way to classify asthma on wheeze alone, although, in many studies, children with more than four wheeze episodes per year are regarded as having "asthma". Robertson et al4 found that among 6-7-year-olds who report current wheeze 34.7% reported more than four wheeze episodes (about 8% to 9% of the population). In comparison with other countries, Australia has the second-highest percentage of children aged 6-7 years who report more than four wheeze episodes in the previous 12 months.19 It can be calculated from the data reported by Bauman et al5 that children who wheeze are symptomatic about 14% of the time. Adults: In contrast to the information available for childhood wheeze, there is a paucity of data on the prevalence of current wheeze in Australian adults. Box 3 shows the prevalence of current wheeze to be between 17% and 29% in adults, with no apparent increase over time. In the European Community Respiratory Health Survey (ECRHS), conducted in 22 predominantly European countries, Australia had the fourth-highest prevalence of self-reported current wheeze in populations aged 20 to 44 years.20 Wheeze and lung function Objective measures of lung function combined with asthma symptoms allow classification of asthma into intermittent and persistent. Persistent asthma is clinically important asthma in that it causes more interference with work and school, requires more treatment, and results in more healthcare utilisation; hence, it represents a greater burden than intermittent asthma.2,27 In Australia, about 9%-11% of children6 and 5%-6% of adults21,22 have persistent asthma. Persistent asthma was not measured in phase one of the ISAAC study. The Australian reporting centre for the ECRHS found that 25.5% of its sample of adults in Melbourne had persistent asthma.28 However, the sample used in that study to determine prevalence of airway hyper-responsiveness (and thus persistent asthma) was not random, but was enriched with an additional 27% of symptomatic subjects. Although data on the prevalence of airway hyperresponsiveness have been published for the ECRHS as a whole, no data on the prevalence of symptoms together with airway hyperresponsiveness (ie, persistent asthma) have been published from this survey. Severity The measurement of severity of asthma is difficult. The nature of mild, moderate, or severe asthma depends on the perspective of the observer. Questionnaire assessments of severity generally focus on symptoms that are regarded by clinicians as indicative of more severe asthma, such as frequent wheeze episodes, severe episodes, hospital and emergency department admissions, and disturbed sleep. In addition, questions relating to disability and handicap arising from the disease, such as time off work or school and inability to carry out normal activities, are used as indicators of severity. None of these could be considered a "gold" standard. In the Australian data from the ISAAC study, among children aged 6-7 years with current wheeze 55.1% have nocturnal waking and 15.3% report severe wheeze episodes.4 In the international comparison, Australia ranked 10th highest for the percentage of children aged 6-7 years who had disturbed sleep in the previous year.19 Rosier et al29 used a statistical approach (item response theory) to develop a questionnaire-based functional assessment of disease severity in children with wheeze. In a population study, they found that the 14% of children who had current wheeze included 47% low, 18% mild, 30% moderate, and 5% high severity. This scale was validated by demonstrating correlations with school absence, functional impairment, practitioner consultations, and medication requirements. In the clinical setting, measurements of airway hyper-responsiveness are often used to determine asthma severity. Peat et al6 showed that of the Australian children with persistent asthma the percentage of children with severe airway hyperresponsiveness was less than 1%. Thus, it appears from both questionnaires and lung function data that the proportion of children with severe asthma is about 0.4%-0.6% of the population. The proportion of the burden of asthma that comes from the small group with severe asthma and from the larger group with mild asthma is open to interpretation. Health planners should target those with severe asthma, as they have a greater potential for adverse health outcomes30 and poorer long term lung function than individuals with intermittent asthma, many of whom remit.30,31 Lung function A proportion of the burden of asthma comes from symptoms of poor lung function. In their study of Busselton adults, Peat et al32 found that individuals with asthma have a more rapid decline of lung function over time compared with normal subjects. In that study, 86% of females and 82% of males with current asthma had abnormal lung function. A study of children in a suburb of an industrial city and in a rural town in New South Wales found that those who had airway hyperresponsiveness had reduced measurements of forced expiratory volume in one second (FEV1) over time.33 The magnitude of the burden of asthma due to poor lung function has not been documented. GP Consultation Data from the Bettering the Evaluation and Care of Health Study, 1998-1999,34 indicate that asthma is the sixth most frequently managed problem by GPs in Australia. Asthma is one of the top 20 reasons for individuals to visit a GP, with a rate of 1.4 per 100 encounters. Hospitalisation During the period 1998-1999, there were 53 907 hospital separations and 7464 same-day separations for asthma in Australia, equating to 147 496 patient-days.35 The average length of stay was 2.7 days. Faniran et al found that about 1.8% of children were admitted to hospital for asthma and 6.8% attended the emergency department in the previous year.7 In Australia, the ISAAC study found that for 6-7-year-olds who reported current wheeze about 7% were admitted to hospital and 14.4% attended the emergency department.4 Between 1998 and 1999, South Australia reported the highest hospitalisation rate (384 per 100 000 people) and Tasmania reported the lowest rate (148 per 100 000 people).35,36 Compared with countries with a similar high prevalence of wheeze, Australia has a very low rate of hospital admissions.37 The ECRHS study found that Australia had the third-lowest hospitalisation rate in adults with current doctor-diagnosed asthma. Only 1% of adults with asthma were admitted to hospital in the previous year. This might indicate that, comparatively, asthma in Australia is reasonably well managed, although many studies suggest that management is still not ideal.38,39 Management Correct prescribing practices and adherence to therapy are core issues in the management of asthma and quality of life, and thus the burden of asthma. One Australian study found that the use of anti-inflammatory medication was unsatisfactory in 26% of children with asthma.38 These children were treated either too aggressively or inadequately. Box 4 shows the patterns of treatment for children in Australia who reported wheeze episodes in the previous year.4 The degree of interventions increased in proportion to the number of wheeze episodes. However, for children who reported more than 12 wheeze episodes, both the use of inhaled steroids and the use of a written asthma action plan were inadequate. Perceptions of treatment efficacy and management among young adults (20-44 years old) in Victoria were examined in the ECRHS study.39 There was generally poor adherence to therapy among this age group. Adults in New Zealand and the UK also have a high prevalence of wheeze, but are three times more likely than Australian adults to take anti-inflammatory medication daily.37 It is difficult to ascertain how much of the GP and hospital attendances are indicative of poorly controlled asthma. Ruffin et al have shown that there is insufficient ownership of asthma management plans in South Australia.40 In 1996, only 33% of patients with asthma had an asthma action plan. Those who had action plans were more aware of asthma severity, used preventer medication more regularly, measured their lung function and understood their asthma. It is acknowledged that self-management plans result in improved health outcomes for patients with asthma.8 Furthermore, regular review and having a written asthma action plan contribute to reduction in hospital and emergency department attendances, and to reduced absenteeism from work or school and reduced nocturnal asthma.41 Morbidity and quality of life The Living with Asthma Study, conducted in 1999, found that asthma had a substantial impact upon child and adult lifestyles. Both groups felt tired and frustrated because of their asthma. One in five children did not ride a bike or play at school or with animals, and one in three did not participate in organised sport. One in four adults avoided socialising in restaurants, pubs and clubs because of the smoky environment. Parents of children with asthma were more anxious than parents of children who did not have asthma. The 1995 National Health Survey, conducted in a sample of the adult Australian population by the Australian Bureau of Statistics, included administration of the SF-36 (Short Form, 36 questions) questionnaire,42 which measures physical functioning, role limitations due to physical problems, bodily pain, general health, vitality, social functioning, role limitations due to emotional problems, and mental health. For all these categories, adults with asthma had lower mean scores than adults without asthma. The NSW Health Survey 1997 (Box 5) showed that many adults who have current doctor-diagnosed asthma suffer considerable morbidity.42 Mortality In 1998, there were 685 deaths from asthma in Australia (Box 6).44 This represents a 28% fall in asthma deaths since they peaked in 1989. The declining trend has occurred across all age and sex groups. Improved asthma management, implemented through the National Asthma Campaign, best explains this trend. There has been greater physician and patient testing of lung function and overall use of management plans. Despite improving mortality rates in Australia, the rate of 0.61 per 100 000 people aged 5-34 years is almost double that of England (0.35 per 100 000),45 indicating that there is still scope for improvement in asthma management practices. Discussion It is widely acknowledged that there are many sources of inaccuracy in studies of asthma prevalence.46,47 Even allowing for the various asthma definitions used in questionnaires, the data indicate that there is a large burden of asthma in Australia, in both children and adults. Moreover, for many measures of asthma, Australia has a high, if not the highest, prevalence when compared with other countries. However, large gaps remain in knowledge about the prevalence, severity and morbidity of persistent asthma in Australia and internationally. More information is needed about treatment practices and the groups of people most at risk for poor outcome. To accurately assess the burden, it will be necessary to relate asthma prevalence and severity to the indicators of morbidity and make international comparisons. There are many things that can be done now to reduce the burden of asthma. Patients and families can manage their own asthma by increasing their knowledge and awareness of asthma medication and control and removing barriers to adherence to treatment regimens. Clinicians should find efficient ways to diagnose and treat people with asthma, and form partnerships with patients to implement asthma management and action plans. Researchers should decide on useful definitions of asthma so that prevalence, severity and health outcomes can be compared with time and with changes in treatment practice. Although there is no cure for asthma, the disease can be controlled by good management. Improving quality of life and keeping prevalence, mortality and hospital admission rates low is well within the scope of clinicians and patients. This represents the preventable burden of asthma. Many questions about the burden of asthma, and how best to reduce it, remain to be answered. These include: What responsibility for reducing the burden of asthma should be borne by government, the National Asthma Campaign and asthma clinicians? How much of the burden is due to poor management by the doctor or individuals with asthma? Can asthma be prevented if treated early? Are there protective factors that can be introduced to reduce the prevalence of asthma? The Cooperative Research Centre for Asthma will address these questions and it is hoped that, together with other researchers, it will answer them. References Peat JK, van den Berg RH, Green WF, et al. Changing prevalence of asthma in Australian children. BMJ 1994; 308: 1591-1596. Toelle BG, Peat JK, Salome CM, et al. Towards a definition of asthma for epidemiology. Am Rev Respir Dis 1992; 146: 633-637. Global initiative for asthma. Global strategy for asthma management and prevention. NHLBI/WHO workshop report. March 1993. National Institutes of Health Publication No. 95-3659. National Heart, Lung and Blood Institute: Bethesda, Maryland, 1995. Available at <http://www.ginasthma.com/xwork.html> Robertson CF, Dalton MF, Peat JK, et al. Asthma and other atopic diseases in Australian children. Australian arm of the International Study of Asthma and Allergy in Childhood. Med J Aust 1998; 168: 434-438. Bauman A, Mitchell CA, Henry RL, et al. Asthma morbidity in Australia: an epidemiological study. Med J Aust 1992; 156: 827-831. Peat JK, Toelle B, Gray L, et al. Prevalence and severity of childhood asthma and allergic sensitisation in seven climatic regions of New South Wales. Med J Aust 1995; 163: 22-26. Faniran AO, Peat JK, Woolcock AJ. Prevalence of atopy, asthma symptoms and diagnosis, and the management of asthma: comparison of an affluent and a non-affluent country. Thorax 1999; 54: 606-610. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Hurry VM, Peat JK, Woolcock AJ. Prevalence of respiratory symptoms, bronchial hyperresponsiveness and atopy in schoolchildren living in the Villawood area of Sydney. Aust N Z J Med 1988; 18: 745-752. Bauman A. Has the prevalence of asthma symptoms increased in Australian children? J Paediatr Child Health 1993; 29: 424-428. Henry RI, Abramson R, Adler JA, et al. Asthma in the vicinity of power stations: 1. A prevalence study. Pediatr Pulmonol 1991; 11: 127-133. Robertson CF, Heycock E, Bishop J, et al. Prevalence of asthma in Melbourne schoolchildren: changes over 26 years. BMJ 1991; 302: 1116-1118. Pearce N, Weiland S, Keil U, et al. Self-reported prevalence of asthma symptoms in children in Australia, England, Germany and New Zealand: an international comparison using the ISAAC protocol. Eur Respir J 1993; 6: 1455-1461. Gray EJ, Peat JK, Mellis CM, et al. Asthma severity and morbidity in a population sample of Sydney schoolchildren: Part 1 — prevalence and effect of air pollutants in coastal regions. Aust N Z J Med 1994; 24: 168-175. Robertson CF, Bishop J, Dalton M, et al. Prevalence of asthma in regional Victorian schoolchildren. Med J Aust 1992; 156: 831-833. Crockett AJ, Cranston JM, Alpers JH. The changing prevalence of asthma-like respiratory symptoms in South Australian rural school children. J Paediatr Child Health 1995; 31: 213-217. Volkmer RE, Ruffin RE, Wigg NR, Davies N. The prevalence of respiratory symptoms in South Australian preschool children. I. Geographic Location. J Paediatr Child Health 1995; 31: 112-115. Downs SH, Marks GB, Sporik R, et al. Continued increase in the prevalence of asthma and atopy. Arch Dis Child 2001; 84: 20-23. Worldwide variations in the prevalence of asthma symptoms: the International Study of Asthma and Allergies in Childhood (ISAAC). Eur Respir J 1998; 12: 315-335. Variations in the prevalence of respiratory symptoms, self-reported asthma attacks, and use of asthma medication in the European Community Respiratory Health Survey (ECRHS). Eur Respir J 1996; 9: 687-695. Peat JK, Gray EJ, Mellis CM, et al. Differences in airway responsiveness between children and adults living in the same environment: an epidemiological study in two regions of Australia. Eur Respir J 1994; 7: 1805-1813. Peat JK, Haby M, Spijker J, et al. Prevalence of asthma in adults in Busselton, Western Australia. BMJ 1992; 305: 1326-1329. Abramson M, Kutin J, Bowes G. The prevalence of asthma in Victorian adults. Aust N Z J Med 1992; 22: 358-363. Woods R, Wharton C, Walters H, Abramson M. The rising prevalence of asthma in young Victorian adults. Respirology 2000; 5 Suppl June: A26. Woods RK, Burton DL, Wharton C, et al. Asthma is more prevalent in rural New South Wales than metropolitan Victoria, Australia. Respirology 2000; 5: 257-263. Gibson PG, Mitchell C, Bauman A, et al. Asthma morbidity and management among adults in Australia, 1998. Respirology 2000; 5 Suppl June: A27. Van Asperen PP. Towards a better understanding of childhood asthma. J Paediatr Child Health 1995; 31: 272-275. Abramson M, Kutin JJ, Raven J, et al. Risk factors for asthma among young adults in Melbourne, Australia. Respirology 1996; 1: 291-297. Rosier MJ, Bishop J, Nolan T, et al. Measurement of functional severity of asthma in children. Am J Respir Crit Care Med 1994; 149: 1434-1441. Lange P. Prognosis of adult asthma. Monaldi Arch Chest Dis 1999; 54: 350-352. Martinez FD, Helms PJ. Types of asthma and wheezing. Eur Respir J 1998; 27: 3s-8s. Peat JK, Woolcock AJ, Cullen K. Rate of decline of lung function in subjects with asthma. Eur J Respir Dis 1987; 70: 171-179. Xuan W, Peat JK, Toelle BG, et al. Lung function growth and its relation to airway hyperresponsiveness and recent wheeze. Results from a longitudinal population study. Am J Respir Crit Care Med 2000; 161: 1820-1824. Britt H, Sayer GP, Miller GC, et al. Bettering the evaluation and care of health: general practice in Australia, 1998-99. Sydney: University of Sydney and Australian Institute of Health and Welfare, 1999. Australian Institute of Health and Welfare. Australian hospital statistics 1998-99. Canberra: AIHW, 2000. (AIHW cat. no. HSE 11. Health Services Series no. 15.) Australian Bureau of Statistics. Australian demographic statistics, March quarter 1999. Canberra: ABS, 1999. (Catalogue no. 3101.0.) Janson C, Chinn S, Jarvis D, Burney P. Physician-diagnosed asthma and drug utilization in the European Community Respiratory Health Survey. Eur Respir J 1997; 10: 1795-1802. Paterson NAM, Peat JK, Mellis CM, et al. Accuracy of asthma treatment in schoolchildren in NSW, Australia. Eur Respir J 1997; 10: 658-664. Reid D, Abramson M, Raven J, Walters EH. Management and treatment perceptions among young adults with asthma in Melbourne: The Australian experience from the European Community Respiratory Health Survey. Respirology 2000; 5: 281-287. Ruffin RE, Wilson D, Southcott A, et al. A South Australian population survey of the ownership of asthma action plans. Med J Aust 1999; 171: 348-351. Gibson PG, Coughlan J, Wilson AJ, et al. Self-management education and regular practitioner review for adults with asthma. The Cochrane Library. 2000(2): CD00117. Australian Bureau of Statistics. National health survey: SF-36 population norms. Australia. Canberra: ABS, 1995. (Catalogue no. 4399.0.) NSW Health Survey 1997 Electronic Report. <http://www.health.nsw.gov.au/ public-health/hs97/> Accessed 8 August 2000. Australian Bureau of Statistics. Causes of death: Australia. Canberra: ABS, 1998. (Catalogue no. 3303.0.) Twentieth Century Mortality. (England & Wales 1901 -1995) CD-ROM. London: Office for National Statistics, 1997. Kemp T, Pearce N, Crane J, Beasley R. Problems of measuring asthma prevalence. Respirology 1996; 3: 183-188. Magnus P, Jaakkola JJK. Secular trends in the occurrence of asthma among children and young adults: critical appraisal of repeated cross sectional surveys. BMJ 1997; 314: 1795-1799. (Received 11 Dec 2000, accepted 24 Apr 2001) Autors' details Cooperative Research Centre for Asthma, Royal Prince Alfred Hospital, Sydney, NSW. Ann J Woolcock, AO, FRACP, FAA, Principal Scientist (deceased); Shalini A Bastiampillai, Research Assistant; Guy B Marks, FRACP, FAFPHM, Project Leader. Victoria A Keena, BS Lib Sc, Information Manager. Reprints will not be available from the authors. Correspondence: Ms V A Keena, Institute of Respiratory Medicine, PO Box M77, Missenden Road, NSW 2050. vakATmail.med.usyd.edu.au Make a comment 1: Definitions Current wheeze A positive answer to the question "Have you [has your child] wheezed in the last 12 months?". Persistent asthma (sometimes called current asthma) Wheeze in the past 12 months together with evidence of abnormal airway function between attacks of wheezing. This abnormal function may include abnormal spirometry, abnormal waking peak flow values or airway hyperresponsiveness. Intermittent asthma Episodes of wheeze in the past 12 months with normal airway function between episodes. Burden of disease Burden can best be defined as the aggregate data from prevalence, lung function, practitioner consultations, hospital admission rates, poor management, quality-of-life indicators, mortality, and estimates of health-sector costs. Airway hyperresponsiveness An increased response to a provoking stimulus (usually inhaled methacholine or histamine), as measured by a 20% fall in forced expiratory volume in one second. Back to text Data are from reference 1, 4-18. The trend is calculated by averaging the prevalences for each year. Back to text Data are from references 8, 20-26. Back to text Back to text Back to text Back to text

Ann J Woolcock · Shalini A Bastiampillai · Guy B Marks · Victoria A Keena

Medicine and the Community A swimming program for children with asthma Does it improve their quality of life? Colleen P Wardell and Clair Isbister MJA 2000; 173: 647-648 Methods - Results - Discussion - References - Authors' details - - More articles on Paediatrics Introduction The Asthma Foundation of NSW started the Asthma Children's Swimming Program in 1964. Previously, it was observed that many asthmatic children tended to be excluded from sport and often had difficulty learning to swim in available "learn to swim" programs. They were generally not physically fit. Many were mouth breathers, often with some chest deformity and chronic rhinitis. Even when adequately medicated, respiration was inefficient, with decreased movement of the diaphragm, and nasal obstruction and recurrent ear and throat infections. Many had low body fat, giving poor insulation against cold water pool conditions, which appeared to aggravate wheezing and exercise-induced asthma. Yet some of Australia's Olympic swimmers of the time (such as Dawn Fraser and Jon Henricks) were asthmatic, which suggested that asthma need not be a barrier to physical fitness. The value of swimming for asthmatics was supported by articles in medical journals1,2 and anecdotal evidence. It was a low weight bearing exercise, potentially life saving, easily supervised, and suited to individual tuition and practice. A swimming program also presented an educational opportunity to teach about health and asthma and efficient breathing. Logically and physiologically, swimming appeared the most suitable exercise relevant to respiratory and overall well being. The program developed by the Asthma Foundation of NSW modified the teaching methods of the day to meet the special needs of asthmatic children (Box 1). By 1994 the program had expanded from one to 36 pools throughout metropolitan and rural NSW. In those 30 years about 25 000 children were taught by 2000 volunteer instructors. This kind of growth, based on the voluntary involvement of unpaid instructors and parents of asthmatic children, is itself a measure of success. The anecdotal evidence of those involved in the program is that it improves health, reduces the frequency of asthma attacks and improves the children's quality of life. The NSW Department of Sport and Recreation had acknowledged the value of the program, and included it as an extension course for AUSTSWIM instructors. In 1994, the Asthma Foundation of NSW allocated $10 000 for an evaluation of the swimming program. That study was a retrospective survey involving a limited statistical analysis and a qualitative evaluation of the effect on the whole child.3 In this article we present the main findings of that evaluation, a full report of which is available from the Foundation.4 Methods Asthma is a multifactorial condition with many variables, including severity, seasonal incidence, and multiple trigger factors, such as allergy, climate, and infection. Medical treatment and school and home management differed, as did the geographic distribution of pools. Under these circumstances, it was not possible to assemble a suitable control group for a case-control study. After studying the relevant literature, we concluded that a quality-of-life study by means of questionnaires administered to parents and volunteer instructors was the most appropriate method. Two rural and three metropolitan swimming groups were selected for the study. Children were randomly selected from those who had attended for over one year (to avoid a seasonal influence on results). Three questionnaires were prepared: two for parents and one for instructors. The first parental questionnaire related to the child's condition on entering the program, and the second to the child's condition at the time of the study. They both asked for information about hospitalisation and doctor's visits; physical signs such as mouth breathing, snoring, and chest deformity; general health; other illnesses and allergies; peak flow readings; severity of asthma; school attendance and performance; height and weight; and participation in other swimming classes and sport. The instructor's questionnaire asked about their participation, how and why they did voluntary work, and their observations on the children and the program. Results One hundred and twenty-three sets of questionnaires were distributed to parents, and 87 sets were returned. However, it was found that one rural swimming group had not adhered strictly to the swimming instruction method and had to be excluded, leaving 73 sets for the survey. These were for 38 boys and 35 girls, with an average time of 2.4 years in the program. The main quantifiable results are shown in Box 2. Asthma medication and medication dosage were highly variable in this group of children. Parents of half the children reported a change in medication since starting the swimming program, with two-thirds showing a decrease. Almost all parents who answered the questionnaire were satisfied with the program and reported that the changes in the children had improved the quality of life of the whole family. Appreciation was expressed for the program, the value of the year-round availability, the individual tuition, and the caring attitude of the volunteers. Also valued was the opportunity to discuss common problems with other parents of asthmatic children, and the asthma education provided. Instructors had joined the program for many reasons and some had stayed over 25 years. They enjoyed their participation, and felt that they were rewarded by the children's achievements and the improvement seen in their general health and attitudes. They commented that many children were timid and anxious at first, and needed much coaxing. This made the children's eventual success and increase in confidence and self-esteem even more rewarding for the instructors. It was often noted that children who could swim before joining the program were breathing inefficiently. When this was corrected they swam longer distances with greater ease. Discussion The results of this study suggest that the program has achieved its purpose and justified its continued demand. For many people the program can improve quality of life and asthma management, and reduce medication, visits to doctors, and hospitalisations. Peak flow meter readings taken at every session have been a useful guide for the instructor regarding the child's possible need for pre-swim medication. Huang et al claim improvement in peak flow readings in a swimming program for asthmatic children conducted in the USA,5 but our study did not find significant change in this variable. Instead, the program produced more general improvements in psychological and physical wellbeing. The acquisition of a lifelong sporting skill provides a psychological boost and assists in developing self-esteem and confidence to take part in other activities. The long term commitment and enthusiasm of the volunteer instructors was most impressive and made one appreciate the special value of these people who gave their time and care. For 1999 it was calculated that, had normal hourly rates for swimming instructors been paid, the cost would have been nearly $500 000. A recent report shows that the cost of asthma to the community is $585-$728 million per year.6 Yet here is a program using volunteers, with no government support, which can improve children's health and reduce medication, hospitalisation and visits to doctors, with consequent reduction in parent absenteeism from employment, all of which should result in economic benefits. We hope that others will be encouraged to establish and evaluate programs designed to assist the overall health of people with a specific illness. References Jones RS, Buston MG, Wharton MI. The effect of exercise on ventilatory function in the child with asthma. Br J Dis Chest 1962; 56: 78-86. McEthenney RR, Petersen KH. Physical fitness for asthmatic boys. A co-operative pilot study. JAMA 1963; 185: 142-143. Meyer J. Using qualitative methods in health action research. BMJ 2000; 320: 178-181. Wardell CP, Isbister C. Report on thirty years of the Asthma Children's Swimming Program. Sydney: Asthma Foundation NSW, 1994. Huang S-W, Veiga R, Sila U, Reed E, Hines S. The effect of swimming in asthmatic children -- participants in a swimming program in the City of Baltimore. J Asthma 1989; 26: 117-121. National Asthma Campaign. Report on the cost of asthma in Australia. Canberra: National Asthma Campaign, 1992: 8. Authors' details The Asthma Foundation of New South Wales, Sydney, NSW, 2065. Colleen P Wardell, BA, Swimming Program Co-ordinator; Clair Isbister, FRACP, DCh, Medical Adviser for the Asthma Children's Swimming Program. Reprints will not be available from the authors. Correspondence: Dr C Isbister, 142 Wentworth Street, Blackheath, NSW 2785. wardelljandcATbigpond.com 1: The Asthma Children's Swimming Program A committee of three specialist clinicians, two thoracic physiotherapists, an Olympic swimmer with asthma and a professional swimming coach designed a swimming program to meet the special needs of asthmatics. The principal differences from a general "learn to swim" program were: the use of indoor heated pools to give a controlled environment, thus reducing the chance of inducing asthma symptoms weekly swimming sessions held all year a minimum admission age of four years, considered desirable for adequate coordination, concentration, and understanding eligibility for the program required parental application, supported by a medical certificate stating details of the child's asthma and current medication the presence of a responsible adult carer, to give pre-swim medication if required pre-swim breathing exercises peak flow meter readings before and after swimming individual tuition, allowing each child to learn at his/her own pace no flotation aids except kickboards strong emphasis, starting at the first lesson, on correct controlled breathing coupled with correct swimming actions An instructor's manual was prepared describing the swimming method, and including information about asthma. Volunteer swimming instructors are trained in the method and in asthma first aid. The program has been operating continuously since 1964 and has expanded to many additional locations. For information about the current swimming program or a copy of the current version of the swimming instructor's manual, contact the Asthma Foundation of New South Wales, Suite 1, 82 Pacific Highway, St Leonards, NSW 2065. Return to text2: Reported changes in children's condition after participating in the Asthma Children's Swimming ProgramNo. of repliesChangesAsthma severity7150% showed improvementNumber of trigger factors72No significant changeMouth breathing7113% showed improvementSnoring7118% showed improvementChest deformity717% showed improvementNumber of other illnesses73No significant changeChild's enjoyment of program7397% enjoyed lessonsSwimming proficiency7390% showed improvement; 63% rated good or betterContinuing swimming7389% intended to continue after leaving the programSelf confidence7277% showed improvementPeak flow readings30No significant change Number of visits to doctor7346% overall reductionNumber of hospitalisations7364% overall reductionSchool absence due to asthma (above kindergarten age)5874% reported less absenceAsthma management7367% reported improvementUnderstanding of asthma7378% reported improvementFeeling disadvantaged by asthma7381% reported improvement Return to text

Colleen P Wardell · Clair Isbister

Research A South Australian population survey of the ownership of asthma action plans Richard E Ruffin, David Wilson, Anne Marie Southcott, Brian Smith and Robert J Adams MJA 1999; 171: 348-351 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Respiratory medicine Abstract Objective: To examine the relationships between ownership of written asthma action plans, asthma morbidity, use of devices, and patients' perceptions of their asthma management. Design and setting: A random population survey (in 1996) of the South Australian population aged 15 years or over, using interviewers to administer a questionnaire. Participants: People who reported that they had current, doctor-diagnosed asthma. Main outcome measures: Prevalence of written asthma action plans; night-time awakenings from asthma; ownership of peak flow meters; and people's perceptions of their asthma management. Results: The ownership of asthma action plans by people with self-reported asthma was 33% and has declined since 1995 (42%; P < 0.001). Fifteen per cent were wakened weekly or more frequently by asthma symptoms. These people were more likely to have a peak flow meter and a written action plan, but less likely to consider they had been provided with enough information about their asthma, to feel comfortable managing their asthma, or to find it easy to see their doctor. Having a written asthma action plan was associated with regular corticosteroid use, understanding asthma, having enough information and owning a peak flow meter. Conclusions: Ownership of asthma action plans in South Australia is suboptimal. Before we develop new strategies to improve asthma outcomes, we must determine whether there is a need to target people with less severe asthma and/or improve the use of guidelines by health professionals. Introduction The Australian and New Zealand Asthma Guidelines, developed in 1989, provide a list of objectives that would be desirable to achieve for every person with asthma,1 and studies of the use of asthma management plans have shown improved health outcomes for people with asthma.2-4 In Australia there is evidence that the promotion of asthma plan guidelines by the Thoracic Society of Australia and New Zealand and the National Asthma Campaign has led to increased uptake of plans.1 In South Australia the prevalence of adults with asthma reporting that they had a written action plan almost doubled between 1992 and 1995.5 However, there is evidence that asthma management is not ideal.6-8In one study in Victoria, 45% of people who died of their asthma had been assessed as having only a history of mild or moderate asthma.6 In another study in Victoria that examined the asthma knowledge of asthma patients, the median score obtained was less than 50%.7The effective implementation of asthma management plans in Australia to date has been seriously questioned by some investigators,8 and Bauman et al have concluded that the treatment and management of asthma is suboptimal.9 Our study aimed to provide representative population information on the ownership of written asthma action plans and the relationship to asthma morbidity and management factors. Methods Survey The data for this study were collected in the 1996 South Australian Health Omnibus Survey,10 a representative survey of people aged 15 years or older (n = 3010; response, 71%) . The survey was a multistage, systematic, clustered area sample of people who live in metropolitan Adelaide and major country centres with a population of over 1000. The survey was selected from a random sample of Australian Bureau of Statistics collector districts. Within each collector's district a random starting point was selected and from this point 10 households were selected using a fixed skip interval. Hotels, motels, hospitals, nursing homes and other institutions were excluded. The person whose birthday was next in each selected household was interviewed in their home by trained health interviewers. There was no replacement for non-respondents. Up to five call-backs were made in an attempt to interview the selected person. The data were weighted by age, sex, and geographic region to the estimated resident population data so that the analysis would be representative of the South Australian population. The part of the survey form dealing with asthma is shown in the Box. A person was classified as having current asthma if they answered yes to the first three questions. Social class was determined by referring to the gradation of occupational prestige given in the Australian Standard Classification of Occupations.11 An asthma action plan was defined as "written instructions of what to do if your asthma is out of control." Data analysis Possession of an asthma management plan and frequency of wakening at night with asthma were used as the two dependent variables for univariate analyses,12 which examined the associations between these variables and reported asthma management, knowledge and attitudes to management. Before conducting multiple logistic regression analyses, the explanatory variables were examined for collinearity or interactions. Stratified analyses were used to check homogeneity of associations across different levels of predictor variables. Smoking status and the information that people with asthma perceive they have for dealing with worsening asthma were found to interact, with an effect of these variables on worsening asthma. An interaction term for the two independent variables was included in the logistic regression analysis for frequency of wakening at night. This interaction term proved significant (P = 0.03), indicating the need to split the model and conduct separate logistic regression analyses of smokers and non-smokers. Therefore, we conducted three logistic regression analyses, using "asthma plan", "waken weekly-non-smokers" and "waken weekly-smokers" as the three response variables. All variables found to be significant at the univariate stage (ie, P = 0.25)13 were entered into each logistic regression. Insignificant variables were progressively omitted until satisfactory models were found that explained possession of an asthma plan and frequency of wakening at night. Results The prevalence of asthma was 11.6% (95% CI, 10.3%-12.9%). Of the 349 survey respondents with asthma, 33% (95% CI, 30.8%-35.2%) had a written asthma action plan and 15.2% (95% CI, 13.7%-15.7%) were awakened by asthma weekly or more frequently. Age, sex, migrant status, education level and socioeconomic status made no significant difference to the rate of possession of an asthma action plan or the rate of wakening with asthma weekly or more frequently. Variables significantly associated with ownership of an asthma action plan at the univariate level are shown in Table 1; those significantly associated with wakening with asthma at night are shown in Table 2. In the multivariate analysis (Table 3), the variables that best described those who had an asthma action plan were: using corticosteroids, understanding the effects of worsening asthma, having a peak flow meter, and believing they have enough information to deal with worsening asthma. The variables that best described non-smokers who waken weekly or more often were: having a peak flow meter, having an asthma action plan, not believing they have enough information to deal with worsening asthma, and not feeling comfortable taking care of their asthma. Only one variable -- not finding it easy or convenient to access their doctor about asthma -- explained wakening weekly or more often for smokers. Discussion The data obtained in this representative population study paint a bleak picture of the effectiveness of asthma management in Australia. As even people with mild asthma can die of the disease,6 every person with asthma may need an action plan. Yet, seven years after the promulgation of Australian guidelines on the implementation of asthma action plans,1 only 33% of people with diagnosed asthma had a written plan. The current level of plan ownership is significantly lower than the 42.1% (P < 0.001) reported 12 months earlier using the same survey methods.5 This may mean that vigilance regarding asthma management is declining. Our study has some limitations. We have no objective data to identify levels of asthma severity and asthma control in the respondents. The validity of the perception questions as repeatable measures has not been verified. Because we focused on ownership of written action plans, our study does not tell us whether patients are making appropriate use of these plans or of verbal instructions. In the multivariate analyses, only use of preventer medication, ownership of a peak flow meter and self-reported understanding of asthma were associated with plan ownership. This association could suggest that the more severe cases have better asthma management. Proof for this requires prospective measures (eg, lung function, medication doses) to assess the two critical factors of asthma severity and asthma control. Such knowledge could inform us of the potential need to target people with less severe asthma. People with asthma with nocturnal symptoms were more likely than those without nocturnal symptoms to report possession of a peak flow meter, and to have asthma action plans, but were less likely to consider they had been provided with enough information about their asthma (non-smokers) or to find it easy to see their doctor (smokers) (Table 2). Thus, although asthmatics with a higher level of morbidity are more likely to receive physical materials to assist in self-care, they continue to have greater unmet needs for general practitioner access and information about asthma self-management. What is the way forward? Randomised studies of the implementation of asthma plans show that good educational and skill objectives can be achieved.2,14-16 However, the complexity of the asthma management problem makes it impossible to provide for every contingency the patient might face in dealing with asthma. Asthma management decisions can be difficult, because the patient, the daily situation, the science base and the disease are constantly changing.2 The objectives of patient asthma management are the development of skills and positive attitudes to problem-solving, accompanied by sufficient knowledge to make sense of changing morbidity and symptoms. A controlled trial evaluation of a brief asthma education program (2.5 to 3 hours group work) demonstrated substantial changes in illness behaviour.2 These programs show that giving the patient the necessary skills cannot be achieved within the normal constraints of general practice. Randomised controlled trials of asthma clinics, where there is an emphasis on self-management, have demonstrated improvements in a range of morbidity and other health-related outcomes in a community-based setting.17 We must identify other ways of training the patient and focus the clinician on that part of the education program that can be managed in general practice. There is evidence that regular review improves asthma outcomes.18 It is pertinent to consider the possibility that inadequate use of guidelines by health professionals may be contributing to the fall in action plan ownership. Ways to improve use of guidelines need to include developments in information technology. Trostle has suggested that the inability of some people to comply with a treatment regimen is an unavoidable byproduct of collisions between the clinical world and other competing worlds of work, family, friends and recreation.19 Often, the process required to inform and empower the patient is more than an educational task. Some of the traditional models of patient education based on health beliefs or compliance frameworks have been seriously questioned.20,21 Patients have to fit their medical problems and medical regimens into the context of their daily lives. In doing so they will vary their compliance with advice and instructions to accommodate the social, psychological, economic and physical influences which are part of their lives.21 We need research that clearly articulates the complexity and variability of how asthma management fits into the context of individual patients' lives. The National Asthma Campaign has provided a guide for health professionals to assist with effective patient communication, which is a starting point for corrective strategies.22 We therefore know what optimal management of asthma is, but its attainment is elusive. Future strategies must be guided by studies defining asthma severity and asthma control, studies identifying factors that influence the use of guidelines by professionals, and studies elucidating the context of asthma management for the individual. References Woolcock A, Rubinfeld AR, Seale P, et al. Asthma management plan, 1989. Med J Aust 1989; 151: 650-653. Yoon R, McKenzie DK, Bauman A, Miles DA. Controlled trial evaluation of an asthma program for adults. Thorax 1993; 48: 1110-1116. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia. Med J Aust 1996; 164: 403-406. Beasley R, Cushley M, Holgate ST. A self-management plan in the treatment of adult asthma. Thorax 1989; 44: 200-204. Adams R, Ruffin R, Wakefield M, et al. Asthma prevalence, morbidity and management practices in South Australia, 1992-1995. Aust N Z J Med 1997; 27: 672-679. Robertson C, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a twelve-month survey. Med J Aust 1990; 152: 511-517. Rubinfeld AR, Dunt DR, McLure BG. Do patients understand asthma? A community survey of asthma knowledge. Med J Aust 1988; 149: 526-530. Bauman A, Young L, Peat JK, et al. Asthma under-recognition and under-treatment in an Australian community. Aust N Z J Med 1992; 22: 36-40. Bauman A, Mitchell CA, Henry RL, et al. Asthma morbidity in Australia: an epidemiological study. Med J Aust 1992; 156: 827-831. Wilson D, Wakefield M, Taylor A. The South Australian Health Omnibus Survey. Health Promotional J Aust 1992; 2: 47-49. Kelley JL, Evans MDR. Using ASCO for socio-economic analysis: assessment and conversion into status and prestige indices. Canberra: Research School of Social Sciences, Australian National University, 1988. SPSS for Windows. Release 8.0 [computer program]. Chicago, IL: SPSS Inc, 1998. Hosmer DW, Lemeshow S. Applied logistic regression. New York: John Wiley, 1989. Wilson-Pessano SR, McNabb WL. The role of patient education in the management of childhood asthma. Prev Med 1985; 14: 670-687. Clark NM, Feldman CH, Evans D, et al. Managing better: children, parents and asthma. Patient Educ Counsell 1986; 8: 27-38. D'Sousa WD, Crane J, Burgess C, et al. Community-based asthma care: trial of a "credit card" asthma self-management plan. Eur Respir J 1994; 7: 1260-1265. Lahdenso A, Haajtela T, Herrala J, et al. Randomised comparison of guided self-management and traditional treatment of asthma over one year. BMJ 1996; 312: 748-752. Asthma management handbook 1998. Melbourne: National Asthma Campaign, 1998. Trostle JA. Medical compliance as an ideology. Soc Sci Med 1988; 18: 1299-1308. Carter WB. Psychology and decision making: modelling health behaviour with multiattribute theory. J Dental Educ 1992, December: 800-807. Morris SL, Schulz RM. Medication compliance: the patients' perspective. Clin Ther 1993; 15: 593-606. Asthma adherence: a guide for health professionals. Melbourne: National Asthma Campaign, 1999. (Received 19 Apr, accepted 26 Aug, 1999) Authors' details The Queen Elizabeth Hospital, Adelaide, SA. Richard E Ruffin, FRACP, MD, Head, Division of Medicine, and Michell Professor of Medicine, University of Adelaide; Anne Marie Southcott, MB BS(Hons), FRACP, Acting Director, Respiratory Medicine; Brian Smith, PhD, FRACP, Director, Clinical Epidemiology and Health Outcomes Unit, and Senior Lecturer, University of Adelaide. Centre for Population Studies in Epidemiology, Department of Human Services, Adelaide, SA. David Wilson, PhD, MPH, Head. Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Robert J Adams, MB BS, FRACP, Research Fellow. Reprints: Professor R E Ruffin, Department of Medicine, University of Adelaide, The Queen Elizabeth Hospital Campus, 28 Woodville Road, Woodville, SA 5011. rruffinATmedicine.adelaide.edu.au Survey questions Have you ever had asthma? Was your asthma confirmed by a doctor? Do you still have asthma? If answer yes to these questions, then: Do you have an asthma action plan (written instructions of what to do if your asthma is out of control)? Do you have a home nebuliser for asthma treatment? Interviewer: if "yes" prompt "have you used it in the last 12 months?" What preventive (not reliever) medicine do you use regularly for your asthma? None - Intal - Becotide - Becloforte Pulmicort - Tilade - Other (specify) Which of the statements shown on this card do you feel are true of your preventer medication? Works by relieving narrowed breathing tubes quickly Needs to be used when you feel unwell Works by slowly reducing inflammation in the breathing tubes Must not have the dose changed Don't know How often do you awaken during the night with asthma? Nightly - Most nights - About twice a week - Weekly - Monthly - Less often than monthly Only at certain times of the year (ie seasonal) Never In the last 12 months have you had any hospital admissions for asthma where you stayed at least one night in hospital? In the last 12 months have you had any days lost from work, school or home duties from asthma? How many days would you estimate? What would you do if you had a bad attack of asthma and six puffs of your reliever (eg, ventolin, respolin) had not helped? Which of these statements shown on this card most closely matches what you would be likely to do? Wait another two hours and take more reliever medication Seek medical advice Take another six puffs of reliever medication and see what happens Call an ambulance Get someone to take you to hospital Do something else (specify) What feelings would you have if you had to get help for a bad attack of asthma? Which of the statements shown on this card most closely match how you would be feeling? You feel that you have failed You would feel embarrassed You do not want to bother others It is the right thing to do You know you will be OK because of past experience Something else (specify) I am now going to read out a number of statements and show you a card for each of them. Could you please tell me which number from 1 to 5 best reflects the way you feel. I am the sort of person who understands all about my asthma Always - Often - Sometimes - Rarely - Never - Don't know/other If I took care of my asthma myself, most of the time, I would . . . Manage well Manage sometimes Not manage at all Don't know/other If I were having a severe attack of asthma I would feel comfortable about going to a doctor or hospital Very comfortable Comfortable Don't mind Uncomfortable Not comfortable at all Don't know/other Going to see a doctor for help with my asthma is Easy and convenient Not easy nor convenient Don't know/other I have information to use (such as "Asthma Action Plan" or other instructions) to deal with worsening asthma. Yes, all I need Some No, none at all Don't know/other Other questions were asked about smoking status, educational level and migrant status. Back to text 1: Variables associated with ownership of an action plan*VariableSubjects (n = 349)%Odds ratioWrong about CS effect10332.01.0Correct about CS effect162†44.41.7 (0.98-2.94) P = 0.04Don't use CS regularly14721.81.0Use CS regularly20241.62.56 (1.54-4.26) P < 0.01No home nebuliser28229.11.0Have home nebuliser6750.72.51 (1.41-4.48) P < 0.01No peak flow meter29626.61.0Have peak flow meter5371.76.99 (3.50-14.14) P <0.01Don't always understand asthma8516.51.0Understand asthma26438.63.19 (1.65-6.27) P < 0.01Not enough information11715.51.0Enough information23255.56.77 (3.98-11.56) P <0.01Feel bad getting help4721.31.0Getting help OK30235.12.26 (1.04-4.90) P = 0.04No hospital admission within 12 months 33432.1 1.0Hospital admission1560.03.17 (1.00-10.32) P = 0.05No days lost from work/school30231.11.0Days lost from work/school4746.81.95 (1.00-3.79) P = 0.05CS = corticosteroids. * Variables tested but not found to be significant were: sex, age, migrant status, educational level, socioeconomic status, weight, access to doctor, uncomfortableness dealing with asthma, perception of dealing with asthma, comfortableness in going to hospital if required, exercise, smoking status, and smoking bans at home. †Only those who regularly used preventive medicine for their asthma (n = 265) were asked about its effects. Back to text 2: Variables associated with the likelihood of wakening with asthma on a weekly basis or more frequently*VariableSubjects (n = 349)%Odds ratioWrong about CS effect1038.71.0Correct about CS effect162†25.83.63(1.60-8.45) P < 0.01No home nebuliser28212.81.0Have home nebuliser6730.81.96 (0.96-3.95) P = 0.04No peak flow meter29612.81.0Have peak flow meter5330.83.02 (1.45-6.27) P < 0.01Not easy to see doctor6033.31.0Easy access to doctor28911.80.27 (0.13-0.53) P < 0.01Uncomfortable taking care of asthma 4836.2 1.0Comfortable taking care30112.30.25 (0.12-0.52) P < 0.01Perception of self-management good 3813.7 1.0Perception poor31129.42.62 (1.09-6.25) P = 0.0 3No days lost from work/school30213.61.0Days lost from work/school4727.72.42 (1.11-5.25) P = 0.02CS = Corticosteroids. * Variables tested but not found to be significant were: sex, age, migrant status, educational level, socioeconomic status, weight, regular use of corticosteroids, not always understanding asthma, not having enough information, feeling bad getting help, comfortableness in going to hospital if required, exercise, smoking status, smoking bans at home, and having an asthma action plan. †Only those who regularly used preventive medicine for their asthma (n = 265) were asked about its effects. Back to text 3: Logistic regression analyses of variables associated with ownership of an asthma management plan and frequency of wakening at night with asthma (n = 349)VariableOdds ratioAsthma planNo peak flow meter1.0Have peak flow meter4.32 (2.91-8.43)Don't always understand asthma 1.0Understand asthma2.01 (1.01-4.02)Not enough information1.0Enough information4.32 (2.11-8.85)Don't use corticosteroid regularly1.0Use corticosteroid regularly2.08 (1.21-3.58)Waken weekly (non-smokers)No peak flow meter1.0Have a peak flow meter7.32 (2.59-20.07)Not enough information1.0Enough information0.12 (0.04-0.39)Uncomfortable taking care of asthma1.0Comfortable taking care0.30 (0.14-0.77)No asthma action plan1.0Asthma action plan2.79 (1.09-7.15)Waken weekly (smokers)Not easy to see doctor1.0Easy to see doctor0.28 (0.10-0.79)All results significant, P < 0.05. Back to text

Richard E Ruffin · David Wilson · Brian Smith · Robert J Adams

Editorial Asthma in general practice: action plans or planned actions There's more than one way to implement effective asthma management in general practice Peter G Gibson MJA 1999; 171: 67 Good general practice is integral to effective asthma management. Asthma prevalence and hospitalisations are high, and, although we don't yet know how to reverse the rise in asthma prevalence, we know that severe exacerbations can be reduced by inhaled corticosteroid therapy and by effective education that involves an individualised, written action plan and regular medical review.1The burden of illness from asthma is concentrated in general practice, but studies of asthma education have mainly been conducted in hospitals. We need to transfer the improvements seen in these randomised trials to Australian general practice. Several approaches have been tried, including public health initiatives conducted by the National Asthma Campaign (NAC), practice audit,2,3 and nurse-run asthma clinics.4 In this issue of the Journal, Abdulwadud et al provide data showing just how different asthma can be in general practice to asthma in a specialist setting.5 Predictably, asthma is less severe in general practice.5 Medication use and understanding about asthma are similar, but fewer general practice patients have a written action plan and understand how to respond to an asthma emergency. Thus, for Australia, where inhaled corticosteroid use is already high, educational interventions in general practice should focus on the early management of exacerbations using written action plans and on smoking cessation. Also in this issue, Heard et al report their trial of a combined nurse educator/general practitioner asthma clinic.6 As part of the intervention, patients attending the asthma clinic received action plans and education about asthma. Patients in the control group also received action plans from their doctors, so that by the end of the study about 70% of patients had a written action plan and 80% were taking inhaled preventer medication. Asthma morbidity was reduced in both groups, and the asthma clinic did not prove to be any better than regular review of asthma by a general practitioner. Presumably outcomes in the control group improved because the participating general practitioners, who were caring for patients in both intervention and control groups, modified their behaviour by appropriately following proven guidelines. This problem is common in studies of asthma education, where blinding is seldom used and participation in the study is enough to improve management. Thus, this article compares asthma clinics to enhanced medical care, and a direct comparison with usual medical practice is lacking. What can we learn from this? Firstly, that the improvements in asthma mordibity that follow education and medical review can be achieved in general practice in Australia, and can be achieved in several ways. Regular review of asthma control and issuing an action plan by a general practitioner can be as effective as a special asthma clinic. General practitioners can now be confident that modifying their practice will improve asthma control. We know that this is needed, as surveys indicate that, although more people use action plans since the NAC, their use is still unacceptably low.7 General practitioners can choose between setting up an asthma clinic or implementing a structured program of regular review in their practices. The NAC and asthma liaison officers within the divisions of general practice are implementing suggested schemes at present. Regular review could turn into complacency, where a general practitioner feels that his or her current practice is satisfactory and that people with asthma are well managed. The best way to avoid this is to conduct regular quality control of asthma management. There are some simple interventions with asthma audit that do reap rewards for patients and doctors alike.2,3 Special asthma clinics also need to conduct regular quality control of their services, as when they provide asthma education without general practitioner consultations and action plans there is no benefit to patients.8 Structured asthma management programs, whether by systematic regular review or a special asthma clinic, will need to be adapted to the organisational structure of the practice. This can be done fairly simply in practices with several doctors. It is more difficult to do so in solo practices, but here it is even more important, as patients from small practices have a higher admission rate for asthma than those from larger practices.9 General practitioners need to adapt the National Asthma Campaign's six-point asthma management plan to their practices and ensure that all patients with asthma understand their disease, have a set of written instructions about when and how to treat exacerbations (all people with asthma are at risk of exacerbations), and are prescribed optimal therapy to control symptoms and exacerbations. Special asthma clinics or a system of regular education and review will suffice, provided that the processes and outcomes are monitored to ensure success. Organising the process of care for asthma in general practice and defining how to do it may be just as important as educating the doctor about what to do. Most general practitioners understand asthma management. Effective implementation is the issue. Peter G Gibson Staff Specialist, Respiratory Medicine John Hunter Hospital, Newcastle, NSW Gibson PG, Wilson AJ, Coughlan J, et al. The effects of self-management asthma education and regular practitioner review in adults with asthma. In: Cates C, DuCharme F, Gibson PG, et al. Airways module. Cochrane database of systematic reviews, issue 4. Oxford, UK: Update Software, 1998. Bryce FP, Neville RG, Crombie IK, et al. Controlled trial of an audit facilitator in diagnosis and treatment of childhood asthma in general practice. BMJ 1995; 310: 838-842. Feder G, Griffiths C, Highton C, et al. Do clinical guidelines introduced with practice based education improve care of asthmatic and diabetic patients? A randomised controlled trial in general practices in east London. BMJ 1995; 311: 1473-1478. Charlton I, Charlton G, Bloomfield J, et al. Audit of the effect of a nurse-run asthma clinic on workload and patient morbidity in general practice. Br J Gen Pract 1991; 41: 227-231. Abdulwadud OA, Abramson MJ, Light L, et al. Comparison of patients with asthma managed in general practice and in a hospital clinic. Med J Aust 1999; 171: 72-75. Heard AR, Richards IJ, Alpers JH, et al. Randomised controlled trial of general practice based asthma clinics. Med J Aust 1999; 171: 68-71. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Premaratne UN, Sterne JAC, Marks GB, et al. Clustered randomised trial of an intervention to improve the management of asthma: Greenwich asthma study. BMJ 1999; 318: 1251-1255. Griffiths C, Sturdy P, Naish J, et al. Hospital admissions for asthma in East London: associations with characteristics of local general practices, prescribing, and population. BMJ 1997; 314: 482-486.

Peter G Gibson

Research Comparison of patients with asthma managed in general practice and in a hospital clinic Omar A Abdulwadud, Michael J Abramson, Larry Light, Francis C K Thien and E Haydn Walters MJA 1999; 171: 72-75 See also Heard et al & Gibson Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Respiratory medicine Abstract Objectives: To compare knowledge and attitudes about asthma, self-management skills and impact of asthma on quality of life between patients managed in general practice (GP) and in a hospital clinic. Design: Cross-sectional survey with six months' follow-up. Patients and setting: 105 adults with asthma: 61 from the Alfred Hospital Asthma and Allergy Clinic, Melbourne, and 44 from nearby general practices, in 1994-1995. Main outcome measures: Patient sociodemographic and clinical characteristics; patient knowledge, attitudes and beliefs about asthma; self-management skills; and impact of asthma on quality of life. Results: GP patients were more educated (P = 0.04) and more likely to smoke (P = 0.04) and to have mild asthma (P = 0.04) than hospital patients; they were less likely to use theophylline (P = 0.006) and to have exercise limitation (P = 0.03), and had fewer previous hospital admissions (P = 0.01). Impact of asthma on quality of life was greater in the hospital group than in the GP group. At baseline, the GP group were less likely to have written asthma action plans (P = 0.018), and were less able to manage rapid onset attacks than the hospital group (P = 0.02). More subjects in the hospital group than the GP group felt their asthma was severe (P = 0.02) and were optimistic about their asthma improving (P = 0.03). GP patients increased their knowledge about asthma significantly (P = 0.002) over six months. Conclusions: Patients with asthma managed in general practice and in hospital differ in clinical parameters, quality of life and attitudes to asthma. Future educational initiatives should take such differences into account. Introduction Asthma is the third most common reason for consultations with general practitioners (GPs) in Australia,1 but is both under-recognised and undertreated.2 The finding that GPs were the usual source of routine asthma treatment for 89% of the people who died of asthma3 demonstrates that GPs have the primary management role even in severe asthma.4To guide both doctors and patients, in 1989 the Thoracic Society of Australia and New Zealand developed the "six-point" Australian Asthma Management Plan (AMP).5 This was adopted by the National Asthma Campaign (NAC) at its inception in 1990. While the Royal Australian College of General Practitioners is a partner in the NAC, the plan was originally drawn up by hospital-based specialists. There is concern among GPs that they do not have sufficient time and knowledge to devise action plans and counsel patients about asthma management,4 as suggested in the AMP. The effectiveness of patient education about asthma as proposed in the AMP has not been widely evaluated in general practice. Only one such study has been reported,6 and only one nationwide survey of selected GPs was conducted before the launch of the NAC intervention.7 We aimed to examine patient knowledge about asthma and its management, self-management skills, impact of asthma on quality of life, and attitudes to asthma. We compared these between patients managed in general practice and in a hospital clinic over a six-month period that coincided with widespread advertising and dissemination of the AMP. Methods Design and setting The study was a cross-sectional survey with six months' longitudinal follow-up during 1994-1995. There was no intervention, and patients received their usual care from their GPs or hospital specialists. The study was conducted at the Alfred Hospital Asthma and Allergy Clinic, Melbourne, Victoria, and at 13 general practices near the hospital. Fourteen GPs were recruited by a practising GP (L L). The study was approved by the Ethics Review Committee at the Alfred Hospital. Subjects Consecutive patients being seen for asthma at the participating general practices were nominated by their GPs. Of 54 patients invited to participate, 44 were recruited (nine refused or did not respond and one died). Sixty-one patients were recruited from the Alfred Clinic. Inclusion and exclusion criteria were reported previously.8 All patients gave written informed consent. Diagnosis of asthma was based on American Thoracic Society criteria.9 Assessments Clinical and demographic characteristics of patients were determined by questionnaire. The term "priority asthmatic" was given to asthmatics who had severe and precipitately acute attacks of asthma; they had usually (but not necessarily) been admitted to an intensive care unit. Forced expiratory volume in 1 second (FEV1) was obtained from the records of the lung function laboratory, and predicted FEV1 at baseline was calculated for males and females separately, as suggested by Gibson et al.10 The mean daily peak expiratory flow (PEF) variability was estimated from patient diaries.5 Severity of asthma was classified as mild, moderate or severe based on medication use, as reported previously.8 Medication was grouped into generic categories. Outcome measures Patients completed the Asthma General Knowledge,11 Quality of Life,12 Self-Management Skills,13 and Attitudes and Beliefs14 questionnaires on entry and six months later. Selection of these outcomes was based on the asthma education targets and outcome measures proposed by the National Asthma Campaign.15 Statistical analysis Data were analysed with the SAS for Windows statistical package.16 Categorical variables were summarised as percentages, and associations were tested in contingency tables by χ2 tests. For continuous variables that were normally distributed, differences in mean scores were assessed by Student's t test. For continuous variables that were not normally distributed, the Wilcoxon signed rank and rank sum tests were used. Results Participation Follow-up questionnaires were returned by 39 of the 44 (87%) GP patients (with five of those with the most severe asthma lost to follow-up) and by 47 of the 61 (77%) hospital patients (with the remaining 14 either lost to follow-up or not responding). Subject characteristics Characteristics of the two patient groups are shown in Box 1. They were similar in age and sociodemographic characteristics, including occupation (data not shown), except that the GP group had a significantly higher proportion of tertiary-educated people and of current smokers than the hospital group. GP patients had less exercise limitation and milder asthma than the hospital patients, and were less likely to have been admitted to hospital and to have priority asthma. There was no significant difference in lung function or other clinical parameters (data not shown). GP patients were significantly less likely to use theophylline and to have a written asthma action plan than hospital patients. Proportions using β-agonists, anticholinergics, and inhaled or oral steroids and owning peak flow meters were not significantly different in the two groups. Asthma outcome measures Asthma knowledge: Asthma General Knowledge scores did not differ significantly between the GP and hospital groups either at baseline (means, 20.2 and 20.5 out of 31, respectively) or six months later. Scores increased in both groups over the six months, but the increase was significant only in the GP group (P = 0.002), which had a mean score increase of 1.66 (95% confidence interval [CI], 0.58 to 2.76) compared with 0.83 (95% CI, 20.39 to 2.03) in the hospital group. Quality of life: Scores for impact of asthma on quality of life are shown in Box 2. Impact at baseline was significantly greater in the hospital group than in the GP group for total quality of life and the subcategories of breathlessness, social disruption, and concern for health, but not mood disturbance. After six months, impact had significantly decreased in the hospital group for all these parameters except mood disturbance, but there was no significant change in the GP group. Despite the significant decrease in the hospital group, impact was still significantly greater than in the GP group for total quality of life (P = 0.03), social disruption (P = 0.008) and concern for health (P = 0.04). None of the improvements in quality of life differed significantly between the two groups over six months. Self-management skills: At baseline, the hospital group had a significantly higher median score for knowledge about self-management of a rapid onset asthma attack than the GP group (P = 0.02), but the two groups had similar scores for a slow onset attack (Box 3). After six months, the hospital group had significantly improved its slow onset scenario score (P = 0.02), but the GP group had not. Overall, there was no difference in the median change over six months in scores for either scenario between the two groups. Attitudes and beliefs about asthma: Patients' attitudes and beliefs about their asthma are shown in Box 4. At baseline, hospital patients were significantly more likely than GP patients to believe that their asthma was severe, but also that it would improve in the future. After six months, hospital patients were significantly less optimistic (P = 0.03), and the difference in this parameter between the two groups was no longer significant. The proportion of patients who said they could do everything they wanted regardless of the effect it might have on their asthma did not differ significantly between the two groups at baseline, but at follow-up hospital patients were significantly less likely to say this than GP patients. More hospital than GP patients wished their doctor would talk more to them about their asthma at both baseline and six-month follow-up, but the difference was significant only at follow-up. Concomitantly, fewer hospital patients than GP patients felt that their doctor had told them everything they wanted to know about their asthma; the difference was significant at both baseline and follow-up. Discussion We found that our samples of GP and hospital patients with asthma differed in sociodemographic and clinical parameters, quality of life, self-management skills and attitudes and knowledge about asthma. Some of our findings about the GP sample were more positive than reported previously. Use of inhaled steroids was significantly higher than found in random community samples,17,18 possibly because our sample of GP patients had more severe asthma, or because of industry promotion of these drugs.18 It is also possible that this form of treatment has become more acceptable in our group of GPs, many of whom had a particular interest in asthma. Use of peak flow meters and prevalence of written action plans in the GP patients were also higher than previously reported,17,18 but, once again, this finding may be confounded by the group of GPs studied. Actual prevalence of peak flow meter use and written action plans may be substantially lower in more typical general practices. There was some evidence from our study that implementation of the AMP may have improved, especially in general practice, over the period of our study. However, despite NAC recommendations, half of the hospital patients and three-quarters of the GP patients had no written asthma action plans; and about a third of the hospital patients and half of the GP patients did not have access to a peak flow meter. While our study sheds no light on the reasons for these findings, it demonstrates that there was room for improvement in asthma management in both settings, but particularly in general practice. Asthma knowledge among the GP patients was similar to that among the hospital patients at baseline, but improved more over the six months to follow-up. This was possibly due to the GP patients' higher educational level, our interaction with them during the study or better than average care from their doctors. As doctors had recruited the patients to the study, they may have put more effort into educating them before follow-up, although we have no evidence for this. The absence of any significant improvement in quality of life among the GP patients after six months suggests that insufficient attention may be given to this aspect of asthma. Furthermore, the potential selection bias towards milder disease and the loss to follow-up of five of those with more severe asthma from the GP group may have biased the results away from detecting improvement. Overall, the general practice group had better quality of life than the hospital group. This would be expected, as the GP group had milder disease with fewer hospital admissions. It is surprising that mood disturbance was the only category which did not differ between the two groups at baseline. Possibly moods such as sadness, depression and frustration are similar in all patients regardless of the severity of asthma. At baseline, the GP group was less able to manage the rapid onset attack, perhaps because they were likely to have experienced fewer such attacks. The hospital group improved their ability to manage slow onset attacks significantly over six months. Maybe their doctors educated them informally, although they did not have access to the results of the questionnaires. Alternatively, participants may have improved their answers with practice, but as this did not happen in the GP group it is unlikely. There was little difference in attitudes and beliefs about asthma between groups. However, at six months, the hospital group was significantly less optimistic about their asthma improving in the future than the GP group. This could result from the difference in asthma severity between the two groups, which resulted in hospital patients having a more realistic appreciation of their poor prognosis after education. At six months, more of the hospital patients than GP patients also wished that their doctors would tell them more about their asthma. Perhaps this reflects a low level of communication between doctors and patients in the hospital asthma clinic compared with general practice and requires further study. This study has some limitations. The GP patients may not be representative of the total general practice population, and recruiting interested GPs may have biased results. In the absence of any viable alternative strategy, evaluation focused on patients rather than GPs. Despite potential sampling and selection biases, the results highlight the impact of patient education among patients attending general practices and the differences between GP and hospital patients. Future educational initiatives should take such differences into account. The type and scope of patient education in general practice and hospitals should be thoroughly evaluated to identify areas in which GPs and specialists could be trained and supported more effectively. Continued dissemination and implementation of the Australian AMP is required to improve the self-management skills of patients in general practice. Acknowledgements We acknowledge a public health postgraduate research scholarship from the National Health and Medical Research Council. Dr Andrew Forbes, Jan Driver and Michael Bailey provided statistical support. We are grateful to the general practitioners who participated in the study. Drs Guy Marks, Rae Allen and Bonnie Sibbald gave permission to use their questionnaires. Dr John Kolbe gave permission to use his scoring system for the asthma attack scenarios. References Bridges-Webb C, Britt H, Miles DA, et al. Morbidity and treatment in general practices in Australia 1990-1991. Med J Aust 1992; 157 Suppl: 1-56. Tse M, Cooper C, Bridges-Webb C, Bauman A. Asthma in general practice. Opportunities for recognition and management. Aust Fam Phys 1993; 22: 736-741. Robertson CF, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a 12 month survey. Med J Aust 1990; 152: 511-517. Antic R. Asthma in Australia: the current understanding. Overview of a national series of interactive meetings for general practitioners. Sydney: Excerpta Medica, 1993. Woolcock A, Rubinfeld AR, Seale JP, et al. Asthma management plan, 1989. Med J Aust 1989; 151: 650-653. Byrne DM, Drury J, Mackay RC, et al. Evaluation of the efficacy of an instructional program in the self-management of patients with asthma. J Adv Nursing 1993; 18: 637-646. Tse M, Bauman A, Bridges-Webb C. Asthma management in general practice. Aust Fam Phys 1991; 20: 1085-1092. Abdulwadud O, Abramson M, Forbes A, et al. Evaluation of a randomized controlled trial of adult asthma education in a hospital setting. Thorax 1999; 54: 493-500. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthma. Am Rev Respir Dis 1987; 136: 225-244. Gibson J, Gallagher H, Johansen A, Webster I. Lung function in an Australian population: spirometric standards for non-smoking adults. Med J Aust 1979; 1: 292-295. Allen RM, Jones MP. The validity and reliability of an asthma knowledge questionnaire used in the evaluation of a group asthma education self-management program for adults with asthma. J Asthma 1998; 35: 537-545. Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol 1992; 45: 461-472. Sibbald B. Patient self care in acute asthma. Thorax 1989; 44: 97-101. Sibbald B, Collier J, D'Souza M. Questionnaire assessment of patients' attitudes and beliefs about asthma. Fam Pract 1986; 3: 37-40. National Asthma Campaign (NAC) National Asthma Strategy. Goals and targets. Melbourne: National Asthma Campaign, 1994. SAS Institute Inc. SAS language guide for personal computers, the SAS system for Microsoft Windows. Release 6.10. Cary, NC: SAS Institute Inc, 1994. 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. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. (Received 28 Sep 1998, accepted 7 Jun 1999) Authors' details Department of Epidemiology and Preventive Medicine, Monash Medical School, The Alfred Hospital, Melbourne, VIC. Omar A Abdulwadud, PhD, Postdoctoral Fellow; Michael J Abramson, PhD, FRACP, Associate Professor. Department of Allergy and Clinical Immunology, Monash Medical School, The Alfred Hospital, Melbourne, VIC. Larry Light, MB BS, Clinical Assistant; Francis C K Thien, MD, FRACP, Staff Physician. Department of Respiratory Medicine, Monash Medical School, The Alfred Hospital, Melbourne, VIC. E Haydn Walters, DM, FRACP, Professor, and Director of Respiratory Medicine. Reprints: Associate Professor M J Abramson, Department of Epidemiology and Preventive Medicine, Monash Medical School, The Alfred Hospital, Prahran, VIC 3181. Email: Michael. AbramsonATmed.monash.edu.au Back to textBack to textBack to text Back to text

Omar A Abdulwadud · Michael J Abramson · Larry Light

Alternative Medicine Buteyko breathing techniques in asthma: a blinded randomised controlled trial Simon D Bowler, Amanda Green and Charles A Mitchell MJA 1998; 169: 575-578 For editorial comment see Hensley & Gibson Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Respiratory medicine Abstract Objective: To evaluate the effect of Buteyko breathing techniques (BBT) in the management of asthma. Design: Prospective, blinded, randomised study comparing the effect of BBT with control classes in 39 subjects with asthma. The study was conducted from January 1995 to April 1995. Participants and setting: Subjects recruited from the community, aged 12 to 70 years, with asthma and substantial medication use. Main outcome measures: Medication use; morning peak expiratory flow (PEF); forced expiratory volume in one second (FEV1); end-tidal (ET) CO2; resting minute volume (MV); and quality of life (QOL) score, measured at three months. Results: No change in daily PEF or FEV1 was noted in either group. At three months, the BBT group had a median reduction in daily beta2-agonist dose of 904 µg (range, 29 µg to 3129 µg), whereas the control group had a median reduction of 57 µg (range, - 2343 µg to 1143 µg) (P = 0.002). Daily inhaled steroid dose fell 49% (range, - 100% to 150%) for the BBT group and 0 (range, - 82% to +100%) for the control group (P = 0.06). A trend towards greater improvement in QOL score was noted for BBT subjects (P = 0.09). Initial MV was high and similar in both groups; by three months, MV was lower in the BBT group than in the control group (P = 0.004). ET CO2 was low in both groups and did not change with treatment. Conclusion: Those practising BBT reduced hyperventilation and their use of beta2-agonists. A trend toward reduced inhaled steroid use and better quality of life was observed in these patients without objective changes in measures of airway calibre. Introduction Proponents of Buteyko breathing techniques (BBT) suggest that hyperventilation resulting in alveolar and airway hypocapnia is a major contributor to the pathophysiology of asthma.1 Advocates claim that exercises designed to reduce minute volume lead to improvements in asthma control and allow reduction of medication.1 To our knowledge, no formal study of the techniques has been reported in accessible publications. Aside from considerations of hyperventilation, a variety of breathing and relaxation techniques have been advocated for the complementary control of asthma. These include yoga,2,3 diaphragmatic breathing4 and progressive muscle relaxation.5 Although varying claims of efficacy have been made, no technique has been adopted by mainstream medical practice. We undertook a blinded, prospective, controlled, randomised study in people with asthma, in which we compared BBT with a placebo breathing technique, and measured lung function, medication use and quality of life. Methods Participants Subjects aged 12 to 70 years were recruited following a publicity campaign about breathing techniques in asthma by the Asthma Foundation of Queensland. People telephoning the Foundation enquiring about BBT were referred to the investigators. Individuals were accepted if they reported a history of asthma (variable difficulty in breathing, wheeze or chest tightness with response to beta2-agonist) and were taking substantial doses of asthma medication. To match the BBT and control groups for symptomatic asthma severity, trial participants were stratified by whether they were taking more or less than 5000 µg of salbutamol or equivalent a day, and were randomly allocated to treatment groups on the basis of a sealed envelope prepared by a clerical staff member not involved in the study. Trial participants, investigators and attending staff were blinded to which group randomisation had occurred; the term Buteyko was not used at any time by either control or BBT instructors. Subjects were excluded if there had been a change in inhaled steroid dose or use of oral steroids within the four-week run-in period, if there were other significant unstable medical conditions, or if they had undertaken BBT previously. Subjects were randomised if they were using at least 1400 µg of short acting beta2-agonist or equivalent doses of nebulised or long acting beta2-agonist in the last week of the run-in period. Nebulised beta2-agonist was considered one-fifth as effective as a dose delivered by metered dose inhaler.6 Standard doses of terbutaline and salbutamol were considered equipotent. Two doses of salmeterol (25 µg) via metered dose inhaler twice a day (100 µg/day) was considered equivalent to 200 µg of a short acting beta2-agonist every four hours (1200 µg/day).7 Intervention Trial participants underwent training simultaneously in two separate groups. Teaching occurred over seven days; each session lasted 60-90 minutes. BBT was taught by a representative of Buteyko Australia. Buteyko training consisted of the teaching of a series of exercises in which subjects reduced the depth and frequency of respiration. Breath holding exercises measured the impact of this training and gauged progress. Participants were encouraged to practise these exercises several times a day. The BBT instructor made follow-up phone calls to participants as she considered necessary, and people experiencing difficulty with the technique were given extra breathing classes, in accordance with standard Buteyko practices. In the control group, subjects were given general asthma education and relaxation techniques, and were taught abdominal breathing exercises which did not involve hypoventilation. The control group instructor made one follow-up phone call to each participant. In both groups subjects were directed to use beta2-agonists only when symptomatic. Subsequently, we telephoned the participants from both groups fortnightly and reiterated the beta2-agonist advice. Subjects were advised to reduce long acting bronchodilator dose only when short acting therapy was used once a day or less. At clinic review, six weeks after tuition, subjects using one dose a day or less of short acting beta2-agonists were directed to reduce their inhaled steroid dose. Further review and, where possible, inhaled steroid reduction was undertaken every two weeks by telephone. The study design is summarised in Figure 1, below. Outcome measures Patients kept diary cards at home for scoring symptoms (0 = no symptoms, 3 = maximal symptoms) and recording daily peak expiratory flow (PEF) and medication use. At clinic visits at the end of the run-in period and three months later, flow volume loops were recorded before and after administration of bronchodilator, and patients completed a self-administered quality of life questionnaire.8,9 The questionnaire measured the effect of asthma on quality of life across four domains: breathing, mood, social interaction and concerns for the future. At each clinic visit, indices of resting ventilation were measured. Subjects were told these techniques were to "assess breathing patterns" and were asked to "breathe normally". End-tidal (ET) CO2 (as a surrogate for arterial CO2) was recorded using continuously sampled nasal expired air, aspirated by nasal cannula and analysed using infra-red absorption (POET, Sensormedics, Wawkesha, USA). Minute volume (MV) was recorded with a 5 L water-sealed spirometer with a CO2 absorber using a mouthpiece and noseclip (Gould 2400, Sensormedics, Yoba Linda, USA). Twenty non-smoking healthy subjects age and sex matched with subjects with no history of upper or lower respiratory tract disease or other illness were recruited from hospital staff to provide comparative data for ET CO2 and MV. Statistical analysis Data were analysed using Statview.10 Paired data were compared using paired t test for normally distributed data, and Wilcoxon signed-rank test for non-parametric data. For unpaired data, unpaired t tests and Mann-Whitney U tests were used for parametric and non-parametric data, respectively. For non-parametric data Spearman's rank was used to investigate correlation. Data are expressed as median (range), or mean ± standard deviation. Ethical approval The Mater Adult Hospitals Ethics Committee approved the protocol, and informed consent was obtained from all subjects. Results Participants One hundred and seventy patients were screened for the study. Most proved either not to have asthma or to have unstable asthma as described above. Thirty-nine patients were randomised, 20 to the control group and 19 to the BBT group. No significant differences existed between the groups (Box). One person from each group was lost to follow-up after the intervention. Twenty normal subjects (10 women) were recruited; their median age was 43 years (range, 25-68). Follow-up calls BBT subjects each received a mean of seven (range, 0-20) follow-up telephone calls from the instructor, and extra classes were scheduled for seven BBT subjects who had difficulty with the technique. Indices of airway function There was no difference between the groups in measures of airway function. Morning pre-bronchodilator PEF was similar at both run-in (BBT, 385 ± 90 L/min; control, 375 ± 117 L/min; P = 0.3) and at three months (BBT, 374 ± 115 L/min; control, 383 ± 103 L/min; P = 0.6). Pre-bronchodilator percentage predicted FEV1 was also no different at run-in (BBT, 75% ± 17%; control, 73% ± 19%; P = 0.4) and at three months (BBT, 72% ± 22%; control, 72% ± 15%; P = 0.4). Indices of resting ventilation End-tidal CO2: No significant difference in mean ET CO2 existed between BBT and control groups either at run-in (BBT, 33 ± 5 mmHg; control, 32 ± 4 mmHg) or at three months (BBT, 35 ± 3 mmHg; control, 33 ± 3 mmHg). The normal subjects had significantly higher mean ET CO2 levels (41 ± 4 mmHg) than both the BBT and the control groups (Figure 2a). Minute volume: The normal subjects recorded a mean MV of 11.9 ± 0.8 L/min. Despite a trend (Figure 2b), there was no significant difference between these subjects and the BBT and control groups either at run-in (BBT, 14.0 ± 6.5 L/min; control, 14.2 ± 4.9 L/min) or at three months (BBT, 9.6 ± 3.1 L/min; control, 13.3 ± 4.0 L/min). At three months the mean MV for the BBT group was significantly less than for the control group (P = 0.004). The relative reduction in beta2-agonist use in the BBT group was related to the proportionate reduction in minute volume (r = 0.51; P = 0.04) Medication use Three months after intervention, there was a significant difference in beta2-agonist use between the BBT group and the control group (P = 0.005). The BBT group had a median reduction in daily adjusted beta2-agonist dose of 904 µg (range, 29 µg to 3129 µg) and the control group had a median reduction of 57 µg (range, - 2343 µg to 1143 µg) (P = 0.002) (Figure 3a). Despite a trend in inhaled steroid use (Figure 3b), there was no significant difference between the groups in absolute daily doses or change in dose at any time. The median reduction in daily dose at the third month, compared with run-in, was 49% (range, - 100% to + 83%) for BBT subjects and 0 (range, - 82% to + 100%) for control subjects (P = 0.06). Serious adverse events During the study, three subjects from each group were admitted to hospital for exacerbations of asthma. Apart from these, six BBT and seven control subjects received short courses of prednisone at some stage during the eight months after intervention. Quality of life No significant difference existed between the mean quality of life score of the two groups at any stage (Figure 4). At three months, there was a trend towards greater improvement in the BBT group: median improvement of 1.2 units (range, 5.2 to - 1.6) in the BBT group compared with 0.4 units (range, 3.4 to - 2.9) in the control group (P = 0.09). These changes were spread fairly evenly across all four domains. Discussion In this largely self-selected cohort of asthma sufferers with high medication use, those randomised to BBT lowered their minute volume, reduced beta2-agonist use, and demonstrated a trend towards lower inhaled steroid doses and greater improvement in quality of life than did those randomised to a control breathing program. No change in lung function was noted. To minimise the effect of environmental influences and to maintain blinding, BBT and control group classes ran simultaneously. This posed logistic problems not often encountered in asthma intervention studies, where subjects are usually enrolled sequentially over a substantial period of time, giving an opportunity to adjust treatment. The need to complete randomisation for all subjects before the interventions precluded comprehensive pre-study medication optimisation. Conventional teaching argues that hyperventilation and hypocapnia are the result rather than the cause of airway narrowing in asthma. Thus, increases in ventilation are seen in normal subjects with methacholine-induced bronchoconstriction.11 On the other hand, hyperventilation may cause bronchoconstriction.12,13 Gardner suggests that asthma and hyperventilation may interact through a process in which symptoms due to asthma and the consequent induced hyperventilation result in anxiety and further increases in minute volume.14 We could not show any change in ET CO2 in either BBT or control subjects; for both groups, ET CO2 remained significantly below that of normal individuals. MV was high (accepting a mean predicted resting MV of 5 L/min) in both BBT and control groups, and to a lesser (although statistically similar) extent in the normal subjects. Perhaps this may be explained in part by the use of a water-sealed spirometer, mouthpiece and noseclip, which have been shown to elevate tidal volume and respiratory rate.15 MV declined in the BBT group. Because MV and ET CO2 were measured at different times and on different devices, no direct correlation of MV and ET CO2 is possible. What alternative explanations are there for the observed improvements with BBT? Both groups were contacted fortnightly by the research team. In addition, some of the BBT subjects who were experiencing difficulties with the technique were contacted frequently by the Buteyko therapist. We did not anticipate this contact, which leaves the study open to the criticism that the BBT group were influenced in ways the control group were not. The study clearly would have been stronger with matched, controlled phone contact between both BBT and control practitioners and subjects. BBT might also have altered subjects' perceptions of asthma severity without affecting the underlying disease. This could account for the reduction in medication use and trends toward improvements in quality of life, and is consistent with the absence of any change in objective measures of airway calibre. On the other hand, the reduction in medication use in the BBT group did not lead to a decline in lung function, and rates of oral steroid use and hospital admission were similar in each group. Reduction in beta2-agonist use itself might have led to an improvement in asthma control. There are suggestions that excess beta2-agonist use may adversely affect asthma control.16 To our knowledge, no study has suggested the converse, that reduction in beta2-agonist use may improve asthma control. In conclusion, we found that those practising BBT reduced hyperventilation and their use of beta2-agonists. A trend toward reduced inhaled steroid use and better quality of life was observed in these patients without changes in objective measures of airway calibre. Acknowledgements A grant from the Australian Association of Asthma Foundations and assistance from Buteyko Australia supported the study. Ms Tess Graham of Buteyko Australia conducted the Buteyko breathing classes and reviewed the manuscript. Ms Jeanette Martin undertook the control group classes. The technical assistance of Mr Andrew Coates; the administrative help of Mr John Laing; and the assistance of the staff of the Asthma Foundation of Queensland are gratefully acknowledged. References Stalmatski A. Freedom from asthma: Buteyko's revolutionary treatment. Hale Clinic Health Library. London: KyleCathie Ltd, 1997; 175. Singh V, Wisniewski A, Britton J, Tattersfield A. Effects of yoga breathing exercises (pranayama) on airway reactivity in subjects with asthma. Lancet 1990; 335: 1381-1383. Jain SC, Talukdar B. Evaluation of yoga therapy programme for patients of bronchial asthma. Singapore Med J 1993; 34: 306-308. Girodo M, Ekstrand KA, Metivier GJ. Deep diaphragmatic breathing: rehabilitation exercises for the asthmatic patient. Arch Phys Med Rehabil 1992; 73: 717-720. Renfroe KL. Effects of progressive relaxation on dyspnea and state anxiety in patients with chronic obstructive pulmonary disease. Heart Lung 1988; 17: 408-413. Gibson PG, Wlodarczyk JH, Borgas T. Drug delivery in asthma: a comparison of spacers with a jet nebuliser. Aust N Z J Med 1995; 25: 324-329. Smyth ET, Pavord ID, Wong CS, et al. Interaction and dose equivalence of salbutamol and salmeterol in patients with asthma. BMJ 1993; 306: 543-545. Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol 1992; 45: 461-472. Marks GB, Dunn SM, Woolcock AJ. An evaluation of an asthma quality of life questionnaire as a measure of change in adults with asthma. J Clin Epidemiol 1993; 46: 1103-1111. Statview [computer program]. Version 4.1. Cary, North Carolina: SAS Institute, 1995. Chadha TS, Schneider AW, Birch S, et al. Breathing pattern during induced bronchoconstriction. J Appl Physiol 1984; 56: 1053-1059. Gayrard P, Orehek J, Grimaud C, Charpin J. Bronchoconstrictor effects of a deep inspiration in patients with asthma. Am Rev Respir Dis 1975; 111: 433-439. Van den Elshout FJ, van Herwaarden CL, Folgering HTM. Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects. Thorax 1991; 46: 28-32. Gardner WN. The pathophysiology of hyperventilation disorders. Chest 1996; 109: 516-534. Gilbert R, Auchincloss JH Jr, Brodsky J, Boden W. Changes in tidal volume, frequency, and ventilation induced by their measurement. J Appl Physiol 1972; 33: 252-254. Taylor DR, Sears MR, Herbison GP, et al. Regular inhaled beta agonists in asthma: effects on exacerbations and lung function. Thorax 1993; 48: 134-138. (Received 11 Aug 1997, accepted 18 Aug 1998) Authors' details Mater Adult Hospital, South Brisbane, QLD. Simon D Bowler, FRACP, Thoracic Physician. Brompton Hospital, South Kensington, London, UK. Amanda Green, GradDipPhys, Physiotherapist. Department of Medicine, University of Queensland, Princess Alexandra Hospital, Woolloongabba, QLD. Charles A Mitchell, FRACP, Associate Professor. Reprints: Dr S D Bowler, Director, Respiratory Medicine, Mater Adult Hospital, South Brisbane, QLD 4101. Email: sbowlerATmater.org.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Simon D Bowler · Amanda Green · Charles A Mitchell

Alternative Medicine Chinese herbal medicines in the treatment of acute respiratory infections: a review of randomised and controlled clinical trials Chaoying Liu and Robert M Douglas MJA 1998; 169: 579-582 For editorial comment see Hensley & Gibson Abstract - Introduction - Methods - Results - Discussion - References - Authors' details Make a comment - - - More articles on Complementary medicine Abstract Objective: To review clinical trials of Chinese herbal medicines (CHMs) in the management of acute respiratory infections (ARIs). Data sources: MEDLINE, the Cumulative Index to Nursing and Allied Health Literature, the Cochrane Library and three Chinese medical journals available in Australia. Study selection: Studies in which a control group was used in comparing CHMs with a placebo or "Western medicine" (usually antibiotics) for treating ARIs were included. Data synthesis: 27 of 46 studies identified in the search of the databases and the Chinese journals fulfilled the inclusion criteria. Twenty-six of these were published in Chinese, and one in English. Twenty were randomised controlled trials and seven were "controlled clinical trials". Although most of the studies reported that CHMs are better than antibiotics for the treatment of ARIs, the quality of the studies was generally poor when evaluated for patient allocation, treatment description, outcome measurement and data analysis. Conclusions: Because the trial methodology of these studies was often inadequate or insufficiently documented, it is difficult to recommend the use of CHMs in ARIs. However, Shuang Huang Lian does appear to be useful for treating lower respiratory tract infections. More rigorous evaluation of CHMs is needed, as they are becoming popular treatments in many countries, including Australia. Introduction Acute respiratory infection (ARI) is the most common illness in childhood and is the leading cause of death in children younger than five years.1,2 In Western medicine, although ARIs are most commonly caused by viral infection, antibiotic agents are widely used in their treatment, despite evidence that the clinical benefits of antibiotics may be slight.3-5 In China, many physicians believe that traditional agents are effective in alleviating symptoms of ARIs, shortening the course of disease, helping recovery from severe illness, and minimising potential long term consequences of lung infections (Box 1).6-8 Chinese herbal medicines (CHMs) are not only routinely used for most respiratory ailments in hospitals in China, but are also commonly used by many Chinese people in the community. The effort to integrate Western and traditional approaches has resulted in a number of publications comparing the benefits of CHMs with Western medicine. Our aim was examine the available evidence in order to explore the generalisability of the traditional Chinese approach to clinical management and determine whether CHMs might be advocated in Australia, where CHMs are now widely marketed.9 Methods Data extraction MEDLINE (1966 to May 1997), the Cumulative Index to Nursing and Allied Health Literature (1982 to May 1997) and the Cochrane Library (1995 to May 1997) were searched for all studies in which CHMs were used to treat ARIs. We also performed a search of three Chinese publications available in Australia: Chung Kuo Chung Hsi I Chieh Ho Tsa Chih (the Chinese Journal of Integrated Traditional and Western Medicine) (1982 to 1996), Chinese Traditional Patent Medicine (1991 to 1996) and Chung Huo I Hsueh Tsa Chih (Taipei) (the Chinese Medical Journal of Taipei) (1986 to 1996). The search keywords were CHMs and acute respiratory infections (or bronchiolitis, pneumonia or viral infections); random allocation; treatment group/control group; CHMs group/Western medicine group. Inclusion criteria Studies were included in our review if they had used a control group to compare CHMs with a placebo or Western medicine. We assessed the quality of these studies from four perspectives: patient allocation, treatment description, outcome assessment, and data analysis. Results Of the 46 studies identified from the search, 27 fulfilled our inclusion criteria.10-36 Ten studies involved upper respiratory tract infections (URTI) (Box 2), and 17 involved lower respiratory tract infections (LRTI) (Box 3). Twenty-six studies were published in Chinese, and one in English.29 Only the article written in English was found in the databases. Treatment Most studies used a herbal tea or patent medicine, although six used parenteral preparations and one study36 used a topical herbal preparation. Treatment duration was three to seven days for URTIs, and more than seven days for LRTIs. The control treatment was antibiotics in 18 studies, antiviral agents in five, symptomatic and supportive therapy in three, and a placebo in one. Clinical outcomes Various methods of reporting outcome were described; a common approach was to report an "effect rate" from less effective to significantly effective. CHMs were reported to have a significantly higher effect rate in 15 of 22 studies (Box 4). Generally, CHMs were reported to produce greater improvement in clinical symptoms and physical signs and a shorter hospital stay. Five out of seven studies testing Maxingshigangton20-24,28,32 and all studies using Shuang Huang Lian29,31,34 reported better treatment effects on bronchiolitis and pneumonia. Assessment of study quality We rated only two studies as of high methodological quality. Both examined the efficacy of intravenous Shuang Huang Lian for LRTIs.29,34 Patient allocation: Twenty studies reported a randomisation strategy, but only three21,30,35 described the allocation method. Three studies29,30,36 reported using single- or double-blind methods in the study. Treatment description: Most studies provided information about the main herbs included in the formulation, dose, course and treatment approach. Information on safety or side-effects of the herbal medicines tested was provided in only four studies.11,17,23,29 In eight studies11,12,14,16,18,21,23,31 the treatment applied to the control group was not described or was manifestly not identical to that of the experimental group in manner of administration. Outcome assessment: Twenty-two studies used a rate to assess the outcome. Eight of these14,15,19,22,23,28,30,36 did not provide adequate information on what constituted the degree of effect or on the defined time point for outcome measures. Satisfactory outcome measures were identified in only eight studies.11,12,22,26,27,29,32,34 Data analysis: Thirteen studies reported baseline data about the participants; only one29 tabled the baseline comparison. Six studies11,17,20,21,29,34 presented statistical results such as mean and standard deviation. Two studies18,28 drew a conclusion regarding efficacy without any reference to statistical analysis. Discussion Although CHMs are the subject of many Chinese research publications, definitive conclusions about their efficacy are difficult to draw. There are perceived ethical constraints about conducting rigorous randomised controlled trials in China, and placebo and double-blind methods are not generally accepted in clinical research, especially for time-honoured and widely used treatments. The inadequate methods of most studies make it difficult to transfer the Chinese confidence in CHMs to other settings. In the articles we reviewed, there was insufficient information on randomisation and baseline comparisons, outcome measures were either complicated or of doubtful validity, and terms were poorly defined or explained. Data analysis and presentation were generally too limited to enable us to assess the adequacy of the statistical analysis. Most of the studies failed to deal with potential confounding factors, and for several reports the timing of outcome measures was inappropriate. Nevertheless, in Chinese practice these traditional approaches are seen as appropriate treatment for ARIs. They are often used as life-saving remedies in preference to antibiotics. From this review, we have been impressed by the "clinical effects" of Maxingshigantong and intravenous Shuang Huang Lian for treating bronchiolitis and pneumonia. On the evidence provided, Shuang Huang Lian appears to be a promising remedy worthy of further study. Interestingly, no studies evaluated the herbs and formulas most widely used in the community for treating the common cold and other common URT infections in China. Perhaps the most widely used herbal medicines, such as Banlangen Chong Ji (tea) and Ganmaoqingre Chong Ji, are so firmly trusted by both clinicians and the community that evaluation is not considered necessary. The one trial published in English was carried out collaboratively between the University of Newcastle, Australia, and the Harbin Medical University, China, and used rigorous procedures to conclude that bronchiolitis was better treated with Shuang Huang Lian than with antibiotics.29 More studies of this calibre are needed. In our view, the scientific evidence that CHMs are more effective than antibiotics in ARIs is inadequate. Our analysis indicates the need for more rigorous evaluation of CHMs, including descriptions of their derivation, preparation, standardisation, potency, safety, and efficacy, if they are to meet modern Western criteria for their use. We suggest that, acknowledging the difficulty in conducting randomised controlled trials in China, the following approaches may be needed: further studies should examine herbs and formulas that are widely used and accepted by Chinese practice as well as those that show promise in treating ARIs; further international collaborations should be encouraged; protocols for studies in which CHMs are tested in clinical settings outside China should be developed; and training for Chinese doctors in clinical trial methodology should be supported through the International Clinical Epidemiology Network, with a view to more rigorously testing the clinical value of CHMs. References BOSTID Researchers. The epidemiology of acute respiratory tract infection in young children: comparison of findings from several developing countries. Rev Infect Dis 1990: 12 Suppl 8: S870-S888. Garcia J. Epidemiology of acute bronchopulmonary infections in children [abstract]. Rev-Prat 1996; 46: 2056-2061. Del Mar CB, Glasziou PP. Antibiotics for the symptoms and complications of sore throat. In: Douglas R, Bridges-Webb C, Glasziou P, et al, editors. Acute respiratory infections module of the Cochrane database of systematic reviews, 3 June 1997. The Cochrane Library [database on disk and CDROM]. Oxford: Update Software; 1997. Glasziou PP, Hayem M, Del Mar CB. Treatments for acute otitis media in children: antibiotic versus placebo. In: Douglas R, Bridges-Webb C, Glasziou P, et al, editors. Acute respiratory infections module of the Cochrane database of systematic reviews, 3 June 1997. The Cochrane Library [database on disk and CDROM]. Oxford: Update Software; 1997. Randolph AG, Wang EEL. Ribavirin for respiratory syncytial virus lower respiratory tract infection. In: Douglas R, Bridges-Webb C, Glasziou P, et al, editors. Acute respiratory infections module of the Cochrane database of systematic reviews, 3 June 1997. The Cochrane Library [database on disk and CDROM]. Oxford: Update Software; 1997. Wen ZY. [TCM-WM diagnosis and treatment of paediatric pneumonia.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1983; 3: 44-45. Chinese. Zhang ZJ. [TCM-WM diagnosis and treatment of severe pneumonia in children.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1987; 7: 112-114. Chinese. Zhang ZJ. [Recent development on treatment of repeated respiratory infection in children.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1996; 17: 571-573. In Chinese. Shenfield G, Atkin P, Kristoffersen S. Alternative medicine -- an expanding health industry. Med J Aust 1997; 166: 516-517. Yu RH. [Investigation on preliminary therapeutic effect of combined Chinese and Western medicine for treatment of acute tonsillitis.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1984; 4: 750. Chinese.* Luo H, Zou DW, Qie JR, et al. [Treatment of upper respiratory tract infection with a mixt 716 compound.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1993; 13: 730-732, 709. Chinese. Chang GZ, Li QC, Li M, et al. [Investigation on therapeutic effect of Yanholer powder in treatment of 220 cases of acute tonsillitis.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1994; 14: 309-311. Chinese.* Gao JF, Ma YX, Lin HP. [A report of 112 children with herpes simplex treated with Jiaweiyinxiao powder.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1994; 14: 620. Chinese.* Yang LP. [Treatment of 60 children with herpes simplex with Qingkailing injection.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1995; 15: 119. Chinese.* An ZY. [Investigation on treatment of 329 cases of acute tonsillitis with Yinma powder.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1995; 15: 428. Chinese.* Zhou ZQ, Xu J, Ding YF. [Clinical investigation on treatment of acute pharyngitis with Shangdogen liquor.] Chinese Traditional Patent Medicine 1995; 17: 20-21. Chinese.* Liu H, Ding PL, Li HC, et al. [Investigation of clinical therapeutic effect of Kanggantuireling tea for treating 301 patients with wild cold.] Chinese Traditional Patent Medicine 1995; 17: 25-27. Chinese.* Lo GQ, Tang WY. [Clinical investigation on children with upper respiratory tract infections treated with Qingjie decoction.] Chinese Traditional Patent Medicine 1996; 18: 26-27. Chinese.* Wang GX, Ho HX. [Investigation on therapeutic effect of Yanhouwan in treatment of pharyngitis.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1996; 16: 43. Chinese.* Hu J. [A clinical study on curative effect of 529 cases of pneumonia in children.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1984; 4: 672. Chinese. Zhang HC, Li FX, Zhu XD. [Therapeutic effects of febrifugal and detoxicant drugs in treating pneumonia in adults: an analysis of 118 cases.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1985; 5: 537-539, 515. Chinese. Xue D, Cheng SH, Wu XF. [Treatment of severe infantile pneumonia with traditional Chinese medicine and herbs.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1988; 8: 234. Chinese.* Yan CR, Shen W, Zhang DS, Zheng JX. [A report of 38 cases of infantile pneumonia treated with Chinese herbal aerosol.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1988; 8: 748. Chinese.* Sun XD. [A report of 94 cases of paediatric bronchopneumonia treated with combined Chinese and Western medicines.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1988; 8: 749. Chinese.* Zhang DY, Yang WW, Gao XC. [Comparison of Chinese medicine with Western medicine for treatment of paediatric bronchitis.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1989; 9: 30. Chinese.* Pang JC. [Clinical investigation on 50 cases of severe paediatric pneumonia treated with Danshi (Salviae miltiorrhirae) injection.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1990; 11: 566. Chinese.* Zhu CY. [A report of 56 cases of paediatric pneumonia with heart failure treated by combined Chinese and Western medicine.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1991; 11: 56. Chinese.* Hu RS, Li YQ, Yuan W, Zhang SL, et al. [Clinical and experimental study of Xiao Er Ke Chaun Ling oral liquid in treating infantile bronchopneumonia.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1992; 12: 719-737. Chinese. Kong XT, Fang HT, Jiang GQ, et al. Treatment of acute bronchiolitis with Chinese herbs. Arch Dis Child 1993; 68: 468-471. Wu KH, Hu TC, Liu XF. [Clinical investigation on 119 cases of paediatric pneumonia treated with Jieduling (defebrile and detoxication) injection.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1994; 14: 116-117. Chinese.* Li MZ, Lu S, Tong QM, et al. [Investigation on therapeutic effect of Shuang Huang Lian injection for treatment of paediatric pneumonia.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1994; 14: 232-233. Chinese.* Li YX, Zhang YH. [Investigation on therapeutic effect of Chinese medicine in treating paediatric pneumonia.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1994; 14: 573. Chinese.* Hong JX, Xie T, Gao YW, et al. [Clinical and experimental study on oral liquor night-cough tranquiller in treating infantile cough.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1995; 15: 25-27. Chinese. Yu JE, Zheng Y, Tang WY, et al. [Analysis of curative effect of Shuang Huang Lian powder for injection for paediatric pneumonia in 110 cases.] Chinese Traditional Patent Medicine 1996; 15: 24-25. Chinese. Shi YM, Zhang YQ, Fang SQ. [Clinical and experimental studies of Zhenkeling Oral Liquor on treatment of infantile cough.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1996; 16: 390-393. Chinese. Weng CX, Li G, Zheng SL. [Application of modified therapeutic system in treatment of upper respiratory viral infection in childhood with Chinese medicine.] Chung Kuo Chung Hsi I Chieh Ho Tsa Chih 1996; 16: 693. Chinese.* * Title translated by C L. (Received 24 Feb, accepted 23 Jul, 1998) Authors' details National Centre for Epidemiology and Population Health, The Australian National University, Canberra, ACT. Chaoying Liu, MB BS, PhD, Visiting Fellow; Robert M Douglas, MB BS, MD, Director. Reprints will not be available from the authors. Correspondence: Dr C Liu, National Public Health and Planning Branch, Public Health Division, MDP 16, Commonwealth Department of Health and Aged Care, Woden, ACT 2601. Email: chaoying.liuAThealth.gov.au Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> We appreciate

Chaoying Liu · Robert M Douglas

Something particular in the air we breathe? Australian research is needed to refine recently set Australian standards for air pollution MJA 1998; 169: 452-453 There is now a mounting body of evidence that fine airborne particles have significant adverse health effects. In this issue of the Journal, Lewis and colleagues report the results of a cross-sectional study of school children conducted as part of the Hunter Illawarra Study of Airways and Air Pollution (HISAAP).1 In brief, the HISAAP investigators found that, in children, outdoor PM10 (particles with an aerodynamic diameter less than 10 µm) concentrations are associated with chest colds and night time cough, but not with wheezing. An important point is that these associations were found at relatively low particulate concentrations -- the most polluted area had an annual average PM10 of 43.7 µg/m3. A good response rate was achieved and appropriate multivariate statistical analysis was conducted to control for confounders such as indoor environmental and individual factors. These results are consistent with previous time series, cross-sectional and cohort studies of the effects of air pollution on both children and adults, predominantly conducted in Europe and North America. The Box contains a summary of the overall health effects found in these studies. Although many of the criteria for causation have now been satisfied (such as a dose-response relationship, consistency of association, and correct sequence of exposure and effect), the lack of data from controlled clinical trials or relevant animal experiments means that the underlying biological mechanisms are not yet understood. Epidemiological studies consistently find associations between exposure to airborne particles and short-term human health effects, and there is no threshold concentration below which these associations disappear. These facts have spurred some regulatory agencies to action. In July 1997, the United States Environment Protection Agency (EPA) set 24-hourly average concentration limits of 65 µg/m3 and an average annual limit of 15 µg/m3 for PM2.5 (particles less than 2.5 µm diameter). These complement the 1987 limits for PM10 of 150 µg/m3 for a 24-hour average and 50 µg/m3 for an annual average. There is some evidence that fine particles (PM2.5) may be even more relevant to public health than PM10.3 In Australia, the development of airborne particle standards to protect public health has proceeded more slowly. In 1990, Streeton first proposed PM10 objectives of 120 µg/m3 for a 24-hour average and 40 µg/m3 for an annual average not to be exceeded for "acceptable" air quality.4 Shortly afterwards, one of us (MJA) expressed the hope that "politicians and bureaucrats would not shirk the task" of introducing the necessary legislation and regulations.5 On 26 June 1998, the National Environment Protection Council finalised the National Environment Protection Measure (NEPM) for Ambient Air Quality.6 This has at last set an air quality standard of 50 µg/m3 for a 24-hour average for PM10. However, because Australian cities are subject to bushfire smoke, the NEPM still permits five allowable exceedance days per year. Closer examination of the evidence summarised in the Box reveals some inconsistencies. It is difficult to envisage a mechanism which results in less exacerbation of mild effects such as cough (1.2% increase per 10 µg/m3) than of respiratory mortality (3.4% increase per 10 µg/m3). Issues such as these have led to continuing controversy over the role of particles in short term health effects.7,8 This was acknowledged in Australia when the National Environment Protection Council agreed, in response to input during the consultation process, that the NEPM and the standards within it will need review within 10 years. There was also agreement that the particle standard needed review, especially the need for a PM2.5 standard. Such a review should be commenced by 2001. Furthermore, a review of the whole NEPM and all six criteria pollutants (airborne particles, sulfur dioxide, ozone, oxides of nitrogen, carbon monoxide, and lead) should be started by 2005. The US National Research Council recently recommended that the US EPA develop a long term (14-year) research program to examine particulate matter.9 Their top 10 priorities are to: investigate quantitative relations between particulate matter and individual exposure; assess the most biologically important constituents of particulate matter; identify the most susceptible subpopulations; analyse exposure to the most biologically important constituents; develop advanced mathematical, modelling and monitoring tools; apply modelling to link sources to exposed individuals; investigate deposition patterns and fate of particles; analyse interactions between particulate matter and gaseous pollutants; explore toxicological mechanisms; and develop advanced methods for statistical analysis of epidemiological studies. Australia needs to conduct similar research because the air quality, the population's exposure to it, and the resulting health effects will differ from those in other countries. The composition, size distribution, and other characteristics of particles differ from those in the United States, as does the mix of background air pollutants in which the particles are suspended, and the susceptibility of the population exposed to such particles. For example, the prevalence of asthma and other allergic disorders is significantly higher in Australia than in either the United States or Europe.10 The results from studies such as HISAAP allow Australian researchers to contribute to this process of examining, in greater detail, the relations between particles and health. It is to be hoped that during the time-frame for revision of the NEPM for ambient air quality, the necessary environmental, epidemiological and toxicological research will be supported to resolve some of the uncertainties. Indeed, although not without considerable economic pain, the forthcoming closure of the steel mills offers a unique opportunity to determine whether improved air quality will actually result in any improved health outcomes for Newcastle residents. Only when such evidence is available can we be confident of setting airborne particle standards that will adequately protect the health of the Australian population. Michael J Abramson Associate Professor, Department of Epidemiology and Preventive Medicine Monash University, Melbourne, VIC Tom Beer Coordinator, Environmental Risk Network, CSIRO Atmospheric Research Melbourne, VIC, and Adjunct Professor of Risk Management Southern Cross University, Lismore, NSW Lewis PR, Hensley MJ, Wlodarczyk J, et al. Outdoor air pollution and children's respiratory symptoms in the steel cities of New South Wales. Med J Aust 1998; 169: 459-463. Dockery DW, Pope CA III. Acute respiratory effects of particulate air pollution. Annu Rev Public Health 1994; 15: 107-132. Abbey DE, Ostro BE, Petersen F, Burchette RJ. Chronic respiratory symptoms associated with estimated long term ambient concentrations of PM2.5 and other air pollutants. J Expo Anal Environ Epidemiol 1995; 5: 137-159. Streeton JA. Air pollution, health effects and air quality objectives in Victoria. Melbourne: Environment Protection Authority, 1990. Abramson M. Air pollution, health effects and air quality objectives. Med J Aust 1991; 154: 716-717. Ambient air quality. National environment protection measure and revised impact statement. Adelaide: National Environment Protection Council, 1998. Reichhardt T. Regulators face questioning on particulate rules. Nature 1996; 380: 11-12. Cooney CM. NRC advises long-term particulate matter research plan needed. Environ Sci Technol 1998; 32: 209A. US National Research Council Committee on Research Priorities for Airborne Particulate Matter. Research priorities for airborne particulate matter: I. Immediate priorities and a long range research portfolio. Washington, DC: National Academy Press, 1997. European Community Respiratory Health Survey. Variations in the prevalence of respiratory symptoms in the European Community Respiratory Health Survey. Eur Respir J 1996; 9: 687-695. Reprints: Associate Professor M Abramson, Department of Epidemiology and Preventive Medicine, Monash University, Clayton, VIC 3168. - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Michael J Abramson · Tom Beer

Outdoor air pollution and children's respiratory symptoms in the steel cities of New South Wales Peter R Lewis, Michael J Hensley, John Wlodarczyk, Ruth C Toneguzzi, Victoria J Westley-Wise, Trevor Dunn and Dennis Calvert MJA 1998; 169: 459-463 For editorial comment, see Abramson & Beer Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health - ©MJA1998 Abstract Objective: To investigate the relationship between outdoor air pollution and the respiratory health of children aged 8 to 10 years. Design: A cross-sectional survey (between October 1993 and December 1993) of children's health and home environment. Summary measures of particulate pollution (levels of particles with an aerodynamic diameter less than 10 µm [PM10] each 6th day) and SO2 (daily mean and maximum hourly values) were estimated for each area (using air quality monitoring station data from July 1993 to June 1994). Setting and survey participants: Parents of 3023 primary school children (Years 3, 4 and 5) from industrial and non-industrial areas with air quality monitoring stations in the Hunter and Illawarra regions of New South Wales. Main outcome measures: Reported occurrence of four or more chest colds, four or more attacks of wheezing, and night-time cough without a cold for more than two weeks, all within the previous 12 months. Results: 77% response rate, ranging by area from 66% to 88%. The average annual outdoor air pollution for the nine areas was 18.6-43.7 µg/m3 for PM10 and 0.16-0.90 parts per hundred million for SO2. The proportion of children reported to have the main outcome symptoms were: chest colds, 3.0%-9.7%; night cough, 12.3%-30.5%; and wheeze, 3.4%-11.3%. There was no significant association with SO2, but a significant increase in the odds of symptoms per 10 µg/m3 increase in PM10 on chest colds (odds ratio [OR], 1.43; 95% confidence interval [CI], 1.12-1.82) and night-time cough (OR, 1.34; 95% CI, 1.19-1.53), but not wheeze. Passive smoking was significantly associated with chest colds but not with the other symptoms. Maternal allergy was associated with all three respiratory symptoms, most strongly with wheeze. Conclusion: These results provide evidence of health effects at lower than expected levels of outdoor air pollution in the Australian setting. They also suggest differences in contributions of environmental and hereditary factors to cough and chest colds compared with wheeze. Introduction The effect of outdoor air pollution on the respiratory system has been investigated and reviewed often.1,2 Various health outcomes have been studied; for example, the relationship between exposure to elevated sulfur dioxide, total suspended particulates (TSP) and respiratory symptoms;3 the association between increased air pollution and hospital admissions for asthma;4,5 and studies of air pollution and mortality.6,7 These studies consistently report associations between air pollution and health outcomes, and illustrate the coherence of effects8 across the range of outcomes. There have been few studies of the relationship between air quality and health in Australia. Studies of asthma in school children living near power stations in the Hunter region of New South Wales had very low levels of exposure and lacked the power to detect small associations.9,10 Other studies in south-eastern Australia confirmed the high prevalence of asthma in Australia but had no exposure measures.11-13 The lower Hunter and Illawarra regions of New South Wales are on the coast, about 150 km north and 80 km south of Sydney, respectively. The main cities are Newcastle, in the Hunter region, and Wollongong, in the Illawarra region. The estimated resident populations in 1993 for Newcastle and Wollongong were 451 100 and 248 700, respectively.14 Both regions have fully integrated steelworks, combining coke ovens, blast furnaces, steel-making vessels and rolling mills, and the main pollutants are coke oven gases, blast furnace gases and particulates. In addition, lead smelting occurs in the Hunter region, and copper smelting in the Illawarra region. The Hunter Illawarra Study of Airways and Air Pollution (HISAAP) arose out of longstanding community concerns about the health effects of air pollution near heavy industry in Newcastle and Wollongong. The generalisability of overseas studies to Australia was not known, because of differences in climate, geography, population and pollution sources. Public health workers need local data to initiate action on air quality at the community level and to formulate air quality guidelines. This study, the first part of HISAAP, investigated the association between outdoor air quality, as particulates and sulfur dioxide, and respiratory symptoms among primary school children. Methods The study was a cross-sectional survey to measure the prevalence of respiratory and atopic symptoms among primary school children and relate these to measures of ambient air quality. Study areas To make best use of resources, study areas were selected on the basis of existing or proposed air quality monitoring stations. In the lower Hunter region, the study areas close to industrial sources of air pollution were North Lake Macquarie, Mayfield and Stockton, and distant areas were Beresfield and Wallsend (Figure 1a). In the Illawarra region, we estimated that there would be an increasing gradient of exposure to air pollution, from Wollongong, to Albion Park, Kembla Grange and Port Kembla (Figure 1b). Wallsend, Beresfield, Wollongong and Albion Park were expected to have background levels of air pollution. We were able to compare these multiple control areas with those areas close to point sources of air pollution. Sampling strategy All primary schools within a three-kilometre radius of the air quality monitoring sites were approached to be involved in the study. The sampling frame included all children in Years 3 and 4, aged 8 to 10 years, whose parents or guardians approved their child's participation. In areas that had small numbers of children, children in Year 5 were included. We aimed to enrol about 300 children in each of the nine areas. Questionnaire Our questionnaire incorporated features used by previous investigators in the Hunter region and NSW,9,11,12 the International Study of Asthma and Allergies in Childhood,15 the American Thoracic Society questionnaire16 and the Six Cities study.17 It addressed demographic data and parental education; child's health (cough, chest colds, wheeze) and atopic symptoms (hayfever, eczema); child's use of respiratory medications; family's symptoms; and home environmental factors (indoor smoking, heating, cooking, carpets, cats). The questionnaire was piloted in both regions.18The primary health outcomes were night-time cough, chest colds and frequent wheeze. They were the responses to the following questions: In the last 12 months has your child had a dry cough at night, apart from a cough with a cold or chest infection? If yes, has this cough lasted for more than 2 weeks? In the last 12 months how many chest colds did your child have? . . . 4 or more chest colds. How many attacks of wheezing has your child had in the last 12 months? . . . 4 or more attacks. Exposure to indoor tobacco smoke was assessed by asking whether the respondent, other adult or any other person smoked cigarettes inside the home. The survey was conducted from October 1993 to December 1993. Children received consent forms and questionnaires at school. Parents completed the questionnaires, and children returned them to their teachers. If a questionnaire was not returned after two weeks, a copy was posted to the parents for completion and return by reply-paid post. Exposure measurement The lower Hunter and Illawarra Air Pollution Monitoring Networks19 consist of sites operated by the Environment Protection Authority (EPA) and industry self-monitoring sites audited by the EPA. Particulate and sulfur dioxide measures were collected for all study areas, from January 1993 to December 1994. As air pollution data were incomplete for some sites in 1993, the goal was to have representative data for 12 consecutive months close to the reference period of the questionnaire (the 1993 calendar year). The most complete data were found to be from July 1993 to June 1994. Sensitivity analyses using data from adjacent 12-month periods showed very little effect on the results. Particulate pollution as PM10 (particles with an aerodynamic diameter less than 10 µm) was measured for 24 hours every sixth day using high volume air samplers with a size-selective inlet, and these measures were averaged over the 12 months. North Lake Macquarie, Mayfield and Stockton measured only TSP, so local data in which both TSP and PM10 were measured for shorter periods20,21 were used to derive a conversion factor to PM10. In North Lake Macquarie, PM10 was estimated to be 60% of TSP, close to the value used by others.22 In Mayfield and Stockton, PM10 was estimated to be 45% of TSP. Sulfur dioxide measurements were obtained hourly using pulsed fluorescent spectrophotometry. Twelve-month averages of the daily maximum values and of the daily mean values were calculated. There were no major trends in air pollution during this time. Seasonal changes did not affect the relative ranking of the areas in terms of air pollution. Analysis We used SAS software for the analysis.23 Descriptive statistics were produced for participation rates, health measures and environmental measures for each of the nine study areas. Logistic regression analysis using generalised estimating equations (GEEs) was used to model the reported symptom (outcome variable) on the following explanatory variables: PM10 and sulfur dioxide measures, unflued gas heating, adults smoking inside the home, indoor cats, age, sex, and maternal allergy.24 The level of clustering for this analysis was the school (ie, clusters of children within schools), with 35 schools in the study. Although schools were also clustered within study areas, area was not chosen as the clustering level because of the allocation of exposure measure by area. Ethical approval The study received ethical approval from the NSW Education Department, the Regional Catholic Education Office, and the Ethics Committees of the Hunter Area Health Service, the University of Newcastle, the Illawarra Area Health Service, and the University of Wollongong. Results Subjects Questionnaires were given to 3023 primary school children -- 1554 children (from 18 schools) in the Hunter region, and 1469 (from 17 schools) in the Illawarra region. In the Hunter region, 1284 (82%) questionnaires were returned, and in the Illawarra region 1056 (72%) were returned. There were no significant differences in age and sex profiles across the study areas (Table 1). Respiratory symptoms About a quarter of the children were reported to have had at least one of the primary respiratory symptoms in the preceding 12 months (Table 2). While some areas with high proportions of children with symptoms were close to industry (Mayfield and Stockton with children having chest colds), this was not a consistent pattern (Beresfield and children with night cough). The proportion of children who had ever been diagnosed with asthma ranged from 17.4% to 38.4%. Home environment and outdoor air pollution Depending on the study area, a third to half of the children lived in homes where one or more adults smoked cigarettes in the home (Table 3). The proportion of children in homes with gas heating that did not have a flue to the outside varied greatly between the areas. The levels of particulate pollution in Mayfield and Stockton approached the US EPA standard for PM10 of 50 µg/m3 (annual mean) (Table 3) and the Australian standard, at that time set for TSP at 90 µg/m3 (annual mean). The annual mean sulfur dioxide levels (daily means) were below the Australian standard of 2 parts per hundred million (annual mean).19 Within study areas, particulate levels were not necessarily high in high sulfur dioxide areas, and vice-versa. Scatter plots of primary health outcomes by air quality measures suggested some positive associations between PM10 and both night cough and chest colds (Figure 2). Generalised estimating equation analysis For each 10 µg/m3 increase in annual mean PM10, children were 43% more likely to be reported as having four or more chest colds (odds ratio [OR], 1.43; 95% confidence interval [CI], 1.12-1.82). The approximate difference in particulate pollution between the area with the highest PM10 level and the area with the lowest was 25 µg/m3, and children were 144% more likely to be reported to have frequent chest colds per 25 µg/m3 increase in annual mean PM10 (OR, 2.44; 95% CI, 1.33-4.49). There was a consistent significant association between particulate pollution and symptoms of night cough and chest colds (Table 4). No association was found between sulfur dioxide and the three respiratory symptoms. An adult smoking in the home was associated with chest colds, and unflued gas heating was associated with frequent wheeze. Boys were more likely to experience frequent wheeze, and there was a significant association between increasing age and likelihood of frequent wheeze. Maternal allergy was consistently associated with an increased risk for all health outcomes, but strongest for wheeze. To estimate the possible impact of the two areas with the largest particulate pollution (Mayfield and Stockton, in the Hunter region), the GEE analysis was repeated excluding those areas. There was little change in the coefficients for most variables, including maternal allergy, for each outcome. However, the odds ratio for chest colds per 10 µg/m3 increase in annual mean PM10 increased substantially -- with Mayfield and Stockton excluded, the odds ratio was 2.05 (95% CI, 1.46-2.87), compared with 1.43 for the full dataset. Discussion This cross-sectional study of primary school children has shown an important association between relatively low levels of particulate air pollution and respiratory symptoms. The importance is reflected in the finding that the odds ratios for particulates were of the same order as for exposure to indoor tobacco smoke. We found an association with maternal allergy across all three symptom outcomes, but strongest for wheeze. The prevalence estimates of respiratory symptoms are similar to those found in other Australian and New Zealand studies.11-13,25 The association between air pollution and respiratory symptoms in children is also consistent with similar cross-sectional studies from other countries. An Italian study found that children living in polluted areas experienced more cough, rhinitis, pneumonia and early respiratory infections than control subjects,26 but that study did not measure actual air pollution exposure. A British study found that children were more likely to miss school because of respiratory symptoms of cough and wheeze if their school was exposed to a higher coal dust burden (OR, 1.55; 95% CI, 1.17-2.06).27 Our results are directly comparable with those of the Six Cities and 24 Communities studies in North America;17,28,29 effects of particulate pollution on respiratory symptoms and effects of indoor smoking were of the same order in those studies and ours. Two results of particular note are the relationship between frequent wheeze and age, and the effect of removing from the analysis the areas with the highest particulate pollution. The increase in wheeze with age is quite large (OR, 1.38 per year). Stratified analysis revealed similar coefficients for younger and older age groups, suggesting that a sampling bias may explain the strength of the relationship. The substantial increase in the odds ratio of particulate pollution and chest colds after removal of the areas with highest PM10 suggests that the dose-response curve for particulate pollution and chest colds is curvilinear and much steeper at lower pollution levels. Potential limitations of our study include possible reporting bias by residents of industrial areas and the variability in the measurement methods for particulate air pollution. It is not possible to estimate the level of possible reporting bias, but its effect may be reduced by selection bias in that families with children with lung disease may not come to, or may leave, polluted areas. The difference in measurement of particulates was unavoidable. A subsequent diary study obtained comparisons of TSP and PM10 which provided evidence on which to convert the measures for local conditions.20,21 Particularly striking are the results which show differences in the determinants of wheeze compared with coughs and colds. While maternal allergy played a part in all, passive smoking was restricted to colds, and particulates to coughs and colds. This suggests differences in underlying pathology which deserve further exploration. Our data lead us to question the current air quality standards, which are based on the premise that levels at or below recommended ambient levels are not likely to produce a clinically important effect. In particular, recommended levels do not consider increased individual sensitivity caused by a disease such as asthma. While this study cannot infer causation, it adds to other local and overseas work that increasingly indicates the role of air pollution in respiratory health -- alone and synergistically with other aeroallergens.30 This information contributes to the review of Australian air quality guidelines, and to the broader societal debate about lifestyle, transport and energy consumption. Individuals, communities, industry and organisations need to reassess their environmental performance not only for the environment, but also for health. Acknowledgements Our thanks to members of the following organisations which supported the study: Newcastle Environmental Toxicology Research Unit (especially Randall Robertson and Julie Holt), University of Newcastle, Hunter Public Health Unit, Hunter Area Pathology Service, Newcastle City Council, Lake Macquarie Council, Illawarra Public Health Unit, University of Wollongong, NSW Health Department, NSW Environment Protection Authority, Australian Nuclear Science and Technology Organisation, BHP (Newcastle and Port Kembla), Incitec, Pasminco Metals Sulphide, Southern Copper. We are grateful to the schools, parents, and children who participated in this study. HISAAP was partly funded by the NSW Health Department as part of its Health and Air Research Program. Dr P Lewis received an NHMRC Public Health Fellowship for two years. References Committee on the Medical Effects of Air Pollution. Asthma and outdoor air pollution. London: HMSO, 1995. Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society. Health effects of outdoor air pollution. Am J Respir Crit Care Med 1996; 153: 3-50. Lunn FE, Knowelden J, Handyside AJ. Patterns of respiratory illness in Sheffield infant schoolchildren. Br J Prev Soc Med 1967; 21: 7-16. Pope CA III. Respiratory admissions associated with PM10 pollution in Utah, Salt Lake and Cache Valleys. Arch Environ Health 1991; 46: 90-97. Bates DV, Baker-Anderson M, Sizto R. Asthma attack periodicity: a study of hospital emergency visits in Vancouver. Environ Res 1990; 51: 51-70. Anderson HR, Ponce de Leon A, Bland JM, et al. Air pollution and daily mortality in London: 1987-92. BMJ 1996; 312: 665-669. Dockery DW, Pope CA III, Xu X, et al. An association between air pollution and mortality in six US cities. N Engl J Med 1993; 329: 1753-1759. Bates DV. Health indices of the adverse effects of air pollution: the question of coherence. Environ Res 1992; 59: 336-349. Henry RL, Abramson R, Adler JA, et al. Asthma in the vicinity of power stations: I. A prevalence study. Pediatr Pulmonol 1991; 11: 127-133. Henry RL, Bridgman HA, Wlodarczyk J, et al. Asthma in the vicinity of power stations: II. Outdoor air quality and symptoms. Pediatr Pulmonol 1991; 11: 134-140. Bauman A, Mitchell CA, Henry RL, et al. Asthma morbidity in Australia: an epidemiological study. Med J Aust 1992; 156: 827-831. Peat JK, Toelle BG, Gray EJ, et al. Prevalence and severity of childhood asthma and allergic sensitisation in seven climatic regions of New South Wales. Med J Aust 1995; 163: 22-26. Robertson CF, Bishop J, Dalton M, et al. Prevalence of asthma in regional Victorian schoolchildren. Med J Aust 1992; 156: 831-833. Australian Bureau of Statistics. Regional population growth 1991 and 1996. Canberra: ABS, 1997. (Catalogue No. 3218.0.) Asher M, Keil U, Anderson H. International study of asthma and allergies in childhood (ISAAC): rationale and methods. Eur Respir J 1995; 8: 483-491. Ferris BG. Epidemiology standardisation project. Part II. Am Rev Respir Dis 1978; 118: 1-53. Ware JH, Dockery DW, Spiro A III, et al. Passive smoking, gas cooking and respiratory health of children living in six cities. Am Rev Respir Dis 1984; 129: 366-374. Lewis PR, Toneguzzi R, Long K, et al. The Hunter Illawarra study of airways and air pollution: refining the process. NSW Public Health Bulletin 1995; 6: 110-112. State Pollution Control Commission. Quarterly air quality monitoring report No 4, 1990. Sydney: SPCC, 1992. Lewis P, Holt J, Fryer J. Daily particulate monitoring in the Speers Point/Boolaroo area -- Lake Macquarie Research Grant 94-9. Newcastle: University of Newcastle, Newcastle Environmental Toxicology Research Unit, 1997. Environment Section, BHP. Mayfield quality control: measures of particulate pollution. BHP, 1995. Dockery DW, Pope CA III. Acute respiratory effects of particulate air pollution. Annu Rev Public Health 1994; 15: 107-132. SAS for Windows [computer program]. Version 6.03. Cary, North Carolina: SAS Institute, 1988. Karim MR. PC version of GEE1 [computer program]. Baltimore: Department of Biostatistics, The Johns Hopkins University, 1989. Moyes CD, Waldon J, Ramadas D, et al. Respiratory symptoms and environmental factors in schoolchildren in the Bay of Plenty. N Z Med J 1995; 108: 358-361. Corbo GM, Forastiere F, Dell'Orco V, et al. Effects of environment on atopic status and respiratory disorders in children. J Allergy Clin Immunol 1993; 92: 616-623. Brabin B, Smith M, Milligan P, et al. Respiratory morbidity in Merseyside schoolchildren exposed to coal dust and air pollution. Arch Dis Child 1994; 70: 305-312. Cunningham J, O'Connor GT, Dockery DW, Speizer FE. Environmental tobacco smoke, wheezing and asthma in children in 24 communities. Am J Respir Crit Care Med 1996; 153: 218-224. Dockery DW, Speizer FE, Stram DO, et al. Effects of inhalable particles on respiratory health of children. Am Rev Respir Dis 1989; 139: 587-594. Devalia JL, Rusznak C, Herdman MJ, et al. Effect of nitrogen dioxide and sulphur dioxide on airway response of mild asthmatic patients to allergen inhalation. Lancet 1994; 344: 1668-1671. (Received 29 Oct 1997, accepted 21 Jul, 1998) Authors' details Newcastle Environmental Toxicology Research Unit, University of Newcastle, Newcastle, NSW. Peter R Lewis, MPH, FAFPHM, Public Health Research Fellow; Michael J Hensley, MB BS, PhD, Director and Professor of Medicine; John Wlodarczyk, BEc, PhD, Statistician; Ruth C Toneguzzi, RN, DipClinEpi, Clinical Nurse Specialist. Illawarra Public Health Unit, Wollongong, NSW. Victoria Westley-Wise, MPH, FAFPHM, Director; Trevor Dunn, GdDipSc(Nursing), MPH(Occ Health), Project Manager. University of Wollongong, Wollongong, NSW. Dennis Calvert, MD, FRACP, Professor in Medicine and Public Health. Reprints will not be available from the authors. Correspondence: Dr P R Lewis, Newcastle Environmental Toxicology Research Unit, Division of Medicine, John Hunter Hospital, Locked Bag 1, Hunter Regional Mail Centre, NSW 2310. E-mail: plewiATdoh.health.nsw.gov.au - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Peter R Lewis · Michael J Hensley · John Wlodarczyk · Ruth C Toneguzzi · Victoria J Westley-Wise · Trevor Dunn · Dennis Calvert

Asthma and other atopic diseases in Australian children Australian arm of the International Study of Asthma and Allergy in Childhood Colin F Robertson, Marita F Dalton, Jennifer K Peat, Michelle M Haby, Adrian Bauman, J Declan Kennedy and Louis I Landau MJA 1998; 168: 434-438 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1998 Abstract Objective: To determine the prevalence of asthma, eczema and allergic rhinitis in Australian schoolchildren using the protocol of the International Study of Asthma and Allergy in Childhood (ISAAC). Design: Questionnaire-based survey. Setting: Melbourne, Sydney, Adelaide (in winter-spring, 1993) and Perth (in winter-spring, 1994). Subjects: All children in school years 1 and 2 (ages 6-7 years) or in year 8 (ages 13-14 years), attending a random sample of 272 schools, stratified by age and city. Main outcome measures: Parent-reported (for 6-7 year olds) or self-reported (for 13-14 year olds) symptoms of atopic disease in the previous 12 months, or ever; treatment of asthma; and country of birth. Results: 10 914 questionnaires were completed for 6-7 year olds and 12 280 for 13-14 year olds (84% and 94% response rates, respectively). Prevalence of wheeze in the past 12 months was 24.6% for the 6-7 year olds and 29.4% for the 13-14 year olds, and, among 6-7 year olds, was significantly higher in boys (27.4%) than girls (21.7%). Children born in Australia were more likely to report current wheeze than those born elsewhere (6-7 year olds: odds ratio [OR], 1.82; 95% confidence interval [CI], 1.55-2.15; and 13-14 year olds: OR, 1.88; 95% CI, 1.68-2.11). Prevalences of current eczema and allergic rhinitis were 10.9% and 12.0%, respectively, for the 6-7 year olds, and 9.7% and 19.6%, respectively, for the 13-14 year olds. Asthma, eczema and rhinitis coexisted in 1.8% of 6-7 year olds and 2.8% of 13-14 year olds. Conclusion: This study provides evidence that asthma prevalence in Australian schoolchildren is continuing to increase and is higher among Australian-born children than among those born elsewhere. Asthma, eczema and allergic rhinitis coexist to a lesser extent than expected. These results form the basis for future Australian and international comparisons. Introduction There is now substantial evidence that the prevalence of asthma and other atopic disorders is increasing worldwide.1,2 While the prevalence of asthma has been documented in the past 30 years, variation in methods and lack of uniform diagnostic criteria make direct comparison between studies difficult. Little is known about the prevalence of the other atopic disorders -- eczema and allergic rhinitis -- both throughout the world and particularly in Australia. The International Study of Asthma and Allergy in Childhood (ISAAC) is a collaborative project which has developed a standardised methodology to describe the prevalence and severity of asthma, rhinitis and eczema in children throughout the world.3 Such data will provide a framework for aetiological research into lifestyle, environmental and genetic factors affecting these disorders. Phase 1 of ISAAC is to determine the prevalence of the disorders throughout the world. Phases 2 and 3 will be more comprehensive, using more detailed questionnaires and objective measures to confirm the differences seen in Phase 1 and to identify important aetiological factors. Our study was part of Phase 1 of ISAAC. It aimed to determine the prevalence of asthma and other atopic diseases in Australian schoolchildren, to determine the burden of atopic disease in this country, and to provide a basis for international comparison. Methods We used the protocol of ISAAC3 to survey two age groups: 6-7 year olds (school years 1 and 2) and 13-14 year olds (school year 8). Subjects were all children in the relevant years of a random sample of primary and secondary schools. The sample comprised about 10% of all government, Catholic and independent schools in the metropolitan areas of Adelaide and Perth; the area within a radius of 20 km from the GPO in Melbourne; the area within a radius of 10 km from the GPO in Sydney for primary schools (school years 1 and 2); and the Western Region of Sydney for secondary schools (school year 8). Previous studies have shown these areas of Sydney and Melbourne to be representative of the metropolitan areas of these cities.4,5 A five-page questionnaire was issued by teachers for completion by parents of the 6-7 year olds, and by the 13-14 year olds in the classroom under examination conditions. The questionnaires contained the three standard ISAAC modules, asking about symptoms of asthma, eczema and allergic rhinitis3 (see Box 1 for definitions), an additional module about treatment of asthma, and two extra questions about the children's and mothers' country of birth. No translations were provided. If the first questionnaire was not returned by the 6-7 year olds, a second was issued. A second visit was made to the secondary schools, if necessary, to recruit students absent at the initial visit. Data were analysed with the statistical package SPSS-X.9 Results were adjusted for cluster effect, and chi-squared tests were used to compare prevalences, while significance of odds ratios (OR) was assessed with 95% confidence intervals (CIs). Results Details of schools and subjects surveyed are shown in Box 2; 201 primary schools and 71 secondary schools participated, comprising 7%-42% of schools in the sampling area; 9% of schools selected declined to participate. A total of 12 952 questionnaires were issued to the 6-7 years age group (response rate, 84%) and 13 078 to the 13-14 years age group (response rate, 94%). Prevalence of atopic diseases in the two age groups is shown in Box 3. Asthma Prevalence of current wheeze was 24.6% for the 6-7 year olds (95% CI, 23.8-25.4), and 29.4% for the 13-14 year olds (95% CI, 29.1-29.7) (Box 3). In the younger group, current wheeze was significantly more common in boys than in girls (OR, 1.36; 95% CI, 1.25-1.49), but this sex difference was reversed in the older group (OR 0.82; 95% CI, 0.76-0.89). Figure 1 (below) compares the prevalence of atopic diseases between the four cities. For the 6-7 year olds, there was no significant difference in prevalence of current wheeze between cities, but for the 13-14 year olds prevalence was slightly higher in the western cities (Adelaide and Perth: 32.3%) than in the eastern cities (Sydney and Melbourne: 25.9%) (OR, 1.37; 95% CI, 1.26-1.48). There was a similar difference between west and east in percentage of 13-14 year olds who had had more than 12 episodes of wheeze per year (4.1% versus 3.1%) and who had attended the emergency department (3.5% versus 2.9%) (data not shown). The prevalence of current wheeze was generally higher in the older age group. The spectrum of asthma among children who reported current wheeze is shown in Box 4. While most children in both age groups reported only one to three asthma episodes in the previous 12 months, 8.0% of 6-7 year olds and 12.2% of 13-14 year olds reported more than 12 episodes. Sleep disturbance due to asthma was common, with 11.2% of 6-7 year olds and 9.8% of 13-14 year olds reporting sleep disturbance on one or more nights per week. About 7% of both age groups reported a hospital admission for asthma in the previous 12 months. Patterns of asthma treatment are shown in Box 5. Regular b2-agonists were taken as sole therapy by 5.5% of 6-7 year olds and 7.4% of 13-14 year olds with current wheeze, while regular inhaled steroids were taken by 21.1% of 6-7 year olds and 14.6% of 13-14 year olds, rising to 49.7% and 36.9% for those with more than 12 episodes per year. While overall 26.5% of 6-7 year olds with current wheeze and 15.8% of 13-14 year olds had a written asthma management plan, this increased to 46.5% and 25.9% in those who reported 12 or more attacks in the past 12 months. Most children attended a doctor at least once during a wheezy episode throughout the year, but only 42.2% of 6-7 year olds and 31.3% of 13-14 year olds visited a doctor for a regular check-up. Eczema Prevalence of current eczema did not vary significantly between the cities (Box 3). Eczema was less common in boys than in girls in both age groups (6-7 year olds: OR, 0.81; 95% CI, 0.72-0.92; 13-14 year olds: OR, 0.57; 95% CI, 0.51-0.65). Sleep disturbance due to itching was common among those with current eczema; it was reported to occur at least weekly by 7.9% of 6-7 year olds and 13.4% of 13-14 year olds, and at a lesser frequency by 27% of 6-7 year olds and 30.4% of 13-14 year olds. Allergic rhinitis The prevalence of current allergic rhinitis was significantly higher in Adelaide and Perth than in Sydney and Melbourne (6-7 year olds: OR, 1.62; 95% CI, 1.44-1.82; 13-14 year olds: OR, 1.53; 95% CI, 1.40-1.68). Like wheeze, rhinitis was more common in boys than girls in the younger group (boys versus girls: OR, 1.19; 95% CI, 1.06-1.33), while this sex difference was reversed in the older group (boys versus girls: OR, 0.64; 95% CI, 1.40-1.68). Among those with current rhinitis, 71% of 6-7 year olds and 76% of 13-14 year olds reported that it interfered with their daily activity to some extent (troublesome rhinitis), while 18.5% of 6-7 year olds and 19.1% of 13-14 year olds described this interference as moderate to "a lot". Atopic disease and country of birth Children born in Australia were more likely to report current wheeze than those born elsewhere (6-7 year olds: OR, 1.81; 95% CI, 1.54-2.14; 13-14 year olds: OR 1.89; 95% CI, 1.69-2.12). This trend was similar for children whose mothers were born in Australia compared with those whose mothers were born elsewhere (6-7 year olds: OR, 1.29; 95% CI, 1.18-1.42; 13-14 year olds: OR, 1.58; 95% CI, 1.45-1.71). When children born outside Australia were analysed by region of birth (United Kingdom, Central Europe, South-East Asia or the Middle East), there was no difference in the prevalence of wheeze between regions. Eczema and rhinitis were also more common in children born in Australia than those born elsewhere. For eczema the OR was 1.31 (95% CI, 1.06-1.63) for 6-7 year olds and 1.36 (95% CI, 1.14-1.61) for 13-14 year olds. For rhinitis, the OR was 1.79 (95% CI, 1.42-2.26) for 6-7 year olds and 1.5 (95% CI, 1.32-1.70) for 13-14 year olds. The proportion of children born outside Australia was higher in the eastern cities among 13-14 year olds (23%) than in the western cities (15%). Similarly, the proportion of mothers born outside Australia was higher in the eastern cities (54%) than in the western cities (39%). When the odds ratio comparing prevalence of wheeze among 13-14 year olds in western versus eastern cities was adjusted for child's country of birth, it fell from 1.37 to 1.25 (95% CI, 1.15-1.36). Interrelations of atopic diseases Figure 2 (below) shows the overlap of asthma, eczema and allergic rhinitis. While 35.2% of 6-7 year olds reported having at least one of these conditions in the past 12 months, only 1.8% reported having all three. Corresponding figures for 13-14 year olds were 41% with at least one condition and 2.8% with all three. Among those with current wheeze, only 19% of 6-7 year olds and 18% of 13-14 year olds reported coexistent current eczema, with no apparent age effect in the relationship. Discussion This study describes the burden of atopic disease in Australian schoolchildren. The prevalence of current wheeze was similar to that reported in recent epidemiological studies in Australia.10 However, comparison with results of a similar questionnaire given to Melbourne schoolchildren in 1990 suggests that, although the spectrum of asthma remains unchanged, the prevalence of recent wheeze has increased from 23.1% in 1990 (95% CI, 21.7-24.5)4 to 27.2% in 1993 (95% CI, 25.6-28.8) (P < 0.01). The rate of increase (1.4% per annum) is similar to that reported in an earlier Australian study (1.24%)10 and higher than that reported in European studies (0.1%-0.4%).1 Morbidity due to asthma remains significant, with high levels of symptoms, emergency department attendances and hospital admissions. Asthma is the second most common reason for admission to a paediatric hospital bed in Victoria (after otolaryngological conditions), with a rate in children of 738 per 100 000 population in 1994-1995.11 The total annual cost to the community associated with asthma management in Australia was estimated in 1989 as $627 million, or $769 per asthmatic person.12 These costs are likely to have increased because of the increases in medication costs and asthma prevalence. There was a significant difference in the prevalence of current wheeze and current rhinitis between the eastern and western States. A possible explanation is the difference in patterns of immigration, with more children in the eastern cities born outside Australia than in the western cities. Indeed, the odds ratio comparing prevalence of wheeze among 13-14 year olds in western versus eastern cities fell from 1.37 to 1.25 after adjustment for country of birth. Internationally, ISAAC has collected data on over half a million children from 120 centres in 48 countries. Australia ranks third-highest in prevalence of current wheeze for 13-14 year olds and second-highest for 6-7 year olds.13 For "current rhinitis", Australia ranks fifth and, for eczema, eleventh. Australia's high ranking for asthma prevalence is supported by data for asthma mortality. This was not collected by ISAAC, but comparison of available data from 11 developed countries shows Australia had the highest mortality rate due to asthma in 1990.14 We found evidence from throughout Australia for continuing lack of effective treatment of asthma. Among children with more than 12 episodes of wheeze per year, only 64% of 6-7 year olds and 43% of 13-14 year olds were taking regular preventive treatment. Further, 5.5% and 7.4% of those reporting "current wheeze" used regular b -agonists in the absence of any preventive therapy, despite the cumulative evidence against the practice. Sodium cromoglycate was used by 19% of the 6-7 year olds and 11% of the 13-14 year olds who reported taking regular preventive therapy, showing some support for the Australian paediatric asthma guidelines, which recommend cromoglycate as first-line therapy for mild to moderate persistent asthma.15 We also found eczema and rhinitis to be common and to cause significant morbidity among Australian schoolchildren. Eczema was less common in boys than in girls in both age groups, a trend seen throughout the world.16 It is not life-threatening, but may cause considerable physical and psychological disability (including discomfort from itching, which may result in sleep loss and secondary infection, as well as the psychological effects of a visible skin disease). Treatment can be expensive and time consuming. Recent Australian estimates of the cost to the family were $330 to $1255 a year, depending on eczema severity.17 Additional costs to the community for consultations ranged from $209 to $642 a year for each child. Allergic rhinitis also carries significant morbidity. The effect on quality of life of perennial rhinitis has been estimated to be similar to, or worse than, mild to moderate asthma.18 In adults, hayfever is estimated to cause, on average, the loss of a third of a day from work each year, in addition to loss of productivity through symptoms or the sedating effects of some drug treatments.18 There are no precise estimates for the cost of therapy, as many sufferers do not consult a medical practitioner,8 and most treatment is available "over the counter". The higher prevalence of "current wheeze" found among 13-14 year olds compared with 6-7 year olds should be interpreted with caution, as the respondents differed between the two groups (parents for the 6-7 year olds and the children themselves for the 13-14 year olds). In an earlier study of Melbourne 7-year-olds and 15-year-olds, in which parents completed the questionnaire for both age groups, prevalence of "current wheeze" was lower among the 15-year-olds (18.6%) than among the 7-year-olds (23.1%).4 Further, comparison of adolescent and parent responses to an Australian asthma morbidity questionnaire showed that the adolescents reported a higher incidence of symptoms than their parents.19 The correlation between the three atopic diseases was less than anticipated. Atopy is usually associated with increased serum levels of IgE and positive skin reactivity to common allergens and has a strong genetic basis. The factors that determine the phenotypic expression of atopy and direct it to asthma, eczema or hayfever are unclear. This diverse expression of the genotype needs to be considered when studying the genetics of asthma. In conclusion, Australia has a high prevalence of atopic disorders, ranking among the highest in the world. Our study, part of a much larger international study, provides an opportunity to gain new insights into the causes and natural history of these disorders. Acknowledgements We would like to thank the schools, parents and children who participated, the research assistants who helped collect the data, and the State departments of education that approved the study. In Adelaide, the study was supported by Rotary, in Perth by the Asthma Foundation of Western Australia, and in Melbourne and Sydney by internal department funds. References Magnus P, Jaakkola JJK. Secular trends in the occurrence of asthma among children and young adults: critical appraisal of repeated cross sectional surveys. BMJ 1997; 314: 1795-1799. Wuthrich B. Epidemiology and natural history of atopic dermatitis. Allergy Clin Immunol Int 1996; 83: 77-82. Asher I, Kiel U, Anderson HR, et al. International study of asthma and allergies in childhood (ISAAC): rationale and methods. Eur Resp J 1995; 8: 483-491. Robertson CF, Heycock E, Bishop J, et al. Changes in prevalence of asthma in Melbourne schoolchildren over 26 years. BMJ 1991; 302: 1116-1118. Peat JK, Toelle BG, Gray EJ, et al. Prevalence and severity of childhood asthma and allergic sensitisation is seven regions of New South Wales. Med J Aust 1995; 163: 22-26. Jenkins MA, Clarke JR, Carlin JB, et al. Validation of questionnaire and bronchial hyperresponsiveness against respiratory physician assessment in the diagnosis of asthma. Int J Epidemiol 1996; 25: 609-616. Williams HC, Burney PGJ, Pembroke AC, Hay RJ. Validation of the UK diagnostic criteria for atopic dermatitis in a population setting. Br J Dermatol 1996; 135: 12-17. Sibbald B, Strachan DP. Epidemiology of rhinitis. In: Busse WW, Holgate ST, editors. Mechanisms in asthma and rhinitis: implications for diagnosis and treatment. Oxford: Blackwell Scientific Publications, 1994: 32-43. Norusis MJ. SPSS/PC+ Advanced Statistics. V5.0 [computer program]. Chicago, Ill:SPSS Inc, 1992. Peat JK, van den Berg RH, Green WF, et al. Changing prevalence of asthma in Australian children. BMJ 1994; 308: 1591-1596. Information Analysis Unit, Acute Health, Victorian Department of Human Services. Victorian inpatient mordibity database. Melbourne: Department of Human Services. Sighted Oct 1997. Toelle BG, Peat JK, Mellis CM, Woolcock AJ. The cost of childhood asthma to Australian families. Pediatr Pulmonol 1995; 19: 330-335. Beasley R, Keil U, von Mutius E, et al. Worldwide variation in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis and atopic eczema: the international study of asthma and allergies in childhood (ISAAC). Lancet 1998. In press. Robertson CF, Sennhauser F, Mallol J. The change in prevalence and severity of asthma in developed and developing countries. Phelan PD (ed). Baillieres Clin Paediatr 1995; 3: 253-275. National Asthma Campaign. Asthma management handbook. 3rd edition. Melbourne: National Asthma Campaign, 1996. Williams HC, Robertson CF, Stewart AW, et al. Worldwide variation in the prevalence of symptoms of atopic eczema in the International Study of Asthma and Allergies in Childhood. J Allergy Clin Immunol 1998. In press. Su JC, Kemp AS, Varigos GA, Nolan TM. Atopic eczema: its impact on the family and financial cost. Arch Dis Child 1997; 76: 159-162. Juniper EF. Measuring health-related quality of life in rhinitis. J Allergy Clin Immunol 1997; 99: S742-S749. Bishop J, Robertson CF, Caust J, et al. Concordance between adolescent and parent response to an asthma morbidity questionnaire. Am Rev Respir Dis 1993; 147: A373. Received 30 Oct 1997, accepted 10 Mar 1998 Authors' details Department of Thoracic Medicine, Royal Children's Hospital, Melbourne. Colin F Robertson, MSc, FRACP, Deputy Director; Marita F Dalton, Assoc Dip Med Rec, Research Assistant. Department of Medicine, University of Sydney, Sydney. Jennifer K Peat, PhD, Senior Research Fellow; Michelle M Haby, MAppSc, Research Assistant. School of Community Medicine, University of New South Wales, Sydney. Adrian Bauman, PhD, FAFPHM, Associate Professor. Department of Respiratory Medicine, Women's and Children's Hospital, Adelaide. J Declan Kennedy, MD, FRCP, Physician. Department of Respiratory Medicine, Princess Margaret Hospital for Children, Perth. Louis I Landau, MD, FRACP, Professor of Paediatrics. Reprints will not be available from the authors. Correspondence: Dr C F Robertson, Department of Thoracic Medicine, Royal Children's Hospital, Flemington Road, Parkville, VIC 3054. E-mail: cfrobATcryptic.rch.unimelb.edu.au Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1998 Medical Journal of Australia.

Colin F Robertson · Marita F Dalton · Jennifer K Peat · Michelle M Haby · Adrian Bauman · Louis I Landau

Smoking -- time to ring the alarm bells again 1998 offers a golden opportunity for evolutionary tobacco control legislation MJA 1998; 168: 204-205 The mortality rate from tobacco-related disease remains inordinately high, with one Australian death every 30 minutes.1Hill, White and Scollo, in this issue of the Journal, report smoking rates of Australian adults for 1995 and look at trends in smoking prevalence over time.2 The 1995 figures show that, compared with the previous uniformly downward trend in smoking prevalence in Australia, there has been a disturbing stabilising in prevalence of smoking in both men and women. For other countries, comparative 1995 data are sparse, and, high mortality rates notwithstanding, Australian (and New Zealand) smoking rates are among the lowest on the international ladder, together with those of Sweden, Finland, the United Kingdom, the United States (especially California), and a small number of other exemplar countries or States. The average smoking rate for this group is about 25%-30% or less,3 and consistently measured data are available over a considerable period. Despite their similar smoking patterns, the countries and environments in which lower smoking rates have been achieved differ remarkably, making generalisation about the most effective tobacco control policies perilous. Australia began with health warnings in the early 1970s, and a patchwork quilt of State and federal laws to control advertising, which evolved (amid much controversy) into good, but not perfect, comprehensive federal legislation in 1992, with final implementation achieved only in 1996. We also have good research-based education programs. Finland and Sweden have had comprehensive legislation in place for two decades (which cannot, of course, prevent cross-border advertising) and have backed this up with competent education programs. California has spent very large amounts of money in recent years on well researched antismoking campaigns, which have been competing with vigorous and clever tobacco advertising (only radio and TV advertising is banned). At present, antismoking campaigns are being conducted amid enormous public debate.4 Mean smoking prevalence in 1995 was 16.7%.5 The United Kingdom can be best classified as having modest advertising controls and modest education programs. Although implementation of tobacco control policy has been somewhat erratic, there is historical and international agreement6 on the necessity for a comprehensive approach (including comprehensive legislation) which prohibits all forms of tobacco promotion, conducts public education campaigns, implements programs to help smokers to quit, restricts smoking in public places and sales to minors, and regularly increases prices. More recently, the emphasis has been on smoke-free workplaces, generic packaging and banning point-of-sale promotions. Probably the only generalisations possible are that no country has been successful in shielding its population from all tobacco advertising and that no country has consistently spent commercially large amounts of money on education over a significant period of time (such as amounts spent by Coca-Cola -- $30-$35 million nationally in Australia7 -- or the Victorian Traffic Accident Commission -- $24 million8). Meanwhile, the resilient and resourceful tobacco industry has responded to tobacco control by focusing increasingly on cross-border and global advertising and global brands. A topical example of global advertising -- Formula One car racing -- is illustrative. Excluded from the Australian prohibition on television and radio advertising in 1975 by a last-minute amendment9 which opened a suitable loophole, Grand Prix racing is still favoured by specific exclusion in 1998. Winfield, which otherwise may be advertised only at point of sale in Australia, is to be launched as a global brand in 1998 through Formula One, and will therefore be advertised back into Australia, as well as globally, by this means. One can only marvel at the tobacco industry's advertising ingenuity10 in using the kangaroo symbol, placing it on the red background of the new packet, and incidentally turning Qantas tailplanes into surrogate Winfield advertisements. Continued broadcasting of the tobacco-sponsored Grand Prix from the United Kingdom will occur until the year 2006. This decision was preceded by a controversial pre-election gift of £1 million to the British Labour Party by the key promoter of the Formula One Grand Prix,11 a feat which the public health fraternity will have difficulty matching. The Australian situation is indeed serious, and, as with the other developed industrialised countries mentioned, prevalence averages conceal both the better and the worse aspects of smoking habits -- all these countries have the same education and occupation gradients. Regardless of how impressive the low smoking prevalence of 18.7% (16.7% for women) is among the highest occupational level of Australian households, it is profoundly depressing to observe the prevalences of 40.9% and 31.8%, respectively, for the lowest occupational level, even though these blue collar levels have seen quite large falls over time. Clearly more effort is needed. Hill et al collated data on smoking prevalences and antismoking campaigns and found that the levelling off in previously declining prevalences is related to lower per capita expenditure on antismoking campaigns. The solution, in essence, requires renewed action on two major interrelated fronts. One is money; the other is legislation. Money need not be a problem. The popular principle of allocation of tobacco tax for health promotion purposes was established by the Victorian Tobacco Act 1987 (a world first), which established the Victorian Health Promotion Foundation (VicHealth). Similar Acts followed in Western Australia and South Australia. The original mandate of VicHealth included spending 30% of its then $28 million budget on sport, plus significant amounts on arts sponsorship and outdoor advertising, to buy out and replace the vested interests then advertising tobacco. This is no longer necessary, as federal legislation now consolidates advertising prohibition in these fields. As a consequence, in 1997, the Victorian Quit campaign received 10% of VicHealth's $23 million. Australian tobacco tax is low by UK and Scandinavian standards and should be increased. Lifting the Victorian Quit allocation from under $3 million to $12 million would equal about $3 per head of population, and would cost less than a packet of cigarettes per head. If followed by other States and matched by 1997 level federal expenditure a serious national campaign could be mounted. State (and possibly federal) tobacco legislation now requires rewriting, both because State tobacco licence fees have been declared unconstitutional and because national competition policy requires it.12 So, 1998 offers a golden opportunity to rewrite the prescription, and some evolutionary legislation is indeed timely: Generic packaging should be introduced; Sales to minors should be more effectively restricted and the restrictions implemented; Point-of-sale advertising should disappear; and Exemptions for international sporting events should be phased out over time, preferably in conjunction with similar action in the United States and Europe. Finally, enough is now known about nicotine-driven compensatory smoking13 and differential carcinogen levels in cigarette brands14 to legislate for control of nicotine content and to introduce, and progressively reduce, upper limits for specific carcinogens. New tobacco legislation is needed in 1998-99. It should be about tobacco, its control and the proper funding of programs to reduce its use and effects. Smoking prevalence and tobacco disease should then continue to decline. Nigel J Gray Consultant European Institute of Oncology, Milan, Italy English DR, Holman CDJ, Milne E, et al. The quantification of drug caused morbidity and mortality in Australia. 1995 edition. Canberra: Commonwealth Department of Human Services and Health, 1995. Hill DJ, White VM, Scollo MM. Smoking behaviours of Australian adults in 1995: trends and concerns. Med J Aust 1998; 168: 209-213. Tobacco or health: a global status report. Geneva: World Health Organization, 1997. Gray N. The global settlement -- a global view [editorial]. J Surg Oncol 1997; 66: 79-80. Glantz SA. Tobacco control in Australia: it's time to get back on top down under. Health Promot J Aust 1997; 7(1): 72-73. Gray NJ, editor. Lung cancer prevention: guidelines for smoking control. Geneva: Union International Contre le Cancer, 1997. Business Review Weekly 1997; Feb 7: 73. Victorian Traffic Accident Commission, Annual Report, Melbourne: VTAC, 1997. Gray NJ. Forty years of plotting for public health. Med J Aust 1997; 176: 587-589. Toy M-A. Outrage as Rothmans plans kangaroo label on cigarettes. The Age (Melbourne) 1998; Jan 17: 1. Morrison J. Row blights Blair's honeymoon. The Sunday Age (Melbourne) 1997; Nov 16: 15. Colebatch T. States' $5b tax rescue plan. The Age (Melbourne) 1997; Aug 6: A.1. Kozlowski LT, Ricket WS, Pope MA, et al. Estimating the yields to smokers of tar, nicotine and carbon monoxide from the lowest yield ventilated filter cigarettes. Br J Addict 1982; 77: 159-165. Hoffmann D, Hoffmann I. Tobacco consumption and lung cancer. In: Hansen HH, editor. Lung cancer. Advances in basic and clinical research. Dortrecht: Kluwer Academic Publications, 1994: 1-42. o - Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/>

Nigel J Gray