Risk factors for onset and remission of atopy, wheeze, and airway hyperresponsiveness.

BACKGROUND: Although many children with asthma may have a remission as they grow and other children who did not have asthma may develop asthma in adult life, knowledge about the factors that influence the onset and prognosis of asthma during adolescence and young adulthood is very limited. METHODS: A cohort of 8-10 year old children (n=718) living in Belmont, New South Wales, Australia were surveyed six times at 2 yearly intervals from 1982 to 1992, and then again 5 years later in 1997. From this cohort, 498 subjects had between three and seven assessments and were included in the analysis. Atopy, airway hyperresponsiveness (AHR), and wheeze in the last 12 months were measured at each survey. Late onset, remission, and persistence were defined based on characteristics at the initial survey and the changes in characteristics at the follow up surveys. RESULTS: The proportion of subjects with late onset atopy (13.7%) and wheeze (12.4%) was greater than the proportion with remission of atopy (3.2%) and wheeze (5.6%). Having atopy at age 8-12 years (OR 2.8, 95% CI 1.5 to 5.1) and having a parental history of asthma (OR 2.0, 95% CI 1.02 to 4.13) were significant risk factors for the onset of wheeze. Having AHR at age 8-12 years was a significant risk factor for the persistence of wheeze (OR 4.3, 95% CI 1.3 to 15.0). Female sex (OR 1.9, 95% CI 1.01 to 3.60) was a significant risk factor for late onset AHR whereas male sex (OR 1.9, 95% CI 1.1 to 2.8) was a significant risk factor for late onset atopy. CONCLUSIONS: The onset of AHR is uncommon during adolescence, but the risk of acquiring atopy and recent wheeze for the first time continues during this period. Atopy, particularly present at the age of 8-10 years, predicts the subsequent onset of wheeze.

Markers of airway inflammation and airway hyperresponsiveness in patients with well-controlled asthma.

In steroid-naive asthmatics, airway hyperresponsiveness correlates with noninvasive markers of airway inflammation. Whether this is also true in steroid-treated asthmatics, is unknown. In 31 stable asthmatics (mean age 45.4 yrs, range 22-69; 17 females) taking a median dose of 1,000 microg inhaled corticosteroids (ICS) per day (range 100-3,600 microg x day(-1)), airway responsiveness to the "direct" agent histamine and to the "indirect" agent mannitol, lung function (forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow (PEF)), exhaled nitric oxide (eNO), and number of inflammatory cells in induced sputum as a percentage of total cell count were measured. Of the 31 subjects, 16 were hyperresponsive to mannitol and 11 to histamine. The dose-response ratio (DRR: % fall in FEV1/cumulative dose) to both challenge tests was correlated (r=0.59, p=0.0004). However, DRR for histamine and DRR for mannitol were not related to basic lung function, eNO, per cent sputum eosinophils and ICS dose. In addition, NO was not related to basic lung function and per cent sputum eosinophils. In clinically well-controlled asthmatics taking inhaled corticosteroids, there is no relationship between markers of airway inflammation (such as exhaled nitric oxide and sputum eosinophils) and airway responsiveness to either direct (histamine) or indirect (mannitol) challenge. Airway hyperresponsiveness in clinically well-controlled asthmatics appears to be independent of eosinophilic airway inflammation.

The burden of asthma in Australia.

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.

Asthma in preschool children: prevalence and risk factors.

BACKGROUND: The prevalence of asthma in children has increased in many countries over recent years. To plan effective interventions to reverse this trend we need a better understanding of the risk factors for asthma in early life. This study was undertaken to measure the prevalence of, and risk factors for, asthma in preschool children. METHODS: Parents of children aged 3-5 years living in two cities (Lismore, n=383; Wagga Wagga, n=591) in New South Wales, Australia were surveyed by questionnaire to ascertain the presence of asthma and various proposed risk factors for asthma in their children. Recent asthma was defined as ever having been diagnosed with asthma and having cough or wheeze in the last 12 months and having used an asthma medication in the last 12 months. Atopy was measured by skin prick tests to six common allergens. RESULTS: The prevalence of recent asthma was 22% in Lismore and 18% in Wagga Wagga. Factors which increased the risk of recent asthma were: atopy (odds ratio (OR) 2.35, 95% CI 1.49 to 3.72), having a parent with a history of asthma (OR 2.05, 95% CI 1.34 to 3.16), having had a serious respiratory infection in the first 2 years of life (OR 1.93, 95% CI 1.25 to 2.99), and a high dietary intake of polyunsaturated fats (OR 2.03, 95% CI 1.15 to 3.60). Breast feeding (OR 0.41, 95% CI 0.22 to 0.74) and having three or more older siblings (OR 0.16, 95% CI 0.04 to 0.71) decreased the risk of recent asthma. CONCLUSIONS: Of the factors tested, those that have the greatest potential to be modified to reduce the risk of asthma are breast feeding and consumption of polyunsaturated fats.

Eosinophilia, interleukin-5, and tumour necrosis factor-alpha in asthmatic children.

BACKGROUND: There are few paediatric studies of the interrelationships between inflammatory markers and asthma severity. We therefore assessed the relationships between eosinophil-associated markers, cytokines, and asthma severity in asthmatic children aged 8-12 years. METHODS: Forty-five children were tested twice, 2 weeks apart. Asthma severity was measured in terms of symptoms, lung function, medication needs, and histamine responsiveness. Peripheral inflammatory markers measured included eosinophil numbers, serum ECP, IL-5, and TNF-alpha and mononuclear cell IL-5, and TNF-alpha production. RESULTS: Histamine responsiveness was correlated with circulating eosinophils (r = 0.56, P = 0.0001) and serum ECP (r = 0.54, P = 0.003). Eosinophilia was increased in children with severe as opposed to mild airway hyperresponsiveness (P = 0.02) and those who lost days at school as opposed to those who did not (P = 0.01). There were no other associations between markers of asthma severity and inflammation. Children taking inhaled corticosteroids had lower serum IL-5 levels than those on beta-agonists +/- cromolyn (mean and 95% CI: 20.5 [11.7-35.7] pg/ml vs 64.3 [26.6-155.4] pg/ml; P = 0.04). Cellular IL-5 production correlated with serum TNF-alpha (r = 0.63, P = 0.0062) and IL-5 (r = -0.59, P = 0.005). CONCLUSION: Serum levels of TNF-alpha and IL-5 were not related to peripheral eosinophilia and asthma severity in these children but were related to their own cellular production ex vivo. This study confirms that eosinophilia is the index of inflammation that is most closely related to the clinical severity of childhood asthma.

Predictive markers of asthma exacerbation during stepwise dose reduction of inhaled corticosteroids.

To determine predictors for failed reduction of inhaled corticosteroids (ICS), in 50 subjects with well-controlled asthma (age 43.7 [18-69]; 22 males) taking a median dose of 1,000 microg ICS/d (100-3,600 microg/d), ICS were halved every 8 wk. Airway hyperresponsiveness (AHR) to a bronchial provocation test (BPT) with histamine was measured at baseline. AHR to BPT with mannitol, spirometry, exhaled nitric oxide (eNO), and, in 31 subjects, sputum inflammatory cells were measured at baseline and at monthly intervals. Thirty-nine subjects suffered an asthma exacerbation. Seven subjects were successfully weaned off ICS. Using a Kaplan- Meier survival analysis, the significant predictors of a failure of ICS reduction were being hyperresponsive to both histamine and mannitol at baseline (p = 0.039), and being hyperresponsive to mannitol during the dose-reduction phase of the study (p = 0.02). Subjects older than 40 yr of age tended to be at greater risk of ICS reduction failure (p = 0.059). Response to mannitol and percentage sputum eosinophils were significantly greater before a failed ICS reduction than before the last successful ICS reduction, whereas there were no significant differences in symptoms, spirometry, or eNO. These findings suggest that documentation of patient's AHR or sputum eosinophils may be useful in guiding the reduction of ICS doses.

Obesity is a risk for asthma and wheeze but not airway hyperresponsiveness.

BACKGROUND: A study was undertaken to assess whether the recent increases in prevalence of both asthma and obesity are linked and to determine if obesity is a risk factor for diagnosed asthma, symptoms, use of asthma medication, or airway hyperresponsiveness. METHODS: Data from 1971 white adults aged 17-73 years from three large epidemiological studies performed in NSW were pooled. Doctor diagnosis of asthma ever, history of wheeze, and medication use in the previous 12 months were obtained by questionnaire. Body mass index (BMI) in kg/m(2) was used as a measure of obesity. Airway hyperresponsiveness (AHR) was defined as dose of <3.9 micromol histamine required to provoke a fall in forced expiratory volume in one second (FEV(1)) of 20% or more (PD(20)FEV(1)). Adjusted odds ratios (OR) were obtained by logistic regression. RESULTS: After adjusting for atopy, age, sex, smoking history, and family history, severe obesity was a significant risk factor for recent asthma (OR 2. 04, p=0.048), wheeze in the previous 12 months (OR 2.6, p=0.001), and medication use in the previous 12 months (OR 2.83, p=0.005), but not for AHR (OR 0.87, p=0.78). FEV(1) and forced vital capacity (FVC) were significantly reduced in the group with severe obesity, but FEV(1)/FVC ratio, peak expiratory flow (PEF), and mid forced expiratory flow (FEF(25-75)) were not different from the group with normal BMI. The underweight group (BMI <18.5 kg/m(2)) had increased symptoms of shortness of breath, increased airway responsiveness, and reduced FEV(1), FVC, PEF, and FEF(25-75) with similar use of asthma medication as subjects in the normal weight range. CONCLUSIONS: Although subjects with severe obesity reported more wheeze and shortness of breath which may suggest a diagnosis of asthma, their levels of atopy, airway hyperresponsiveness, and airway obstruction did not support the suggestion of a higher prevalence of asthma in this group. The underweight group appears to have more significant respiratory problems with a higher prevalence of symptoms, reduced lung function, and increased airway responsiveness without an increase in medication usage. This group needs further investigation.

Optimal asthma control, starting with high doses of inhaled budesonide.

The aim of this study was to determine whether outcomes in poorly controlled asthma can be further improved with a starting dose of inhaled budesonide higher than that recommended in international guidelines. The study had a parallel-group design and included 61 subjects with poorly controlled asthma, randomized to receive 3,200 microg or 1,600 microg budesonide daily by Turbuhaler for 8 weeks (double-blind), then 1,600 microg x day(-1) for 8 weeks (single-blind), followed by 14 months of open-label budesonide dose down-titration using a novel algorithm, with a written asthma crisis plan based on electronic peak expiratory flow monitoring. The primary outcome variable for weeks 1-16 was change in airway hyperresponsiveness (AHR), and, for the open-label phase, mean daily budesonide dose. By week 16, there were large changes from baseline in all outcomes, with no significant differences between the 3,200- and 1,600-microg x day(-1) starting dose groups (AHR increased by 3.2 versus 3.0 doubling doses, p=0.7; morning peak flow increased by 134 versus 127 L x min(-1), p=0.8). Subjects starting with 3,200 microg x day(-1) were 3.8 times more likely to achieve AHR within the normal range, as defined by a provocative dose of histamine causing a 20% fall in forced expiratory volume in one second (PD20) of > or = 3.92 micromol by week 16 (p=0.03) [corrected]. During dose titration, there was no significant difference in mean budesonide dose (1,327 versus 1,325 microg x day(-1), p>0.3). Optimal asthma control was achieved in the majority of subjects (at completion/withdrawal: median symptoms 0.0 days x week(-1), beta2-agonist use 0.2 occasions x day(-1), and PD20 2.4 micromol). In subjects with poorly controlled asthma, a starting dose of 1,600 microg x day(-1) budesonide was sufficient to lead to optimal control in most subjects. The high degree of control achieved, compared with previous studies, warrants further investigation.

Salmeterol/fluticasone propionate combination therapy 50/250 microg twice daily is more effective than budesonide 800 microg twice daily in treating moderate to severe asthma.

Three hundred and fifty-three asthmatic patients who remained symptomatic despite treatment with budesonide 800-1200 microg day(-1) (or equivalent) were randomized to a new combination therapy comprising salmeterol 50 microg and fluticasone propionate 250 microg (Seretide, Advair, Viani 50/250 microg) twice daily or budesonide 800 microg twice daily for 24 weeks. Patients kept daily records of their morning and evening peak expiratory flow (PEF), daytime and night-time symptom scores and daytime and night-time use of rescue salbutamol. Mean morning PEF increased by 451 min(-1) (baseline 361 l min(-1)) in the salmeterol/fluticasone propionate combination (SFC) group and by 19 l min(-1) (baseline 358 l min(-1)) in the budesonide group over the 24 weeks. The adjusted mean morning PEF over weeks 1 to 24 was significantly greater in the SFC group, despite the > three-fold lower corticosteroid dose (406 vs. 380 l min(-1); P < 0.001). A significantly greater improvement in evening PEF was also seen in the SFC group (adjusted mean 416 vs. 398 l min(-1); P<0.001). SFC also provided significantly better control of daytime symptoms and a significantly greater reduction in the requirement for rescue salbutamol compared with budesonide. These results demonstrate that SFC 50/250 microg twice daily is superior to budesonide 800 microg twice daily in the management of patients with moderate to severe asthma who are symptomatic on their existing dose of corticosteroid.

The effect of insecticide aerosols on lung function, airway responsiveness and symptoms in asthmatic subjects.

The object of this study was to compare the effect of standard and "low irritant" insecticide aerosols on lung function, airway hyperresponsiveness (AHR) and symptoms in asthmatic subjects. A double blind randomized, crossover study was conducted in 25 asthmatic subjects who reported sensitivity to insecticide aerosols. All subjects were exposed for 30 min, on separate occasions, to two standard insecticide formulations (A and B), one low irritant formulation (C) and a negative control aerosol. Spirometric function and chest, nose and eye symptoms were recorded during, and for 90 min after, the exposure. AHR to methacholine was measured 90 min after the exposure. Compared to the negative control, the maximum fall in forced expiratory volume in one second (FEV1) was slightly greater after standard insecticides (mean differences from control +/-95% confidence interval: aerosol A, 3.3+/-3.6%, p=0.08; aerosol B, 5.1+/-4.7%, p=0.04), AHR was significantly more severe (mean difference from control: aerosol A, 0.35+/-0.29 doubling doses, p=0.028; aerosol B, 0.52+/-0.43 doubling doses, p=0.028), and symptoms were more severe. The low irritant test aerosol (C) did not differ significantly from the negative control with respect to FEV1, AHR or symptoms. It is concluded that some insecticide aerosols trigger symptoms and falls in lung function in some people with asthma. Furthermore, these aerosols may also increase airway hyperresponsiveness, although the mechanism of this effect has not been determined. The low irritant formulation did not appear to have the same effects.

Lung function growth and its relation to airway hyperresponsiveness and recent wheeze. Results from a longitudinal population study.

To evaluate the association between growth in height and growth in lung function, and to identify the potential temporal relationships between airway hyperresponsiveness (AHR), respiratory symptoms, and lung function growth during adolescence and young adulthood, we analyzed data collected from the Belmont cohort. Among the 718 schoolchildren initially studied at 1982 (aged 8-10 yr), 557 were studied between two times and six times at 2-yr intervals until 1992. Baseline lung function, AHR by histamine inhalation test, and recent wheeze by questionnaires, were measured at each visit. We found that between 17 and 19 yr of age, when growth in height had stopped, growth in FEV(1) was approximately 200 ml/yr in boys and 100 ml/yr in girls. Peak growth velocity of height occurred at age 13 both in boys and in girls, whereas peak growth velocity of FEV(1) occurred at the same age only in girls and 1 yr later in boys. Having AHR and recent wheeze at the previous study time were both associated with lower subsequent growth in FEV(1), but not with subsequent growth in FVC. We conclude that lung function continues to grow after the cessation of height growth and that growth in FEV(1) is reduced in subjects with AHR and/or recent wheeze.

Family patterns of asthma, atopy and airway hyperresponsiveness: an epidemiological study.

BACKGROUND: The patterns of inheritance of asthma have largely been explored using data of symptom history collected by questionnaires which are subject to bias and which may therefore distort the measured relationship. OBJECTIVE: The purpose of this study was to examine family patterns of allergic disease using objective measurements of atopy and of airway hyperresponsiveness (AHR). METHODS: A large random sample of children aged 8-11 years was studied and 3 months later, their parents were also invited for study. Of the sample of 1655 children, both parents of 661 children were studied. In all subjects, respiratory illness history was measured by questionnaire, atopy by skin tests and AHR by responsiveness to histamine. RESULTS: The odds ratio for a child to have AHR if either parent had the same condition was approximately 2. 0, which was the same as the odds ratio for wheeze or diagnosed asthma in the presence of the same condition in either parent. The odds ratio for atopy was smaller (approximately 1.4, NS) but the risk of a nonatopic child having AHR if the parent had AHR was 3.0 (P = 0.01). The correlation between weal size in the child and parent was poor and the severity of AHR in the child was only modestly correlated with the severity of AHR in the parent (R = 0.51, P = 0.04). CONCLUSION: The use of objective measurements did not strengthen the association between atopic or asthmatic conditions in the parent and child, but did suggest that atopy and AHR are inherited independently.

Do subjects with asthma have greater perception of acute bronchoconstriction than smokers with airflow limitation?

OBJECTIVE: Smokers who develop chronic airflow limitation (CAL) do not usually present for medical attention until their lung disease is well advanced. In contrast, asthmatic subjects experience acute symptoms and present for care early in the course of their disease. The aim of this study was to determine whether subjects with asthma differ from smokers with CAL in their ability to perceive acute methacholine-induced bronchoconstriction. METHODOLOGY: Thirteen subjects with diagnosed asthma and 10 current smokers with CAL, defined as forced expiratory volume in 1 s (FEV1) < 75% predicted and FEV1/forced vital capacity < 80%, with no previous diagnosis of asthma, were challenged with methacholine. Symptom severity was recorded on a Borg scale. Lung volumes were measured before challenge and after the FEV1 had fallen by 20%. RESULTS: After methacholine falls in FEV1 were similar in the asthmatic subjects and smokers. The regression lines relating change in FEV1 to symptom score were significantly steeper in asthmatic subjects than smokers (0.13 +/- 0.04, 0.03 +/- 0.04, respectively, P < 0.01). At 20% fall in FEV1 there were no significant differences between asthmatic subjects and smokers in the magnitude of change of lung volumes. CONCLUSIONS: In asthmatic subjects, symptoms are closely related to change in FEV1. In smokers with CAL, symptoms change little during bronchial challenge despite large changes in FEV1. The differences in perception between the two subject groups are not due to differences in acute hyperinflation during challenge. We propose that heavy smokers may adapt to poor lung function, or may have damaged sensory nerves as a result of prolonged cigarette smoking.

Prevalence of atopy, asthma symptoms and diagnosis, and the management of asthma: comparison of an affluent and a non-affluent country.

BACKGROUND: The prevalence of childhood asthma and of atopy varies widely between countries. However, few studies have compared the pattern of diagnosis and management of asthma, or the role of atopy in predisposing to asthma between a less affluent country and a more affluent country. The aim of this study was to compare the prevalence of symptoms, diagnosis, and management of asthma, and the prevalence of atopy as measured by skin prick tests in Nigeria and Australia using a standardised methodology. METHODS: Respiratory history was collected using a validated questionnaire administered to parents, and atopy was measured with skin prick tests in 654 Australian and 566 Nigerian children aged 8-11 years (70% consent rate in Australia, 60% in Nigeria). RESULTS: Wheeze and persistent cough were less prevalent in Nigeria (10.2% and 5.1%, respectively) than in Australia (21.9% and 9.6%, respectively), caused less morbidity, and were less likely to be labelled or treated as asthma than in Australia. There was no significant difference in the overall prevalence of atopy between the two countries (Australia 32. 5%, Nigeria 28.2%). Atopy was a strong risk for wheeze in both countries (odds ratio (OR) 3.4 (95% CI 2.3 to 5.1) in Australia, 1.8 (95% CI 1.0 to 3.3) in Nigeria), especially atopy to house dust mites (OR 3.1 (95% CI 2.1 to 4.7) in Australia, 2.4 (95% CI 1.3 to 4. 3) in Nigeria). CONCLUSION: Although there was a similar prevalence of atopy in both countries, Australian children had a higher prevalence of asthma symptoms. Further studies are needed to determine why atopic children in Australia are more at risk of developing asthma. Such studies will have important implications for the prevention of asthma.

Perception of bronchodilation in subjects with asthma and smokers with airflow limitation.

Perception of the efficacy of bronchodilators in relieving airflow obstruction is a likely determinant of compliance with treatment in patients prescribed these drugs on an 'as needed' basis. This study aimed to determine whether bronchodilator-induced improvements in lung function are associated with improvements in breathing difficulty in subjects with asthma or smokers with airflow limitation. Twenty smokers with airflow limitation and 16 subjects with previously physician-diagnosed asthma received salbutamol (200 micrograms) and ipratropium bromide (80 micrograms). Spirometry and lung volumes were measured before and 40 min after bronchodilator. Subjects recorded changes in 'difficult breathing' on a visual analogue scale (VAS). After bronchodilator, forced expiratory volume in 1 s (FEV1) increased by 23.0 +/- 6.4% of baseline (mean +/- 95% CI) in smokers, and by 25.2 +/- 8.5% in the asthmatics, while VAS improved by 31 +/- 23% in smokers and 45 +/- 25% in asthmatics. However, these changes were not significantly correlated in either smokers (r = -0.04) or asthmatics (r = 0.15). In the asthmatic subjects, good perceivers (> 25% improvement in VAS) had greater improvements in lung volumes, as percentage predicted, than did poor perceivers. In the smokers, changes in lung function did not differ significantly between good and poor perceivers. Improvement in FEV1, as percentage predicted, was significantly correlated with improvement in VAS in good perceivers (asthma: r = 0.78, P < 0.01; smokers: r = 0.68, P < 0.05), but not in poor perceivers. Asthmatic subjects had good perception of improvements in lung function. However, in smokers with airflow limitation there is little correlation between improvement in lung function and sensation of breathing difficulty. In these subjects symptoms appear to be an unreliable guide for 'as needed' use of bronchodilators.

Exhaled nitric oxide measurements in a population sample of young adults.

In epidemiologic studies of asthma there is a group with recent wheeze, but with no airway hyperresponsiveness (AHR), in whom it is unclear whether any significant airway abnormality exists. Exhaled nitric oxide (NO) has been proposed as a measure of airway inflammation. We measured exhaled NO in a population sample of 306 young adults who also underwent bronchial challenge with histamine or a bronchodilator test. Subjects blew into a 3-L Tedlar bag against a 2-mm-diameter resistance to close the soft palate and exclude nasal air. The NO content of expired gas from a single breath was analyzed by chemiluminescent analyzer. Exhaled NO was log-normally distributed in the population sample and duplicate measurements were highly reproducible (intraclass correlation coefficient = 0.98). Exhaled NO correlated significantly with airway responsiveness, measured as the dose-response ratio to histamine (r = 0.39, p < 0.001) and with peripheral blood eosinophils (r = 0.35, p < 0.001). Exhaled NO was significantly greater in asthmatic subjects (geometric mean, 22.2; 95% confidence intervals, 16.1 to 30. 7 ppb) than in normal subjects (7.8, 7.1 to 8.4, p < 0.001) or in subjects with wheeze but no AHR (8.8, 7.5 to 10.3, p < 0.001). We conclude that exhaled NO is log-normally distributed, is highly reproducible and discriminates well among subjects, suggesting that it is both a feasible and useful measurement for epidemiologic studies of asthma. The findings suggest that wheeze in the absence of AHR is unlikely to be associated with airway inflammation.

Measuring persistent cough in children in epidemiological studies: development of a questionnaire and assessment of prevalence in two countries.

STUDY OBJECTIVE: Cough is a common symptom in children that is frequently encountered in general practice. However, most of the information on the prevalence of persistent cough has come from studies that use different, often ambiguous, definitions for persistent cough. It is therefore important that a validated questionnaire to accurately measure persistent cough is developed and is appropriate for use in different age groups of children and in different cultures. Such a questionnaire is essential for accurately measuring the prevalence of persistent cough and the factors associated with its occurrence. DESIGN: A parent-administered respiratory questionnaire was developed and administered twice during a 3-week interval pilot study to test repeatability. The questionnaire was then administered to a randomly selected cross-section of Australian children aged 5 to 7 years old and 8 to 11 years old (N = 511 and N = 654, respectively), and to 566 Nigerian children aged 8 to 11 years old. RESULTS: The new questionnaire was reliable, with most of the questions having a kappa value of above 0.6. The prevalence of persistent cough was similar in younger and older Australian children, but significantly less in Nigerian children (p < 0.001). Also, persistent cough was more prevalent in children of high rather than low socioeconomic status among older Australian children (p = 0.04). CONCLUSIONS: The newly developed questionnaire will be an important tool in epidemiological studies for measuring the prevalence, morbidity, and risk factors of persistent cough in childhood. Although our findings showed that persistent cough does not occur more frequently in younger than in older Australian children, it is more frequent in Australian than in Nigerian children.

The message from the World Asthma Meeting. The Working Groups of the World Asthma Meeting, held in Barcelona, Spain, December 9-13, 1998.

The 1998 World Asthma Meeting (WAM) has been the first multidisciplinary event aimed to consider asthma as a global public health problem in children and adults. The purpose of the meeting was to present state-of-the-art scientific information and to make recommendations on the research agenda for the coming years. Five Working Groups of invited experts were appointed to pin-point the established knowledge and the important questions in the areas of epidemiology, prevention, pathogenesis, management, and education. Their reports were discussed during the final plenary session, and are forming the current proceedings of the meeting. The message of the World Asthma Meeting provides a research agenda supported by the major international bodies involved in this disease. An integrated approach is considered to be essential in order to improve the prevention and care of asthma in all countries of the world.