Respiratory disease

Smoking behaviours of Australian adults in 1995: trends and concerns David J Hill, Victoria M White and Michelle M Scollo MJA 1998; 168: 209-213 For editorial comment see Gray Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - ©MJA1998 Abstract Objectives: To estimate the prevalence of smoking among Australian men and women in 1995 and to examine trends in smoking prevalence in Australia over the past 10 years. Design: A representative sample of adults participated in face-to-face interviews conducted by a large market research company. Participants: 2819 men and 2880 women over the age of 16. Main outcome measure: Self-reported smoking behaviours assessed by standard questions. Results: Overall, 27.1% of men and 23.2% of women were smokers of tobacco (factory-made cigarettes, pipes, cigars or roll-your-own cigarettes). This difference in smoking prevalence of men and women was significant. More men (32.1%) than women (21.7%) were past smokers and more women (53.4%) than men (39.3%) had never been regular smokers. On average, male smokers smoked about 20 factory-made cigarettes a day, while women smoked about 18. Occupation and education levels were inversely related to smoking prevalence. Comparisons with earlier data suggest that the decline in smoking prevalence seen in previous surveys has ceased. However, the number of cigarettes consumed daily decreased between 1992 and 1995. In the period between 1983 and 1989, when per capita expenditure on adult antismoking campaigns rose, smoking prevalence declined, but levelled off thereafter in a period when expenditure on campaigns fell. Conclusion: Failure to find a continuing decline in prevalence of smoking among the Australian population is of great concern and indicates the importance of continuing and extending antismoking programs. Introduction Cigarette smoking is still the most important preventable cause of premature death in Australia. Reducing the prevalence of smoking rightly remains a high priority on Australia's public health agenda.1,2 As such, it is important to collect and publish estimates of the prevalence of smoking and its sociodemographic correlates at regular intervals, as indicators of progress towards controlling the virtual epidemic of tobacco-related disease,3 and as a basis for public decisions on action to take. We have published data on national smoking prevalence for the years 1974,4 1976,5 1980,6 1983,7 1986,8 19899 and 1992,10 using a standard method of data collection. Here we report data for 1995. Methods Survey method: A large market research company carried out the sampling and interviewing as part of an omnibus survey in September/October 1995. Procedures were the same as in our previous surveys. In brief, interviews were conducted on the weekend, with respondents within a census collector's district selected at random within specified strata, including State and rural or urban divisions. Within each collector's district an individual residence was chosen at random for the first contact and the adjacent house was contacted next. Further adjacent households were approached until the required number of interviews for that collector's district were obtained (usually eight from about 200 households in each census collector's district). Response rate: Of the households contacted 47% agreed to participate in the survey, 42% refused, and in the remaining 11% either the residents were too old or ill or could not speak English, or call-back was unsuccessful. The response rate for this survey was similar to the rates for the 1992 and 1989 surveys, but it was lower than response rates in earlier years. Thus, if variable response rates influence reported prevalences, this could only have occurred for the period before 1989; recent comparisons are not confounded by response rates. Data collected: Respondents indicated their smoking status by choosing a category from the following list: Current smoker -- cigarettes only, cigarettes plus cigars or pipes, cigars only (ex-cigarettes), pipes only (ex-cigarettes), cigars only (never cigarettes), or pipes only (never cigarettes); Past smoker -- of cigarettes only, of cigarettes plus pipe or cigar, of cigars or pipes only; and Never smoker -- those who had never smoked regularly. Current smokers of factory-made cigarettes indicated the brand usually smoked, the size of the pack usually bought and the number of cigarette packets usually smoked in a week. Respondents' sex, age (in five-year age groups), country of birth, highest level of education achieved, and occupation were recorded, as well as the occupation of the household's main income earner. Analysis of data: We calculated 95% confidence intervals (95% CI) associated with estimates of smoking prevalence among men and women and the difference between estimates. Confidence intervals around prevalence estimates for particular subgroups (eg, men aged 50-59 years) are not given. We used chi-squared tests of association to examine differences in the prevalence of smoking between groups, and logistic regression analyses to explore whether associations between smoking prevalence, educational level, occupation and, for women, country of birth were independent of associations between age and smoking. We used analyses of variance and t tests to examine whether the mean number of cigarettes smoked differed between groups. Finally, to compare the prevalence of smoking across recent years, we age-standardised the data from the 1995, 1992 and 1989 surveys to the age distribution of the 1986 sample. Results Smoking status: Of the 5699 participants, 51% (2880) were women and 49% (2819) were men. A comparison of the distributions of age, occupation, education and country of birth in the sample data with those in the census data indicated no bias in the socio demographic variables in the dataset. Eighty-two per cent of respondents were interviewed on the first visit to their home. The smoking status of these respondents was similar to that of the more hard-to-reach respondents (those who were interviewed on the second or third contact). Cigarettes dominated tobacco use, with only 1% of men and less than 1% of women indicating that they smoked only pipes or cigars. Only 8% of men and 4% of women had smoked roll-your-own cigarettes in the month before the survey. The smoking status of the males and females in the sample is shown in Table 1. Smoking prevalence: In 1995, the estimated prevalence of smoking among Australian men aged 16 years and over was 27.1% (95% CI, 25.6%-28.7%), while among women the prevalence was estimated to be 23.2% (95% CI, 21.7%-24.7%); this difference was significant (3.9%; 95% CI, 1.6%-6.2%). The prevalence of smoking peaked between the ages of 25 and 29 in men (34.7%) and in women (35%), after which age smoking generally decreased among both men and women. Past smoking or non-smoking: More men (32.1%; 95% CI, 30.4%-33.8%) than women (21.7%; 95% CI, 20.2%-23.2%) were past smokers, a highly significant difference (10.4%; 95% CI, 8.1%-12.7%). More women (53.4%; 95% CI, 51.6%-55.2%) than men (39.3%; 95% CI, 37.5%-41.1%) had never been regular smokers, and again this difference was highly significant (14.1%; 95% CI, 11.5%-16.7%). Men and women differed in their age-related patterns of past smoking. Among men, the proportion of past smokers increased with age to reach a peak of 54.4% in those over 70. Although among women the proportion of past smokers peaked at 26% for those over 70, the proportion of past smokers in the other age groups showed little variation from the overall rate of 21.7%. The proportion who had ever smoked was calculated by adding the percentage of those who had smoked in the past to the percentage of current smokers. Overall, 59.2% (95% CI, 57.4%-61.0%) of men and 44.9% (95% CI, 43.1%-46.7%) of women had smoked at some stage in their life. The association between age and ever having smoked differed for men and women. While among men the proportion who had ever smoked increased with increasing age, for women the proportions of ever smokers began to decrease after the age of 35. Quit proportions: The quit proportion (ie, proportion of ever smokers who had given up smoking in each age and sex group) is also shown in Table 1. The overall quit proportion for men (0.54) was slightly higher than that among women (0.48). However, as Table 1 shows, there is little difference in the quit proportions for men and women in most age groups, except for the 16 to 19 years and 60 to 69 years age groups. Factory-made cigarettes: The mean number of factory-made cigarettes smoked per day by smokers was 19.7 (SD, 11.6) for men and 18.1 (SD, 10.8) for women; this difference was statistically significant (t=2.55, df=1238, P=0.01). In 1995, the cigarettes smoked by women had a lower average tar content than the cigarettes smoked by men (t=5.56, df=1022, P<0.001). The average tar content of cigarettes smoked by men was 8.2 mg (SD, 2.8), while for women it was 7.2 mg (SD, 3.0). Education: As in previous reports of this survey series, the prevalence of smoking and the mean number of cigarettes smoked per day differed for people in various sociodemographic groups. As Table 2 shows, smoking prevalence decreased with increased education, so that only 17.0% of men and 14.2% of women who were university graduates smoked. The association between education level and smoking prevalence was significant for both sexes, but was stronger for men (chi-squared=91.3, df=6, P<0.001) than women (chi-squared=35.5, df=6, P<0.001). The proportions of ex-smokers in the different education levels indicate that quitting was common in all groups. However, the greater proportion of never smokers in the better-educated groups indicates that the lower prevalence of smoking among this group was due to their never having smoked in the first place. For both men and women, smokers with more years of formal education smoked fewer cigarettes per day than did those who had fewer years of education (men: F3,618 = 3.15, P<0.05; women: F3,614=8.92, P<0.001). Occupational levels: Respondents were classified into one of four occupation levels based on the occupation of the household's main income earner. Occupational levels differed in the level of skill required for the job, such that unskilled workers (eg, labourers) were classified as "lower blue collar", while skilled workers (eg, plumbers) were classified as "upper blue collar". As occupation status increased, the prevalence of smoking decreased (Table 2). Among men from "upper white collar" households, 18.7% smoked compared with 40.9% of men from "lower blue collar" households. The association between occupation status and smoking was significant for both men (chi-squared=102.3, df=6, P<0.001) and women (chi-squared=46.8, df=6, P<0.001). Among men, the proportion of ex-smokers was slightly lower among "lower blue collar" households than other groups . Among women, the proportion of ex-smokers was similar among all occupation groups. The proportion of never smokers was greatest among higher occupation levels. This pattern of results indicates that the lower prevalence of smoking seen in higher occupation groups is due to the relatively lower rate of taking up smoking among these groups rather than their greater success at quitting. The differences in the mean number of cigarettes consumed per day between occupation groups was not statistically significant for men (F3,618 = 2.0, P=0.12) or women (F3,614=1.4, P=0.24). Country of birth: The prevalence of smoking was lowest among both men and women born in Asian countries. However, while the prevalence of 19.8% among Asian-born men was not significantly different from that found for groups born elsewhere, the prevalence of smoking among Asian-born women was significantly lower than the prevalence of smoking among women born in Australia (chi-squared=7.2, df=1, P<0.01) or the United Kingdom (chi-squared=6.6, df=1, P<0.01). The number of cigarettes smoked per day showed little variation according to place of birth. The overall association between place of birth and cigarette consumption was not significant for either men (F4,617=1.3, P=0.26) or women (F4,614=1.0, P=0.40). However, Asian-born men consumed significantly fewer cigarettes per day than did men born elsewhere (t=2.14, df=620, P<0.05). Logistic regression analyses of demo graphic data: In separate analyses, age was entered before the predictor variable of education level, occupational status or country of birth (for women only), and in each case the association between smoking prevalence and the predictor variable remained significant. Pack size and number of cigarettes smoked: The cigarette packet size most commonly used was 25 (by 36% of smokers), followed by packets of 30 and 40 (19% each), 50 (17%), 20 (6%) and 35 (4%). The number of cigarettes smoked per day was related to packet size (F5,1205=34.93, P<0.001). The mean number of cigarettes smoked per day by those who used packets of 20 was 13, for packets of 25 it was 16, for packets of 30 it was 17, for packets of 40 the mean was 23, and for packets of 50 it was 25. Except for women from lower blue collar households, the packet of 25 cigarettes was the most popular size for all occupation and education groups. After collapsing pack-size categories and combining sexes, 55% of blue collar smokers used pack sizes of 20, 25 or 30 compared with 68% of white collar smokers, and 32% of white collar smokers used packs of 35, 40 or 50 compared with 45% of blue collar smokers (chi-squared=20.0, df=1, P<0.001). Comparisons with previous years Smoking prevalences in Australia from 1986 to 1995 are shown in Figure 1, with a line of best fit superimposed. Of concern from a public health point of view is that the observed prevalence in 1995 is no lower than that in 1992, necessitating an upward adjustment of the projection to 2001 compared with our projection based on the four triennial surveys up to 1992. It was expected that the national prevalence targets for the year 2000 would be bettered.10 Now the trends suggest they will not be met, either for men or women. The results of the 1995 survey also show 5% more men and 3% more women smoking than would have been expected on the basis of the trends to 1992, and, by extrapolation, this means that in 1995, 356 000 more men and 384 500 more women were smoking in Australia than expected . The mean number of cigarettes smoked by men in 1995 was lower than the 22.1 cigarettes smoked per day by men in 1992 (t=3.39, df=1348, P<0.001). Among women, however, the average number of cigarettes smoked per day in 1995 was not significantly less than the number smoked in 1992 (19.1) (t=1.59, df=1322, P=0.113). The legislative and other activity to restrict advertising and promotion of tobacco, as well as expenditure on adult-directed antismoking campigns, between 1989 and 1995 are outlined in Box 1. Discussion This is the first time in eight successive surveys that the reported prevalence of smoking in men was no lower than the previous survey and the first time since 1983 that this was also the case for prevalence of smoking in women. If these data signal an underlying change and the previously falling prevalence of smoking has indeed stabilised, a major public health response is indicated. Attainment of what is arguably the nation's primary public health target1 -- reducing the prevalence of smoking in men and women to 20% by 2000 -- is clearly under threat. Given that this target was and still may be seen as modest, this would be a major public health failure, as the following calculations show. For every percentage point smoking prevalence in Australia exceeds the national goal, nearly 140 000 people are smoking who, had the goal been met, would not have been. So, if the goal is missed by 3%, which would be the case if the prevalence remains stable, nearly 420 000 more people than expected will be smoking. If they remain smokers, according to estimates of Doll et al,15 210 000 will die prematurely as a result of their smoking. Against the above fairly alarming observations must be set some auspicious trends -- smokers are smoking less and are probably less exposed to inhaled carcinogens and this should flow through to modest public health gains. As well as benefiting themselves, it seems plausible that a lower daily consumption by smokers is reducing the passive exposure of others to cigarette smoke, as forgone cigarettes may be some of those previously smoked at work or in public places where others would be exposed to sidestream smoke. Assuming these data indicate a slow-down or stalling in the previous reduction in smoking prevalence, why has this occurred and what needs to be done? Figure 2 suggests one explanation for influences on smoking prevalence. At times when antismoking activity is high, whether it be in the form of policy or programs, smoking declines, but when these abate prevalence stagnates. Clearly, these data call for more extensive and rigorous analysis which might incorporate, in a multivariate analysis, other factors such as price, regulations and pro-cigarette promotions. This could determine the extent to which program expenditure affects smoking prevalence. The trends are extremely worrying. Stasis in public policy and prevention programs paralleled by static smoking levels suggest the importance of continuing to extend antismoking programs in order to restart the reduction in smoking prevalence. The experience of some Scandinavian countries shows that public health authorities cannot rest on their laurels.16 Much remains to be done (Box 2). References Commonwealth Department of Human Services and Health. Better Health Outcomes for Australians. Canberra: AGPS, 1994. Australian Institute of Health and Welfare. Tobacco use and its health impact in Australia. Canberra: AIHW, 1996. English D, Holman CD, Milne E, et al. The quantification of drug caused morbidity and mortality in Australia. Canberra: Commonwealth Department of Human Services and Health, 1995. Gray N, Hill D. Patterns of tobacco smoking in Australia. Med J Aust 1975; 22: 819-822. Gray NJ, Hill D. Patterns of tobacco smoking in Australia II. Med J Aust 1977; 20: 329-330. Hill D, Gray N. Patterns of tobacco smoking in Australia III. Med J Aust 1982; 1: 23-25. Hill D, Gray N. Australian patterns of tobacco smoking and related health beliefs in 1983. Community Health Stud 1983; 8: 307-316. Hill D. Australian patterns of tobacco smoking in 1986. Med J Aust 1988; 149: 6-10. Hill D, White V, Gray N. Australian patterns of tobacco smoking in 1989. Med J Aust 1991; 154: 797-801. Hill D, White V. Australian adult smoking prevalence in 1992. Aust J Public Health 1995; 19: 305-308. Chapman S, Wooward S. Australian court rules that passive smoking causes lung cancer, asthma attacks and respiratory disease. BMJ 1991; 302: 943-945. Schollam v Dept of Health (NSW). District Court (NSW). 25 May 1992, Case 40830/86. Borland R, Mullins R. The increasing prevalence of workplace smoking bans in Victoria. J Occup Health Safety Aust N Z 1994; 10: 35-40. Borland R, Morand M, Mullins R. Prevalence of workplace smoking bans in Victoria. Aust N Z J Public Health 1997; 21: 694-698. Doll R, Peto R, Wheatley K, et al. Mortality in relation to smoking: 40 years' observations on male British doctors. BMJ 1994; 309: 901-911. Rimpela A. Critical analysis of the Finnish Tobacco Act: implementation and legitimacy 1977-89. Tobacco Control 1992; 1: 285-292. (Received 11 Aug 1997, accepted 27 Jan, 1998) Authors' details Centre for Behavioural Research in Cancer, Anti-Cancer Council of Victoria, Melbourne, VIC. David J Hill, PhD, Director; Victoria M White, MA, Behavioural Scientist; Michelle M Scollo, BBSc, GradDipCommHlth, Public Health Consultant. Reprints will not be available from the authors. Correspondence: David J Hill, Director, Centre for Behavioural Research in Cancer, Anti-Cancer Council of Victoria, 1 Rathdowne Street, Carlton South, VIC 3053. E-mail: davidh AT accv.org.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/>

David J Hill · Victoria M White · Michelle M Scollo

Tuberculosis in the young: focusing on those at risk Recognition and workable strategies for children at risk are needed MJA 1998; 168: 100-101 Tuberculosis (TB) is curable and preventable, yet causes more deaths worldwide than any other infectious disease -- three million yearly, with 450 000 involving children. Australia has one of the lowest rates of TB in the world, and multidrug-resistant TB has not emerged as a problem here.1,2 None the less, people born overseas, Aboriginal people, those infected with HIV, the elderly (especially men over 65), and the homeless experience much higher than average rates of disease. Children up to the age of 14 years account for only 3%-6% of all Australian notifications. Children are also much less likely to transmit infection than adults. However, they have a high risk of developing active disease -- 23%-43% for those infected in the first year of life, 8%-25% for those infected between one and 10 years of age, and 16% for those infected when aged 11-15 years.3 Thus, it is important to identify infected children for preventive therapy (i.e., usually isoniazid for six months) to prevent progression to disease. Children born overseas, child contacts of infectious (usually adult) patients and Aboriginal children have much higher than average rates of infection and disease and deserve specific TB control strategies. The primary strategy for TB control is to stop transmission by timely diagnosis and curative treatment of infectious patients. The next priority, especially in children, is to identify by Mantoux testing those infected and to initiate preventive therapy where appropriate. Screening of at-risk groups and contact tracing of cases are important for both these strategies. It is also important that the skills and resources for diagnosing and curing TB are available to health care providers serving those at risk, such as general practitioners working in high risk migrant communities, Aboriginal medical services and regional chest clinics or public health units. The overall age-specific rates in Australia in 1995 were highest in overseas-born children aged 0-4 years (approximately 44, compared with 1 per 100 000 in Australian-born children of the same age).4 By contrast, 5-14-year-olds, whether born in Australia or overseas, have the lowest specific rates of any age groups, a finding that is consistent worldwide. In this issue of the Journal, the Consensus Statement5 on strategies for TB control in children in Australia from two paediatric special interest groups recommends Mantoux screening of immigrant children from high prevalence countries. This recommendation is long overdue, but needs a workable strategy. Issuing a Tuberculosis Undertaking (as is done for any adult migrant considered to be at increased risk of TB) to all children under five years of age emigrating from countries of high TB prevalence (> 25 per 100,000) would obligate a parent or guardian to contact the Health Assessment Service of the Department of Immigration and Multicultural Affairs within a specific period for direction to the nearest centre for Mantoux testing. The Health Assessment Service is currently investigating the feasibility of such a proposal. Findings from the Melbourne study by Johnson and colleagues6 on the prevalence of asymptomatic Mycobacterium tuberculosis infection in secondary school students add to earlier studies from Sydney,7,8 the Northern Territory9 (NT) and South Australia10 (SA) in supporting targeted school screening. Clearly, there is no current evidence to support mass school screening, and efforts should be directed towards students from countries of high TB prevalence to identify those at risk of developing active, contagious TB in adulthood and to offer them preventive therapy. TB is detected in around 1% of contacts of active cases. While contact tracing finds up to 10% of notified cases of TB overall, this percentage is much higher in children. In 0-14-year-olds, 65% of all cases11 and 78% of intrathoracic cases12 were identified by contact tracing. TB in a child which is not found by contact tracing usually signals recent transmission within the family, providing an opportunity to diagnose adult TB and stop further transmission. Alternatively, it may indicate inadequacies in current control methods, such as failure to trace contacts or to promote successful preventive therapy in identified infected children. The forthcoming National Health and Medical Research Council (NHMRC) publication Towards elimination of tuberculosis II emphasises the importance of contact tracing and provides detailed guidelines for contact screening.3 Limited national data are available on TB in Aboriginal children, but reports from Queensland, SA and the NT confirm they are at increased risk of infection and disease. In the NT from 1989 to 1997, Aboriginal children represented 25 of the 28 notified TB cases aged 0-14 years. Twelve of these 25 cases were nodal TB, consistent with the high rate of extrapulmonary disease seen in children; in contrast, only two cases of non-tuberculous (atypical mycobacteria) nodal disease were found. Suspected mycobacterial disease of lymph nodes always requires culture and susceptibility testing, and in Aboriginal as in migrant children should be considered as TB until proved otherwise. This is in contrast to the 1989 NHMRC statement "that in children born in Australia, mycobacterial disease of lymph nodes is almost invariably due to atypical mycobacterial disease".13 Strategies for TB control among Aboriginal children include diligent contact tracing, which may extend to community screening due to sociocultural interactions and overcrowded housing,3 and targeted school Mantoux testing, education and preventive therapy in regions of high TB incidence.9 The Consensus Statement lists BCG vaccination as an important control strategy, and recommends extending this beyond Aboriginal and Torres Strait Islander neonates in regions of high incidence, neonates born to parents with leprosy, and children under the age of five years living or travelling in countries of high TB prevalence for more than three months, as recommended by the NHMRC TB Working Party.3 While BCG vaccination protects against disseminated TB in the young, it has not played a large role in reducing transmission and controlling TB worldwide. Children born in Australia with one or both parents born overseas are at no higher risk of infection than those with Australian-born parents.6,7,8,9,10 Present evidence therefore supports continuing BCG vaccination according to the three recommendations above. Comprehensive information about the actual TB cases notified in all Australian-born children would be useful to further evaluate this issue. The recommendation that specialised State and Territory TB control programs be maintained in a climate of economic rationalism for a disease with low national rates and low rates in children5 is appropriate. However, an international focus is also required. To this end, it is encouraging that TB has been recognised as a priority issue by the Advisory Group on International Health of AusAID. With 75% of cases being in the migrant population, and Australia's location between two regions which the World Health Organization estimates account for two-thirds of the world's 8-9 million cases, we can not work alone towards eliminating TB. Australia needs to be a partner in the region as well as a contributor to global TB-control strategies. Vicki L Krause Director, Centre for Disease Control Territory Health Services, Casuarina, NT Dawson DJ, Cheah DF, Chew WK, et al. Tuberculosis in Australia 1989-1992. Bacteriologically confirmed cases and drug resistance. Med J Aust 1995; 162: 287-290. Dawson D. Tuberculosis in Australia: bacteriologically confirmed cases and drug resistance, 1994 and 1995. Commun Dis Intell 1997; 21: 245. Towards elimination of tuberculosis II -- guidelines and protocols for controlling tuberculosis in Australia. Draft prepared by NHMRC Tuberculosis Working Party -- 2nd stage public consultation. Canberra: NHMRC, June 1996. Oliver G, Harvey B. Tuberculosis notifications in Australia, 1995. Commun Dis Intell 1997; 21: 261-269. Isaacs D, Mellis CM. Tuberculosis in children in Australia: strategies for control. Med J Aust 1998; 168: 121-124. Johnson PDR, Carlin JB, Bennett CM, et al. The prevalence of asymptomatic tuberculosis infection in Melbourne secondary school students. Med J Aust 1998; 168: 106-110. Alperstein G, Fett MJ, Reznik R, et al. The prevalence of tuberculosis infections among Year 8 school children in inner Sydney in 1992. Med J Aust 1994; 160: 197-201. Alperstein G, Morgan K, Fett MJ, et al. Prevalence of tuberculosis infection among primary school entry children in Sydney. Aust J Pub Health 1996; 20: 123-128 . Wright J, Krause V. Outcomes of the NT School Mantoux Program 1991-1994 [abstract]. Program and abstracts. The 2nd National Tuberculosis Conference: Australia's regional role in tuberculosis control. 1997 Nov 17-18: 38. Sydney: The Public Health Association of Australia, 1997. Broomell K, Antic R, Stapledon R. A decade of tuberculosis control in SA. Abst. Program and Abstracts. The 2nd National Tuberculosis Conference: Australia's regional role in tuberculosis control. 1997 Nov 17-18: 38. Sydney: The Public Health Association of Australia, 1997. Goldman JM, Teale C, Cundall DB, Pearson SB. Childhood tuberculosis in Leeds, 1982-90: social and ethnic factors and the role of the contact clinic in diagnosis. Thorax 1994; 49: 184-185. Pineda PR, Leung A, Muller NL, et al. Intrathoracic paediatric tuberculosis: a report of 202 cases. Tubercl Lung Dis 1993; 74: 261-266. National Health and Medical Research Council. Tuberculosis in Australia and New Zealand into the 1990s. Canberra: AGPS, 1989. 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/>

Vicki L Krause

Long-term ventilatory support at home: any progress? Is breathing at home a right or a privilege? MJA 1998; 168: 7-8 Since Newton-John's 1989 editorial in the MJA calling for better support for patients needing long-term mechanical ventilation,1 there has been little progress nationally. However, a start has been made in Victoria with the establishment of the Victorian Respiratory Support Service. It seems self evident that home rather than institutional care is desirable for these patients -- in this age, it is not only Superman,2 but Everyman, who should be able to live at home on a ventilator. However, home care is possible only when the financial costs and caregiver needs can be adequately met, which depends primarily on patients' personal resources and access to government-funded programs. Access to community programs such as the joint federal- and state-funded Linkages program, which provides for up to 32 hours of attendant care per week, is severely restricted, with waiting lists in many areas. In addition, this level of care may be inadequate to meet the needs of severely disabled people. The cost of ventilators is met by the federally funded Program of Aids for Disabled People in New South Wales, but not in Victoria, where it is met by a specific program grant. Further, for patients who need discontinuous (e.g., nocturnal) ventilation, the cost of acute hospital care to introduce the treatment is not adequately addressed under casemix funding. Chronic ventilator dependence has been defined as use of mechanical ventilation for at least six hours daily for at least 21 days.3 In the past, patients who were ventilator dependent for part or all of the day comprised mainly those who failed to wean after bouts of acute respiratory failure (e.g., post-poliomyelitis),4 and a cumbersome negative-pressure "iron lung" ventilator was used. Recent technological advances, particularly development of small portable ventilators and face and nose masks that allow non-invasive, intermittent positive-pressure ventilation, have made mechanical ventilation practical in a wider range of patients. It can improve quality and duration of life in patients with chronic hypercapneic ventilatory failure caused by restrictive chest-wall disease, spinal cord injury, slowly progressive neuromuscular disease, central hypoventilation or obesity-hypoventilation syndrome.5 The awareness that ventilation is effective treatment for a wider range of indications has led to a rapid increase in the number of ventilator-assisted individuals in Australia and other countries. The Victorian Respiratory Support Service, based at Austin and Repatriation Medical Centre, now provides care for over 170 people, an increase from 25 in 1989. Their underlying diagnoses are shown in the Box (below); 15 receive continuous ventilatory support via tracheostomy, five use a negative-pressure ventilator (iron lung) at night, and the remainder use non-invasive positive pressure ventilation via nasal mask. New patients also tend to have more complex needs. For example, of the 40 new patients started on ventilatory support in the six months to January 1997, eight (20%) required a tracheostomy, including five (13%) receiving continuous ventilatory support. Nationally, the National Health and Medical Research Council (NHMRC) identified 19 children and 39 young adults receiving home ventilation in 1993, including six with a tracheostomy.6 In the absence of a national register, it seems likely that there are more than 500 adult ventilator-assisted individuals at present, 95% of whom live at home (Associate Professor Ron Grunstein, Senior Staff Specialist, Centre for Respiratory Failure and Sleep Disorders, Royal Prince Alfred Hospital, Sydney, NSW, personal communication). The proportion of ventilator-assisted individuals cared for at home varies between countries, largely depending on the support available and types of patients undergoing ventilation. In Japan, a national survey of long-term ventilator-assisted children in 1993 found that only 61 (14%) of 434 patients aged under 20 years were ventilated at home, largely because there was no system in place to support their care at home.7 In the United States, Medicaid reimbursement in 1990 was estimated to cover only 46% of the costs of care of the approximately 11 000 chronic ventilator-dependent patients.4 Patient discharge from acute care facilities to home was often delayed by a lack of community resources, and to long term care facilities by a shortage of beds.4 In 1990, this delay was estimated to average 35 days, adding US$27 000 per patient to the cost of acute care.4 In Minnesota, the proportion of ventilator-assisted individuals cared for at home decreased from 81% to 65% between 1986 and 1992, while total numbers increased by 110%.8 Studies of the long term outcomes of home mechanical ventilation and the factors that influence these are limited. However, a case-control study from Papworth Hospital in the United Kingdom showed that patients managed in a specialised weaning centre had a higher rate of survival to discharge from hospital than control subjects receiving conventional management (94% versus 59%) and a three-year survival rate (63.5%) similar to the one-year survival rate for control subjects.9 In France, which has a national program responsible for nearly all ventilator-dependent patients and for 70% of those receiving home oxygen therapy, a survey of ventilator-assisted individuals found mean survival for those with a neuromuscular disease and kyphoscoliosis was 6.5 and 8 years, respectively.10 We believe that initial care for patients who become ventilator dependent should be provided in designated acute care hospitals by specialised units with expertise in their management. Such units can undertake weaning from continuous ventilatory support and/or initiation of nocturnal ventilatory support with a multidisciplinary team approach that focuses on pulmonary and general rehabilitation. Although current casemix formulas include categories for patients requiring continuous ventilatory support, they fail to address adequately the acute hospital costs of those requiring discontinuous support, which vary widely depending on the complexity of care needed. For non-invasive ventilation, initial cost for the ventilator varies between $4500 and $17000, and annual costs for consumables vary between $200 and $3800. Equipment maintenance can exceed $1000 a year, and enteral feeding, if required, can also add up to $4500 a year. For tracheostomy patients, initial costs may be up to $6500 higher and consumables may add another $2400 a year. Ultimately, home rather than institutional care is desirable for ventilator-assisted individuals, but can be considered only when the financial and caregiver needs can be met. When home care is not feasible, supported accommodation must be found in the community. We believe that, ideally, payment for the care of ventilator-assisted individuals after discharge from an acute care hospital should be provided under a program grant that: recognises the need for case management, training of carers, provision of respite and residential care, along with attendant care if required, while recognising that ventilator-assisted individuals have a major role to play in their own case management; provides funding for ventilators and consumables; provides an administrative and clinical supervisory mechanism to ensure accountability; provides funding for core staff, including a respiratory nurse, physician, respiratory physiotherapist and a care coordinator in each State to provide appropriate training for carers (professional and non-professional) of ventilator-assisted individuals in the community; and provides additional funding for ventilator-assisted individuals who require supported residential care in the community, as the new Commonwealth classification of nursing home and hostel residents which came into effect on 1 October 1997 is unlikely to fund their care adequately. There is an urgent need to monitor the characteristics of ventilator-assisted patients and to evaluate treatment outcomes so that policies and programs can be developed to provide effective support services. A national approach is needed, with an NHMRC report on home ventilation for adults as a necesary first step towards identifying the needs of this neglected but growing group. Donald A Campbell Senior Specialist Robert J Pierce Director, Department of Respiratory Medicine Austin and Repatriation Medical Centre, Melbourne, VIC Newton-John HF. Long term mechanical ventilation of patients in Australia. Med J Aust 1989; 150: 3-6. Rosenblatt R. New hopes, new dreams. Time 1996; 26 Aug: 57-68. Health Care Financing Administration. Chronic ventilator-demonstration: technical advisory panel. Washington, DC (USA): HCFA, 1990. Hill NS. Failure to wean: the chronic ventilator-dependent patient. In: Fishman AP, editor. Pulmonary rehabilitation. New York: Marcel Dekker Inc, 1996: 577-617. Make BJ, Gilmartin ME. Care of ventilator-assisted individuals in the home and in alternative community sites. In: Hodgkin JE, Connors GL, Bell CW, editors. Pulmonary rehabilitation: guidelines to success. 2nd edition. Boston: J B Lippincott, 1984: 359-391. Report of the National Health and Medical Research Council Healthcare Committee Expert Panel on Home Mechanical Ventilation for Children and Young Adults. Canberra: AGPS, 1994. Sakakihara Y, Yamanaka T, Kaji M, Kamoshita S. Long term ventilator-assisted children in Japan: a national survey. Acta Paediatr Jpn 1996; 38: 137-142. Adams AB, Whitman J, Marcy T. Surveys of long-term ventilatory support in Minnesota: 1986 and 1992. Chest 1993; 103: 1463-1469. Smith IE, Schneerson J. A progressive care program for prolonged ventilatory failure: outcomes, February 1992 to November 1996. Proceedings of the Sixth International Conference on Home Mechanical Ventilation. 1997 Mar 5-7; Lyon, France. Lyons: Service de Reanimation Medicale et d'Assistance Respiratoire. Hopital de la Croix-Rousse, 1997: 51. Chailleux E, Fauroux B, Binet B, et al. Predictors of survival in patients receiving domiciliary oxygen therapy or mechanical ventilation: a ten year analysis of ANTADIR observatory. Chest 1996; 109: 741-749. 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/> © 1997 Medical Journal of Australia.

Donald A Campbell · Robert J Pierce

Adult domiciliary oxygen therapy Position statement of the Thoracic Society of Australia and New Zealand Iven H Young, Alan J Crockett and Christine F McDonald Evidence shows that patients with chronic obstructive pulmonary disease and a stable daytime PaO2 of 55 mm Hg or less will have longer life expectancy if given supplemental oxygen to keep the PaO2 above 60 mm Hg, preferably for longer than 15 hours a day, including sleep. There is some evidence for improved quality of life. It is reasonable to offer this therapy for other lung diseases which cause chronic hypoxaemia, and there are also less well defined indications for supplemental oxygen during exercise, sleep and air travel. (MJA 1998; 168: 21-25) → This position statement has been superseded by a new statement published in 2005. Click here for the new statement. Introduction - Indications - Contraindications - Investigations - Reassessment - Dangers - Quality of life - Methods of domiciliary oxygen delivery - Authorisation of oxygen therapy - References - Authors' details - - ©MJA1997 Introduction Domiciliary oxygen therapy is an effective but potentially expensive therapy that should be prescribed to those in whom there is evidence for benefit. This position paper is a consensus statement based on evidence from English-language publications up to 1996 obtained by search of MEDLINE with keywords domiciliary oxygen, home oxygen and LTOT (long term oxygen therapy). The paper is an update of the position statement published in the Journal in 1991.1 Supplementary oxygen may benefit patients whose disability is related to decreased oxygen concentration in arterial blood. The most common cause of chronic hypoxaemia in Australia is chronic obstructive pulmonary disease (COPD), and there is more substantial information about use of domiciliary oxygen in this condition than in any other. In COPD, domiciliary oxygen is the only therapy (apart from smoking cessation) shown to reduce mortality.2,3 There is also evidence that it alleviates right heart failure caused by cor pulmonale, enhances neuropsychological function, and improves exercise performance and capacity to undertake the activities of daily living.4 Although long term oxygen therapy has been best studied in COPD, other possible indications include hypoxaemia associated with cyanotic congenital heart disease, severe congestive cardiac failure, diffuse interstitial lung disease, advanced lung cancer or cystic fibrosis,5 and, in general, any illness with chronic hypoxaemia as an important feature. In the absence of hypoxaemia, oxygen therapy is unlikely to contribute usefully to relief of dyspnoea, heart failure or angina. Indications Continuous (at least 15 hours/day) oxygen therapy: Long term continuous oxygen therapy should be considered for patients with stable chronic lung disease, particularly COPD, who have an arterial PO2 (PaO2) consistently less than or equal to 55 mm Hg when breathing air, at rest and awake. At assessment (see Investigations), the patient's condition must be stable and all reversible factors (such as anaemia) should be remediated.6 Because gas exchange may improve substantially on ceasing cigarette smoking, assessment should be made at least a month after the patient has stopped smoking. Polycythaemia (Hb > 170 gm/L), clinical or electrocardiographic (ECG) evidence of pulmonary hypertension, as well as episodes of right heart failure, are consistent with the systemic effects of chronic hypoxaemia and strengthen the case for therapeutic use of oxygen. Patients with these complications should be prescribed continuous oxygen if their stable PaO2 is 55-59 mm Hg. In COPD, continuous oxygen therapy is of most benefit for patients with increased arterial PCO2 ( >45 mm Hg).3 As the benefit has been shown to increase with increasing daily use of oxygen for up to 19 hours per day,3 patients should be advised to use oxygen whenever the physical restriction imposed by the oxygen therapy is not onerous. Intermittent oxygen therapy: The use of intermittent oxygen may be considered for: Patients with fibrotic or obstructive lung diseases during exercise, as supplementary oxygen may improve exercise capacity. Benefit cannot be predicted by a resting test and may occur irrespective of resting or exercise hypoxaemia. Benefit should be established by comparing exercise endurance when breathing oxygen and when breathing air (using a treadmill, stationary bicycle or six-minute walk test). Room air is probably adequate for this comparison, as there appears no difference in exercise endurance between breathing room and cylinder air.7 The Society's position on the controversal use of oxygen during exercise is summarised in Box 1. Patients with acute asthma living in isolated areas or prone to sudden life-threatening episodes while they are awaiting medical attention or evacuation by ambulance. During air travel, particularly long distance flights out of Australia. Commercial passenger aircraft operate at cabin pressures between about 1500 and 3000 metres above sea level, with the lowest pressure likely to be experienced for a significant time being equivalent to 2500 metres above sea level. This is analogous to breathing 15% oxygen at sea level. Sufficient supplementary oxygen should be given during flight to keep the PaO2 above 50 mm Hg, which is commonly achieved by increasing the usual flow by 1-2 L/min. Patients who qualify for continuous oxygen at home will require this supplementation. Others can be tested for the effects of 15% oxygen in the laboratory before the flight. Further, those travelling to high-altitude destinations may need an increase in their oxygen prescription during their sojourn.4 Patients with late stage interstitial or neoplastic lung disease with significant hypoxaemia. Supplementary oxygen may provide symptomatic relief. Patients in the latter category will generally have a life expectancy of three months or less. Duration of use may be extended as long as necessary to relieve symptoms. The prescription of home oxygen for patients with chronic heart failure and/or angina is not well supported by evidence of efficacy, and a decrease in mortality with this therapy has not been verified. A high inspired oxygen concentration of 50% may modestly improve exercise duration in heart failure,8 but concentrations this high are difficult to attain with current home delivery systems. Nocturnal oxygen therapy: This may be indicated in patients with hypoxaemia during sleep. This diagnosis should be considered in patients whose arterial gas tensions are acceptable when awake, but who have daytime somnolence, polycythaemia or right heart failure. The clinical importance of isolated nocturnal hypoxaemia (i.e., without daytime hypoxaemia or obstructive sleep apnoea) was recently established.9 In patients with this condition, nocturnal oxygen at 3 L/min over three years was found to reduce pulmonary hypertension, but not to alter mortality, in comparison with a control group over this relatively short period. Although data are insufficient to make rigorous recommendations for this group, and further studies are needed, the current consensus is that those whose nocturnal arterial oxygen saturation falls to 88% or less should be treated with nocturnal oxygen. Hypoxaemia during sleep should be distinguished from sleep apnoea caused by upper airway obstruction, which requires other forms of therapy (such as continuous positive airway pressure and nocturnal ventilation). The diagnosis is by formal sleep studies. These are essential if obstructive sleep apnoea is suspected in a patient with chronic airflow limitation; this combination is suggested by daytime hypercapnia. Contraindications Supplementary oxygen is not indicated for: Patients with severe airflow limitation whose main complaint is dyspnoea, but who maintain a PaO2 greater than 60 mm Hg and who show no secondary effects of chronic hypoxia; Patients who continue to smoke cigarettes, because of the increased fire risk and the probability that the poorer prognosis conferred by smoking will offset treatment benefit; Patients who have not received adequate therapy of other kinds (e.g., inhaled and oral bronchodilators, treatment of right ventricular failure and of any respiratory infection); and Patients who are not sufficiently motivated to undertake the discipline required in oxygen therapy. Investigations Establish the nature and severity of the pulmonary disorder responsible for hypoxaemia (usually obstructive or fibrotic lung disease) by appropriate tests, including objective tests of pulmonary function. Undertake clinical, ECG, echocardiographic and radiological assessment of right heart failure and pulmonary hypertension. Measure haemoglobin level. Polycythaemia, the usual response to chronic hypoxaemia in otherwise healthy people, is not always seen in those with hypoxaemia of chronic lung disease. The degree to which it is adaptive or adds to the burden of disordered function through increased blood viscosity is controversial. Anaemia is always a burden and should be investigated and corrected. Undertake other appropriate tests, according to clinical findings, for other major diseases which might be expected to seriously limit survival. As noted above, it is appropriate to prescribe oxygen for symptomatic relief in patients with a very limited prognosis. Before introducing oxygen therapy, undertake optimal treatment of the pulmonary disorder while monitoring improvement with objective tests (usually simple tests of ventilatory capacity such as FEV1 and vital capacity).6 Treatment may include maximum therapy of airway obstruction, attention to nutrition and body weight, an exercise rehabilitation program, control of infection and treatment of cor pulmonale. When the patient's condition has been stabilised and drug therapy optimised over about four weeks, the degree of hypoxaemia should be determined by measurement of arterial blood gases while the patient is breathing air at rest. This should include measurements of PaO2 at rest on at least two occasions and, when indicated, measurements of PaO2 or arterial oxygen saturation during sleep. In patients selected for oxygen therapy, assess the adequacy of relief of hypoxaemia (PaO2 > 60 mm Hg, SaO2 > 90%) and/or improvement in exercise capacity or nocturnal arterial oxygen saturation while using a practical oxygen delivery system. Reassessment Patients should be reassessed a month after starting continuous or nocturnal oxygen therapy, both clinically and by measurement of PaO2 and PaCO2 with and without supplementary oxygen. It should then be decided whether the treatment has been properly applied and whether it is worthwhile or should be abandoned. This one-month review is particularly important to confirm that the low entry PaO2 was not spurious because the patient was unstable at the time of sampling. Subsequent review should be undertaken at least annually, or more often according to the clinical situation. Some patients will show a sustained rise in PaO2 to > 60 mm Hg when breathing air, but current thinking is that this represents the reparative effects of supplementary oxygen and should not be a rationale for stopping therapy.4 This recommendation may change with further evidence. A patient having intermittent oxygen therapy should also undergo periodic reassessment, but this may be unnecessary and undesirably disruptive for those with a limited prognosis. Dangers Pulmonary oxygen toxicity has not been seen at the low rates of flow used for long-term oxygen therapy. However, supplementary oxygen in patients with increased arterial PCO2 may depress ventilation, increase physiological deadspace, and further increase arterial PCO2. This is suggested by an obvious decrease in respiratory rate and depth, as well as the development of somnolence and disorientation. In long-term oxygen therapy, the increase in arterial PCO2 is usually small and well tolerated. It was not a practical problem in two large trials, probably because patients were in a stable condition.2,3 However, serious hypercapnia may occasionally develop, making continued oxygen therapy impractical. Risk appears greater during acute exacerbations of disease. Sedatives (particularly benzodiazepines), narcotics, alcohol and other drugs which impair the central regulation of breathing should not be used in patients with hypercapnia receiving oxygen therapy. Quality of life With the potential restriction of movement imposed by long-term continuous oxygen therapy, it is possible that the treatment may only prolong suffering rather than improve quality of life. However, for patients who qualify according to the above criteria, the improvement in quality of life will mostly outweigh the restriction imposed. There is some evidence that women experience more improvement than men in several quality-of-life dimensions.10 Whether oxygen therapy is worthwhile for a particular individual must be determined by a comprehensive clinical assessment rather than solely, or mainly, by the increase achieved in PaO2. Methods of domiciliary oxygen delivery There are three methods of oxygen supply for the home: Cylinders: These contain compressed pure oxygen gas and deliver 100% oxygen at the outlet. Sizes and contents vary (see Box 2), and a regulator, flow meter, spanner and key wheel are needed to connect the tubing to the cylinder. These components are mostly interchangeable for the different cylinder sizes, although cylinder C requires a specific regulator. Several portable light-weight cylinders are available which allow the patient to leave home for several hours. Cylinders are available from Medical Gases Australia, BOC Gases and Sunrise Medical. Oxygen concentrators: These are floor-standing electrically driven devices that entrain room air, extract the nitrogen in molecular sieves and deliver oxygen at the outlet. They run off the domestic electricity supply, and, as they do not store significant amounts of gas, they must run all the time that oxygen is needed. Most of these units deliver 90%-95% oxygen at the outlet when operating at a flow rate of 2 L/min; the percentage falls with increasing flow rate (to about 78% oxygen at 5 L/min), depending on the model. All units currently available in Australia are imported, and there are several distributing agents (including Medical Gases Australia, BOC Gases, Anaesthetic Supplies, and Sunrise Medical). Rental fees are about $100 per month. A back-up standard D-size oxygen cylinder is recommended in case of concentrator breakdown or power failure. Liquid oxygen systems: These systems, now available in Australia, conserve space by storing oxygen in liquid form at 2 1831/4C (30 L of liquid oxygen is equivalent to 25 800 L of gaseous oxygen). The oxygen is delivered through coils, where it vaporises. Two tanks are needed: a large storage tank, which is filled by the supplier as required (e.g., one unit has a 25 800 L gaseous capacity, equivalent to seven E-size cylinders), and a portable unit filled from the larger tank for ambulatory use. Comparisons between supply methods There is no significant difference in the quality of oxygen delivery among the above methods. Advantages and disadvantages of each are compared in Box 3. For patients receiving intermittent oxygen, D-size cylinders or concentrators are the most appropriate mode of supply, while for most patients receiving continuous or nocturnal oxygen concentrators are favoured. Further aspects of concentrators to be considered are: Concentrators are cheaper than cylinders if use is equivalent to three E-size cylinders per month, but electricity costs must be considered (council rebates may apply). Concentrators can be wheeled around the home but are heavy (about 21-26 kg) and difficult to move upstairs and in and out of cars. Concentrators cannot be used for nebulisation, as the pressure delivered is too low (35-63 kPa, compared with 140 kPa for nebuliser pumps). If the anticipated need is for longer than two years, then it is cheaper to buy than to rent a unit. On the other hand, rental is not affected by the hours per day the machine is used and includes maintenance costs (about $180 annually). Regular maintenance of concentrators, including changing and cleaning of filters and checking of alarm systems, is essential. Conservation devices These are small devices introduced between the oxygen source and the patient to ensure that oxygen is delivered only during inspiration and not wasted during expiration. They are useful cost- and time-conserving devices for cylinders and liquid oxygen systems, especially portable units, and can prolong the use of a C-size cylinder from two to 10 hours. As many conservation devices switch on the flow by sensing negative pressure at the nares via the nasal cannula, they may not trigger if the patient mouth-breathes (unless the cannula is transferred to the mouth); many breathless patients become mouth breathers when they are more distressed. These devices are of no value with concentrators and should not be used with transtracheal delivery systems. Delivery to the patient All patients should receive careful and detailed instruction on how to operate and obtain optimal benefit from their oxygen equipment. Flow rate should be set in the range 1-5 L/min, at the lowest rate needed to maintain a resting PaO2 of 60 mm Hg (in practice, most often 2 L/min). It should be increased by 1 L/min during exercise and sleep. Humidifiers are not needed as flow rates are low, and ambient air entrainment supplies sufficient humidification for the total inspired gas. Extrasoft nasal prongs are recommended for continuous oxygen use, but may become uncomfortable at flow rates over 2-3 L/min and in the long term. Facemasks may be preferred for at least some of the time. Simple masks are adequate; complex Venturi masks are not necessary; the appropriate mask should be selected using measurements of arterial oxygen tension. Both nasal prongs and masks are also acceptable for intermittent oxygen use. In selected patients needing 24-hour oxygen therapy, transtracheal delivery systems may have advantages.12 These allow substantially lower flow rates, as the tracheal cannula fills the tracheal and upper airway deadspace with oxygen during each expiration. This may be a crucial advantage in patients needing high flow rates. In addition, portable systems become more useful with this conserving effect, and the delivery tubing can be hidden under clothing. However, care of this relatively invasive appliance is demanding -- the patient must learn to clean and replace the cannula often, as it may become obstructed by formation of "mucous balls" at the tip -- and it will be attractive to only a few. Authorisation of oxygen therapy Current guidelines for prescription through the Program of Aids for Disabled People specify that respiratory physicians and cardiologists are authorised prescribers. It could be argued that other groups should be authorised as long as the guidelines are adhered to. At present, any medical practitioner may order home oxygen if the patient meets the costs. References Breslin AB, Colebatch HJ, Engel LA, Young IH. Adult domiciliary oxygen therapy. Med J Aust 1991; 154: 474-477. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Ann Intern Med 1980; 93: 391-398. Report of the Medical Research Council Working Party. Long-term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981; 1: 681-686. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. ATS Official Statement. Am J Respir Crit Care Med 1995; 152 Suppl: 77-120. Recommendations for long term oxygen therapy (LTOT). Report of a European Society of Pneumology Task Group. Eur Respir J 1989; 2: 160-165. Cooper CB, Waterhouse J, Howard P. Twelve year clinical study of patients with hypoxic cor pulmonale given long term domiciliary oxygen therapy. Thorax 1987; 52: 105-110. McKeon JL, Tomlinson JC, Tarrant PE, Mitchell CA. Portable oxygen in patients with severe chronic obstructive pulmonary disease. Aust N Z J Med 1988; 18: 125-129. Restrick LJ, Davies SW, Noone L, Wedzicha JA. Ambulatory oxygen in chronic heart failure. Lancet 1992; 340: 1192-1193. Fletcher EC, Luckett RA, Goodnight-White S, et al. A double-blind trial of nocturnal supplemental oxygen for sleep desaturation in patients with chronic obstructive pulmonary disease and a daytime PaO2 above 60 mm Hg. Am Rev Respir Dis 1992; 145: 1070-1076. Crockett AJ, Cranston JM, Moss JR, Alpers JH. Initial trends in quality of life and survival in CAL patients on domiciliary oxygen therapy. Monaldi Arch Chest Dis 1996; 51: 64-71. Kampelmacher MJ, van Kesteren RG, Deenstra M, et al. Long-term oxygen therapy. Neth J Med 1994; 44: 141-152. Christopher KL, Spofford BT, Petrun MD, et al. A program for transtracheal oxygen delivery. Assessment of safety and efficacy. Ann Intern Med 1987; 107: 802-808. (Received 8 Apr, accepted 18 Sep, 1997) Authors' details Department of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Iven H Young, PhD, FRACP, Head. Department of Respiratory Medicine, Flinders Medical Centre, Adelaide, SA. Alan J Crockett, MPH, Senior Hospital Scientist. Austin and Repatriation Medical Centre, Melbourne, VIC. Christine F McDonald, PhD, FRACP, Respiratory Physician. Reprints: The Thoracic Society of Australia and New Zealand, 145 Macquarie Street, Sydney, NSW 2000. E-mail: iveny AT mail.med.usyd.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/> © 1997 Medical Journal of Australia.

Iven H Young · Alan J Crockett · Christine F McDonald

Specific allergen immunotherapy for asthma A Position Paper of the Thoracic Society of Australia and New Zealand and the Australasian Society of Clinical Immunology and Allergy MJA 1997; 167: 540-544 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/MJA/>". Introduction - Atopy, allergens and asthma - Rationale for using immunotherapy for asthma - Clinical trials - Allergen extracts and route of administration - Adverse effects - Practical aspects of administering immunotherapy - References - Authors' details Make a comment - - ©MJA1997 Introduction Specific allergen immunotherapy (desensitisation, hyposensitisation) is the technique of treating IgE-mediated disease with increasing doses of an allergen in order to decrease sensitivity to that allergen. First used early this century, 60 million patients annually are now treated with immunotherapy throughout the world. The only absolute indication for immunotherapy is a life-threatening reaction after a Hymenoptera (bee or wasp) sting; all other indications are relative (see indications and contraindications for immunotherapy). Many randomised controlled trials have shown that hayfever caused by airborne pollens and house dust mite responds to this therapy.1 The use of specific allergen immunotherapy in asthma remains controversial. Despite this, the Thoracic Society of Australia and New Zealand and the Australasian Society of Clinical Immunology and Allergy believe that all strategies which may impact on the morbidity and mortality of asthma should be assessed. The cost-effectiveness of this therapy also needs to be addressed in the context of the total cost of asthma in Australia, the mid-estimate of which in 1991 was $652 million (National Asthma Campaign, 1992). We present an overview and do not cover all aspects of this subject. Interested readers are referred to recent reviews.1-9 Atopy, allergens and asthma Allergy is best defined as an exaggerated response on exposure to an allergen following prior exposure, and mediated by an immune reaction involving IgE. The same clinical picture may result from non-immune mechanisms. Atopy is an increased tendency to IgE-based sensitivity resulting in production of specific IgE antibody to common environmental allergens, such as house dust mite, pollens, moulds or animal danders. This sensitisation occurs in genetically predisposed people after exposure to low concentrations of allergen; cigarette smoke and viral infections may assist in the sensitisation process. About 40% of the population is atopic, and about half of this group develop clinical disease ranging from trivial rhinitis to life-threatening asthma. After sensitisation, continuing exposure to allergens leads to a significant increase in the prevalence of asthma.10 Ninety per cent of children and 80% of adults with asthma are atopic.10 Once sensitisation has occurred, re-exposure to allergen is a risk factor for exacerbations of asthma.11 Effective management of allergic asthma includes pharmacological therapy and allergen avoidance. For example, avoiding dust mite allergen can reduce symptoms and the need for medication. Rationale for using immunotherapy for asthma Asthma is an inflammatory disease characterised by the presence of cells such as eosinophils, mast cells, basophils, and CD25+ T lymphocytes in the airway walls. There is close interaction between these cells, because of the activity of cytokines which have a variety of communication and biological effector properties. Chemokines attract cells to the site of inflammation and cytokines activate them, resulting in inflammation and damage to the mucosa.12 With chronicity of the process, secondary changes occur, such as thickening of basement membrane and fibrosis.13 An immunological reaction to allergen is the initiating event of airway inflammation in many cases of asthma.14 Continued exposure to allergen results in chronic inflammation. Current therapy aims to suppress this inflammation with inhaled corticosteroids, sodium cromoglycate, or nedocromil sodium, all of which interfere with the cellular and cytokine interactions by diverse mechanisms, but do not address the initiating event in allergic asthma. By withdrawing the allergen or altering the immune response to allergen, it is theoretically possible to control the allergic trigger of asthma. Immunological changes have been described after immunotherapy. These include an initial rise in specific serum IgE, followed by a fall, and a rise in specific IgG ("blocking antibody"). Specific IgG titres correlate poorly with the degree of protection. Immunotherapy leads to a reduction in mediator release from mast cells in vitro, alterations in lymphocyte subsets, and a downregulation of IL-4 production from T cells.15 Several studies have shown a reduction in inflammation and a decrease in bronchial hyperresponsiveness after immunotherapy.1,16,17 There are strong theoretical arguments why immunotherapy should be used early in the course of the disease, before irreversible secondary changes such as fibrosis have occurred. Further, data are emerging to suggest that immunotherapy may also influence the progression of clinical disease.3,7 Immunotherapy should not be regarded as an alternative to established forms of preventive therapy, as recommended by the National Asthma Campaign.18 A systematic cost-benefit analysis of immunotherapy has not yet been undertaken. Clinical trials There have been numerous randomised placebo- controlled double-blind trials of immunotherapy for asthma. Comparison of these trials is difficult, not only because of the inherent problems of trials involving asthma (such as standardisation of inclusion and outcome criteria), but also because of differences in allergen extracts and dosage regimens. A meta-analysis can address some of these difficulties, and has recently been applied to 20 randomised controlled trials of immunotherapy for asthma in both adults and children.19 This meta-analysis found a clinically useful improvement from immunotherapy with house dust mite and with other allergens (see Box below). It concluded that immunotherapy is a treatment option in highly selected patients (discussed more fully below) with allergic asthma. The reviews cited in this position paper,1-9 the meta-analysis19 and further controlled studies published in the last five years20-24 provide references to the most important trials of immunotherapy. Allergen extracts and route of administration Although several routes of allergen delivery have been used in immunotherapy, only subcutaneous injection has been studied in detail and shown to be effective. Giving allergen extract sublingually is not recommended as studies have failed to show long-term efficacy.25 Trials with giving birch pollen orally appeared promising, but large doses were required and there was a high incidence of side effects. Further studies of oral immunotherapy using modified preparations are under way. Intranasal administration of pollen extracts resulted in an unacceptable level of side effects. Local bronchial immunotherapy with mite extract in patients with asthma has been studied in a controlled trial but failed to produce significant clinical improvement.26 Most allergen extracts used in Australia for immuno therapy of inhalant allergy are alum-precipitated. Such preparation slows the absorption of allergen, reducing the risk of serious anaphylaxis and providing sustained immune stimulation. There is no reliable standardisation of biological activity for many allergen extracts used in Australia. Mass and concentration of active material are not useful guides to biological activity. The concentrations of the slow-release (alum-precipitated) preparations are expressed in "protein nitrogen units" and not biological activity. Aqueous preparations of some allergens, including Dermatophagoides pteronyssinus, are standardised against a WHO standard and are extremely potent. Their use in asthma should be restricted to specialist centres. Adverse effects Local reactions Mild swelling and erythema at the site of the injection is to be expected. It may persist for 24 hours or more and is not a cause for concern. A more severe reaction over 50 mm in diameter is an indication for reduction in the subsequent dose. Systemic reactions These include sneezing, bronchospasm, urticaria and, in more severe cases, anaphylaxis with hypotension and collapse. They must always be regarded seriously. Although they usually occur within 30 minutes of the injection, they may be delayed for several hours with the use of alum-precipitated preparations. Recent data from the UK estimate that the incidence of severe systemic reactions was 1 in 500 injections,1 but most occurred with aqueous extracts, and alum-precipitated extracts appeared to be much safer. The incidence of anaphylaxis with Allpyral (Bayer, Pymble, NSW), the alum-precipitated material available in Australia, was reported to be 1 in 27 854 courses of treatment, and of anaphylaxis and/or bronchospasm, 1 in 14 998 courses of treatment.27 The Committee on the Safety of Medicines, in the United Kingdom, reported in 1986 that in the 29 years from 1957 to 1986 during which 1 459 273 courses of treatment were given, there were 29 deaths from immunotherapy -- 16 in patients where the indication for therapy was asthma.27 Highly purified and potent aqueous extracts were involved in most of these deaths, and no deaths were reported with the Allpyral extract. Subsequent reports indicated a much lower incidence of anaphylaxis and deaths in France and the US,28,29 where one major difference in practice is that treatment is administered by specialists with expertise in the area. In Australia, five deaths from immunotherapy were reported to the Adverse Drug Reactions Advisory Committee in the 21 years from 1972 to 1993. Four were in patients with asthma, and in each case there was a divergence from recommended procedure. Long term adverse effects There is no increase in the prevalence of vasculitis, autoimmune disease or monoclonal gammopathies during or after immunotherapy.30 Further, there is no evidence that long term worsening of asthma occurs with immunotherapy. Practical aspects of administering immunotherapy These guidelines relate to specific allergen immunotherapy for the treatment of asthma in patients with clinical manifestations and/or need for treatment of ongoing bronchial hyperreactivity. The decision to prescribe immunotherapy is based on appropriate patient selection, appropriate antigen selection, and whether potential benefits outweigh associated risks. Only a practitioner or team with training and experience in the management of both asthma and immunotherapy should make the decision. Suitably qualified practitioners include thoracic physicians with training and expertise in allergy, or clinical immunologist/allergists with training and expertise in asthma. It is the responsibility of the supervising consultant to (a) decide whether a patient needs to be treated in a hospital, and (b) ensure that the medical practitioner giving immunotherapy receives written instructions on patient assessment and immunotherapy protocol. Informed consent according to currently accepted guidelines must be obtained from patients before starting immunotherapy. Immunotherapy should be given only by a medical practitioner familiar with immunotherapy, conversant with resuscitative procedures, and in a setting where the following resuscitation equipment is immediately available: adrenaline 1:1000 for intramuscular use (adrenaline is the drug of choice for the immediate management of systemic reactions to immunotherapy), oxygen, an inflatable bag and mask ventilator, a nebuliser and bronchodilator nebuliser solution, needles and tubing for intravenous access, intravenous fluids suitable for volume replacement, parenteral antihistamine, and parenteral corticosteroid. The practitioner and a second appropriately trained health care professional should be present during immunotherapy to assist if resuscitation is required. Each patient requires an individual dosage schedule according to the degree of sensitivity and clinical reaction to the injections. The principle of therapy is to start with a small dose and gradually increase it as tolerated. Supervising consultants will have the training and experience necessary to determine the starting dose and appropriate schedule. Flexibility in dosage is essential and rigid adherence to predetermined dosage schedules is inappropriate. Extracts should be stored in a refrigerator at 4°C , clearly marked with the patient's identifier(s) and replaced in the refrigerator immediately after use. Before injection, the extract should be examined visually and discarded if its appearance has changed. The contents of the bottle should be mixed well to avoid variation in dosage. When changing to a new batch of unstandardised extract (such as Allpyral), the first dose should be reduced by 25% to take account of possible variation in biological activity of the preparations. Each patient should have his or her own individual vial of extract -- laws in some States forbid multiple use of vials for different patients. Every patient should be assessed clinically on each occasion before an injection is given , with particular attention to stability of asthma as indicated by peak flow charts, intercurrent illness, reaction to the last injection and any change in medication. Spirometry or peak flow meter readings must be taken before injection and, if more than 20% below the best recent recorded reading for that patient, the injection should not be given. The readings should be repeated 30 minutes after the injection and immediately any lower respiratory symptoms arise during the period of observation -- a fall of 10% or more is an indication for reducing the dose of the next injection. The medical practitioner must be responsible for selecting the dose and having it checked by a second health professional. Injections are given subcutaneously, a suitable site being the tissue overlying the triceps muscle group. After introducing the needle, and before starting the injection, the plunger should be withdrawn gently to ensure that the needle is not placed intravenously. There is no consensus about the optimal time that a patient must remain under observation . However, we recommend 45 minutes, as serious reactions after that time are rare. Reactions may be delayed with alum-precipitated preparations but they are usually minor. Before discharge patients should be examined to record the size of the local reaction, ensure that there are no signs of a systemic reaction, and to repeat spirometry or peak flow readings. Patients must not engage in strenuous physical exercise or take hot baths or saunas for six hours after the injection. Patients should monitor their peak flow at home ; excessive variability would indicate a need for re-evaluation of asthma and immunotherapy. A local swelling larger than 50 mm requires a reduction in dosage. Patients should be instructed to measure the diameter of any local reaction should it increase in size after leaving medical supervision, and report this before the next injection. Some practitioners "cover" therapy by giving prophylactic antihistamines to reduce the local reactions. This practice may make it difficult to judge the effects of therapy, both locally and systemically, and to modify dosage accordingly. It may also block the initial manifestations of an anaphylactic reaction. Use of this practice is a matter of judgement, but if prophylactic drugs are used use must be consistent. Injection schedules vary with individual patients, but the Allpyral preparations are administered every 1-2 weeks until a maintenance dose is reached. Maintenance injections are administered every 2-4 weeks. It should be re-emphasised that immunotherapy schedules are individualised and fixed schedules are not recommended, particularly when aqueous extracts, which are becoming more readily available in Australia, are used. The duration of therapy for optimal management is unknown at present. With bee and wasp venom immunotherapy, there is evidence that five years of maintenance injections will provide long term protection in almost all patients. There is no corresponding evidence in inhalant allergy and practice varies. Dust mite injections are often continued for 2-3 years if there is a response, and preseasonal immunotherapy with grass pollen is repeated for 2-3 years. References Position paper on allergen immunotherapy. Report of a BSACI Working Party. Clin Exp Allergy 1993; 23 Suppl 3: 1-44. WHO/IUIS Working Group Report. Current status of allergen immunotherapy. Lancet 1989; 1: 259-261. Position paper: immunotherapy. The European Academy of Allergology and Clinical Immunology (EAACI). Allergy 1993; 48 (14 Suppl): 9-35. Platts-Mills TAE. Allergen-specific treatment for asthma. Am Rev Respir Dis 1993; 148: 553-555. Lockey RF, Bukantz SC, editors. Allergen immunotherapy. New York: Marcel Dekker, 1991. Walls RS. Desensitisation injections: do they have a role? Aust Prescriber 1989; 12: 90-92. Bousquet J, Michel F-B. Specific immunotherapy in asthma: is it effective? J Allergy Clin Immunol 1994; 94: 1-11. Malling H-J. Immunotherapy in Europe. Clin Exp Allergy 1994; 24: 515-521. Greenberger PA, editor. Immunotherapy of IgE-mediated disorders. Immunol Allergy Clin North Am 1992; 12: 1-203. Sporik RB, Chapman MD, Platts-Mills TAE. House dust mite exposure as a cause of asthma. Clin Exp Allergy 1992; 22: 897-906. Gelber LE, Seltzer LH, Bouzoukis JK, et al. Sensitization and exposure to indoor allergens as risk factors for asthma among patients presenting to hospital. Am Rev Respir Dis 1993; 147: 573-578. Corrigan CJ, Kay AB. T cells and eosinophils in the pathogenesis of asthma. Immunol Today 1992; 13: 501-506. Roche WR, Beasley R, Williams JH, Holgate ST. Subepithelial fibrosis in the bronchi of asthmatics. Lancet 1989; 1: 520-524. Lenfant C. Global initiative for asthma: global strategy for asthma management and prevention. NHLBI/WHO Workshop Report. Bethesda, Md.: National Institutes of Health, January 1995. (Publication No. 95-3659.) O'Brien RM, Byron KA, Varigos GA, Thomas WR. House dust mite immunotherapy results in a decrease in Der p2-specific IFN- g and IL-4 expression by circulating T lymphocytes. Clin Exp Allergy 1997; 27: 46-51. Rak S, Bjornson A, Hakanson L, et al. The effect of immunotherapy on eosinophil accumulation and production of eosinophil chemotactic activity in the lung of subjects with asthma during natural pollen exposure. J Allergy Clin Immunol 1991; 88: 878-888. Nagata M, Shibasaki M, Sakamoto Y, et al. Specific immunotherapy reduces the antigen-dependent production of eosinophil chemotactic activity from mononuclear cells in patients with atopic asthma. J Allergy Clin Immunol 1994; 94: 160-166. Asthma management handbook. 2nd ed. Melbourne: National Asthma Campaign, 1996. Abramson MJ, Puy RM, Weiner JM. Is allergen immunotherapy effective in asthma? A meta-analysis of randomised controlled trials. Am J Resp Crit Care Med 1995; 151: 969-974. Bousquet J, Hejjaoui A, Soussana M, Michel F. Double-blind placebo-controlled immunotherapy with mixed grass-pollen allergoids. IV. Comparison of the safety and efficacy of two dosages of a high-molecular-weight allergoid. J Allergy Clin Immunol 1990; 85: 490-497. Haugard L, Dahl R. Immunotherapy in patients allergic to cat and dog dander. I. Clinical results. Allergy 1992; 47: 249-254. Alvarez-Cuesta EJ, Cuesta-Herranz J, Puyana-Ruiz J, et al. Monoclonal antibody-standardised cat extract immunotherapy: risk-benefit effects from a double-blind placebo study. J Allergy Clin Immunol 1994; 93: 556-566. Creticos PS, Reed CE, Norman PS, et al. Ragweed immunotherapy in adult asthma. N Engl J Med 1996; 334: 501-506. Adkinson NF, Eggleston PA, Eney D, et al. A controlled trial of immunotherapy for asthma in allergic children. N Engl J Med 1997; 336: 324-331. Bjšrksten B. Local immunotherapy is not documented for clinical use. Allergy 1994; 49: 299-301. Crimi E, Voltolini S, Troise C, et al. Local immunotherapy with Dermatophagoides extract in asthma. J Allergy Clin Immunol 1991; 87: 721. Committee on Safety of Medicines. CSM update. Desensitising vaccines. BMJ 1986; 293: 948. Warner JO, Kerr JW. Hyposensitisation. BMJ 1987; 294: 1179-1180. Stewart GE, Lockey RF. Systemic reactions from allergen immunotherapy. J Allergy Clin Immunol 1992; 90: 567-578. Katelaris CH, Walls RS. A study of possible ill effects from prolonged immunotherapy in treatment of allergic diseases. Ann Allergy 1984; 53: 257-261. Authors' details The Thoracic Society of Australia and New Zealand, Melbourne, VIC. Reprints: Dr P I Field, Honorary Secretary, 145 Macquarie Street, Sydney, NSW 2000. Australasian Society of Clinical Immunology and Allergy, Melbourne, VIC. No reprints will be available. Correspondence: Dr D Gillis, Honorary Secretary, PO Box 204, Mt Albert, VIC 3127. <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia. We appreciate your comments.

Asthma management plans: progress and problems Research on the usefulness, applicability and effectiveness of the Australian Asthma Management Plan should ultimately improve quality of life for people with asthma MJA 1997; 166: 287 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/>". - - ©MJA1997 There have been considerable improvements in morbidity and mortality from asthma in Australia since the publication of the Australian Asthma Management Plan (AMP) in 1989.1,2 The Australian plan was a milestone and many national (e.g., British3 and United States4 ) and international asthma management guidelines (e.g., Global Initiative for Asthma5 ) followed. It outlines six components of good asthma management: (1) assess severity, (2) achieve best lung function, (3) maintain best lung function -- identify and avoid triggers, (4) maintain best lung function with optimal medication, (5) develop an action plan, and (6) educate and review regularly. Within Australia, the AMP was widely disseminated to doctors and allied health professionals by the National Asthma Campaign through the Asthma management handbook, which has since undergone two revisions, the latest in 1996. Any major public health initiative should be rigorously evaluated before its recommendations become established practice, and the National Asthma Campaign has been monitoring asthma management practices and outcomes since 1990.6 What is the role of an AMP if less than half of asthma sufferers report receiving one? In this issue of the Journal, Beilby and colleagues shed more light on current asthma management and the use of the Australian AMP. As part of a larger general population survey, they included questions on asthma which enabled assessment of the use of whole or part of the AMP. It is important to distinguish between an AMP (the complete six-step package) and specific elements within it, such as having an action plan or having identified trigger factors with one's doctor, as research is still needed to assess the usefulness and applicability of the different components of the AMP. For example, action plans can play a vital role in preventing hospital admissions and death from asthma,7 but not all patients will find them helpful or use them when needed.8 The essential ingredients of an action plan should enable a patient to identify an exacerbation (e.g., by increased bronchodilator use or nocturnal asthma or a decrease in peak flow), increase medication and add oral corticosteroids appropriately and seek timely medical attention. A peak flow meter is not essential to this process, although it is extremely valuable for some patients. Those most likely to benefit from using a peak flow meter include those with previous life-threatening asthma, a history of emergency visits and hospital admissions, and a history of poor perception of airway obstruction. Gibson et al.9 have shown that the more severe an asthma exacerbation, the less frequently will patients prefer self-management or use of an action plan. In addition, the elderly are more likely to seek advice from their doctors at the time of an acute attack of asthma, rather than make autonomous decisions based on an action plan. Garrett et al.8 have also shown that, among patients admitted to hospital with acute asthma, a minority used their action plans. On the other hand, many patients manage their asthma effectively at home, and avoid the need for emergency medical treatment, possibly as a result of effective use of action plans, although this has been more difficult to quantify. In long-term management, AMP adherence is better in those with more severe asthma, and use of a self-management plan can reduce unscheduled acute care visits, courses of antibiotics and oral corticosteroids, and improve quality of life.7,10 The finding of Beilby et al. that 46% of respondents with asthma reported being given an AMP is very similar to the 42% estimated in the 1994 NSW Health Promotion Survey,11 and the National Asthma Campaign evaluation in 1993.6 However, they found that only a quarter of this 46%, or 11%-12% overall, had a written AMP. This is lower than the 1993 National Asthma Campaign estimate of 20% and is cause for concern. There is evidence that written advice is more effective than verbal advice alone in improving patient adherence to medication instructions and management strategies.12 Audit data indicate a low rate of use of action plans among people who attend accident and emergency departments with asthma exacerbations. For these reasons the low rate of written AMPs (and therefore, it is assumed, action plans) identified in all studies needs to be addressed. As highlighted by Beilby et al., lack of time in general practice consultations and uncertainty about how to write an action plan may be impediments to more widespread uptake of this important component of the AMP. These observations raise the issue of which components of the AMP matter most. The Australian AMP was written as an expert consensus statement. It provides a systematic and methodical approach to asthma care, but it was not formulated as an evidence-based document -- its recommendations were not based on systematic reviews and have not been ranked according to the strength of the evidence supporting them. Had we waited for this to be done, we would have delayed guidelines which were desperately needed at a time when the prevalence of asthma in Australia was rising,13 asthma mortality was high and morbidity was proving a major cost to the Australian community.14 An evidence-based review of the AMP has been advocated in the National asthma strategies15 and a systematic review of the evidence for the sixth step of the AMP -- educate and review regularly -- is already being undertaken by members of the Thoracic Society of Australia and New Zealand through the Cochrane Collaboration Airways Group. The article by Beilby and colleagues makes an important contribution to monitoring the use of the AMP. Several positive points emerge. Good management was more likely among those who had a regular doctor, and action plans were more common among those who had moderate or severe asthma. The combination of specialist and GP care resulted in the highest rate of possession of an AMP (82%). This finding concurs with other studies showing the benefits of integrated care,16 and highlights the need to improve communication and joint management strategies between specialists and GPs, hospitals and the community. Further work and consultation are needed to address the barriers to wider use of written action plans and to help facilitate this process for GPs. Considerable resources are needed to clarify which aspects of the AMP are making the greatest contributions to improving asthma outcomes, but this investment will be important in developing the AMP into more strongly evidence-based guidelines. Christine R Jenkins Visiting Thoracic Physician, Concord Hospital, Sydney, NSW, and Chairman, National Asthma Campaign Adrian E Bauman Associate Professor of Public Health, School of Community Medicine, University of New South Wales, Sydney, NSW Woolcock AJ, Rubinfeld AR, Seale JP, et al. Asthma management plan 1989. Med J Aust 1989; 151: 650-653. Australian Bureau of Statistics. Deaths due to diseases and cancers of the respiratory system, 1979-94. Canberra: ABS, 1996: 6-7. (Catalogue No. 3314.0.) Guidelines for management of asthma in adults: I -- chronic persistent asthma. BMJ 1990; 301: 651-653. National Asthma Education Program. Expert panel report. Guidelines for the diagnosis and management of asthma. Bethesda, Md.: United States Department of Health and Human Services, August 1991. (Publication No. 91-3042.) Global Initiative for Asthma. Global strategy for asthma management and prevention. NHLBI/WHO workshop report. Bethesda, Md.: National Heart, Lung and Blood Institute, 1995. Comino EJ, Mitchell CA, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Lahdensuo A, Haahtela T, Herrala J, et al. Randomised comparison of guided self management and traditional treatment of asthma over one year. BMJ 1996; 312: 748-751. Garrett J, Mercer Fenwick J, et al. Peak expiratory flow meters (PEFMs) -- who uses them and how and does education affect the pattern of utilisation? Aust N Z J Med 1994; 24: 521-529. Gibson PG, Talbot PI, Toneguzzi RC, et al. Self-management, autonomy and quality of life in asthma. Chest 1995; 107: 1003-1008. Charlton I, Charlton G, Broomfield J, Mullee MA. Evaluation of peak flow and symptoms only self management plans for control of asthma in general practice. BMJ 1990; 301: 1355-1359. Howell S, Bauman A. NSW health promotion survey databook, December 1995. Sydney: NSW Department of Health, 1995. Jones K, Tilford S, Robinson YK. Compliance. Health education. London: Chapman and Hall, 1991: 127-130. Peat JK, van de Berg R, Green WF, et al. Changing prevalence of asthma in Australian children. BMJ 1994; 308: 1591-1596. National Asthma Campaign. Cost of asthma in Australia. Melbourne: Boston Consulting Group, 1993. National Asthma Campaign. National asthma strategies: strategies and implementation. Melbourne: NAC: 1996. Osman LM, Abdulla MI, Russell IT, et al. Integrated care for asthma: matching care to the patient. Eur Respir Dis 1996; 9: 444-448. - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Christine R Jenkins · Adrian E Bauman

Reported use of asthma management plans in South Australia Justin J Beilby, Melanie A Wakefield and Richard E Ruffin MJA 1997; 166: 298 For comment see Jenkins & Bauman 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/>". Abstract - Introduction - Methods - Results - Asthma management plans - Good management - Discussion - References - Authors' details - - ©MJA1997 Abstract Objective: To examine the use of asthma management plans (AMPs) and specific elements of AMPs in a South Australian community. Design: Cross-sectional questionnaire survey by experienced interviewers. Participants and Setting: 307 adults with current asthma, confirmed by a doctor, who were among 3001 respondents of a representative sample of 4065 South Australian adults recruited by multistage systematic clustered area sampling for a larger study in March 1995. Main Outcome Measures: Prevalence of reported use of AMPs and of specific elements of AMPs, such as knowledge of trigger factors and having an action plan, and the proportion of adults with asthma receiving what we defined as "good management". Results: 46% reported having an AMP; 63% had discussed trigger factors with their doctors and 39.5% had action plans. 82% had been told the severity of their asthma, and 23.3% were receiving good management. Conclusion: Less than half of people with asthma use AMPs, although certain elements within the AMPs are reportedly being used more frequently. More research is required on why AMPs are not more generally used and, more importantly, on what elements within the AMP model are useful and effective for people with asthma and likely to be used by their general practitioners (GPs). MJA 1997; 166: 298-301 Introduction Asthma causes substantial morbidity1 and mortality,2 and costs -- in the range of $585-$720 million in Australia in 1991.3 Approximately 9% of Australians (over 1.4 million people) have reported asthma as "either a recent or long term condition in the last 12 months".4 There is evidence that the prevalence of the disease is increasing,5 and that it is both undertreated and underdiagnosed.6 The variability of the condition in both adults and children further complicates these concerns. In an attempt to create a unified approach to the management of asthma, a group of "accepted experts" developed the Asthma Management Plan (AMP), a set of consensus guidelines for health professionals.7 The Australian AMP comprises six steps: Assessing the severity of asthma; Achieving best lung function; Maintaining best lung function by identifying and avoiding triggers; Maintaining best lung function with optimal medication; Developing an action plan; and Educating the patient and reviewing regularly. These steps are aimed at doctors as an aid to achieving good asthma management. Hence, any reported use of elements of the AMP will, in part, be dependent on the use of these steps by doctors as well as on patient factors. In this study we examine the current use of AMPs and determine the specific elements of the plan that have been adopted by people with asthma and their doctors. Such information is important in planning ongoing asthma management campaigns. Methods In March 1995, a representative population sample of adults in South Australia was obtained for the Health Omnibus Survey,8 as follows. A multistage systematic clustered area sample of households was used to give a sample comprising 75% selected from the Adelaide metropolitan area and the rem ainder from country centres with populations of 1000 or more. At each household, one person aged 15 years or over (the person whose birthday was last) was selected for interview. Interviews were conducted in the respondent's home by trained interviewers, with up to six call-back visits if the selected respondent was not at home. For the purposes of our study, we included a number of questions in the Health Omnibus Survey. Respondents were asked whether they had asthma, and if they answered "yes" they were then asked to respond to the questions listed in Box 1. For the purposes of the interviews, we defined: Asthma management plans as "a coordinated method of management that covers aspects of your asthma -- medication, trigger factors, lung function measurement, etc."; Trigger factors as "incidents that can cause you to have an asthma attack"; and An asthma action plan as "written or verbal instructions of what to do if your asthma is out of control, i.e., having a bad attack". We initially examined questionnaire responses against sociodemographic variables, including age, sex, place of birth, educational attainment, and household income. Conventional chi-squared tests were used for comparisons at the univariate level, and unconditional logistic re gression analysis to adjust for potential confounders. In further analyses, we adjusted for confounding and/or interaction between variables such as place of residence, severity, age, sex and whether respondents had been told about their level of asthma severity. Separate logistic regression analyses were run for the subgroup who had been told about their asthma severity to determine the independent contribution of severity level on the dependent variable of interest. Similarly, the responses of those who had a regular doctor were analysed separately to determine differences between sources of care. Finally, we considered that patients who reported having an AMP, being told about trigger factors and having an action plan were receiving "good management", and examined factors related to good management. We excluded the optimisation of pharmacological intervention from our definition. SPSS was used for all statistical analyses.9 Results 3001 of a possible 4065 people responded (response rate, 73.8%). Of these 3001 respondents, 558 (18.6%) indicated that they had ever had asthma, and 521 (93.4%) of these had had their asthma confirmed by a doctor. Of these 521, 307 (58.9%) indicated that they still had asthma, representing 10.2% of the total sample and comprising 120 men and 186 women (one respondent did not indicate sex), with a mean age of 39.4 years (SD, 18.3; range, 15-84 years). Box 2 (below) shows that current medically confirmed asthma was more common among women than men, and declined in prevalence with increasing age. It was also more common among rural than metropolitan respondents, and among Australian-born respondents than those born elsewhere; this difference remained significant after adjusting for age and sex in logistic regression analyses. There was no relationship between current confirmed asthma prevalence and post-secondary education or annual gross household income, even after adjusting for age and sex. Asthma management plans Box 3 (above) summarises our findings on asthma management among respondents with currently confirmed asthma. Further analyses showed that having an AMP was not related to age, sex, area of residence, or whether people had been told their level of severity. However, those who had a regular doctor were more likely to have an AMP (P = 0.03). Those who saw both a general practitioner (GP) and specialist were significantly more likely to have an AMP (81.7%) than those who saw a GP only (47.6%), specialist only (41.1%) or no one (22.6%; P = 0.02). Among respondents who had been told their level of severity, those with moderate or severe asthma were more likely to report having an AMP than those with mild asthma (P < 0.01), after adjustment for other covariates. Women were more likely than men to have been told about their asthma severity (86.3% v. 75.0%; chi-squared = 6.1; P = 0.01), and those who had been told tended to be younger than those who had not (t = 3.1; P = 0.07). Among those who had been told, reported level of severity increased with advancing age (t = 5.3; P < 0.01). Severity did not vary by sex, but was greater among rural respondents than metropolitan respondents (chi-squared = 8.6; P = 0.01). The reported prevalence of discussing trigger factors and having an action plan increased with increasing asthma severity (see Box 4). It is notable that only 14 (25.4%) of those who had not been told their asthma severity had an action plan. Men were more likely than women to have no regular doctor for asthma care (22.7% v. 12.4%; chi-squared = 5.7; P = 0.02); there was no difference by age. Overall, those who had discussed trigger factors did not differ by sex, area of residence or whether they had been told their level of severity. After adjustment for covariates, discussion of trigger factors was more likely among younger respondents (P < 0.05) and those who had a regular doctor (P < 0.01). Among those who had been told their level of severity, logistic regression analysis showed that those with severe asthma were more likely than those with moderate or mild asthma to have discussed trigger factors (P < 0.05). Of those with a regular doctor, source of care was unrelated to discussion of trigger factors. Respondents who reported having an action plan did not vary by age, area of residence or whether they had been told their level of severity. Action plans were more common among women (P < 0.05) and those who had a regular doctor (P < 0.05), and among those who had been told they had moderate or severe asthma than mild asthma (P < 0.01). For respondents with a regular doctor, source of care was unrelated to having an action plan. Good management Seventy-one respondents with currently confirmed asthma (23.3%) were receiving "good management". Good management was unrelated to age, sex, area of residence or whether respondents had been told their level of severity, but was more likely among those who had a regular doctor (P < 0.05). Among those who had been told their level of severity, those with moderate or severe asthma were more likely to be receiving good management than those with mild asthma (P < 0.001). Of those with a regular doctor, source of care was unrelated to receiving good management. Discussion Given that the AMP model was initiated in 1989, our finding of a prevalence of reported use of AMPs of 46%, with much higher prevalences for certain elements of AMPs, is reassuring. It is noteworthy that we found AMPs to be more common among people who had been told their asthma was severe and those with a regular doctor. Our finding that 39.5% of respondents had an action plan is a somewhat higher result than those of previous reports,10,11 possibly indicating an increase in their use. As we found that reported use of action plans did not vary by age, the different age profile of our study compared with that of Comino and colleagues10 (mean, 39.4 years; range, 15-84 years v. mean, 37.4 years; range, 18-50 years) is unlikely to have contributed to the apparent doubling in prevalence of action plan use that we observed. However, unlike the other study, we included verbal as well as written action plans, and this may have been responsible for the difference. Our study was based on self-report, and responses were not validated. However, our method of assessing self-reported asthma has been used in a previous validated epidemiological study.12 There may have been under-reporting in the responses to the questions, even though we used trained interviewers. However, despite these methodological problems, the key measure of the acceptability of the AMP and its elements is their reported use in the community. We are aware that the term "asthma management plan" may have introduced some problems in that our def inition of the AMP encompassed as - sessment of severity, trigger-factor discussions and the development of an action plan. Hence, it is possible that people who reported using an AMP may have been including the other three elements. However, as a main objective was to compare the uptake of the "complete" AMP with that of its individual elements, we believed it was important to include all these questions in the survey. We found that certain elements of the AMP are being adopted more frequently than others, which may indicate that patients find these steps more appropriate to their specific needs, or that doctors (GPs and specialists) find certain elements of the AMP easier to use or implement. GPs are the principal providers of asthma care in the community and it is probable that they have a considerable effect on the uptake of the AMP model. Developing a "complete" management plan may be too onerous a task for a busy GP. Conversely, GPs may find the AMP model does not satisfy their individual needs and, as a consequence, choose specific elements from the AMP model for their everyday practice.13 Over 80% of our respondents, most of whom had mild to moderate asthma, saw a GP for all or part of their asthma care. As there is evidence that GPs' management of asthma is very variable,14,15 it is important to concentrate on providing useful and focused education for GPs. Urgent clarification is needed of the key steps within the AMP model that will reduce mortality and morbidity in people with asthma and improve their quality of life. Interestingly, we found that only 41% of the respondents attending a specialist only had an AMP. As specialists spend more time with their patients and deal with people with more severe asthma, this finding requires further investigation. It has been suggested that some steps of the AMP may be inappropriate for general application. For example, peak flow meters are supposed to be used in both steps 2 and 3, but Ruffin and Pierce have proposed that aiming to have all asthmatic patients record peak expiratory flow over the long term may not be worthwhile,16 and that focusing on, for example, those at risk of dying, those in uncertain clinical situations (e.g., those with exercise-induced asthma) and those who are "particularly interested" in monitoring their asthma would be more cost effective. They emphasised the need for a more rigorous scientific approach to examining "the basis for and benefit of" peak expiratory flow.16 In a more recent paper Gibson et al. state that "action plans have received little controlled evaluation".17 Among 35 adult asthma patients, they found that the current increase in medication recommended in the AMP action plan had a high failure rate. On the other hand, there is evidence that regular review (step 6 of the AMP) can reduce days lost from work or school18 and home visits by GPs,19 and that patient education (step 5) improves symptom control20 and reduces visits to accident and emergency departments.21 The guidelines in the AMP model have come to be accepted as the "gold standard" of asthma management in most countries.22,23 However, what is needed now is a careful re-evaluation 24 to ensure that "unsound practice" does not become formalised.25 A new perspective may be required that embraces the variability in management and clinical encounters.26 Not surprisingly, we found that having a regular doctor is the main determinant of "good management" -- regular review is likely to allow time for the introduction of more steps in the AMP. The challenge in continuing to evaluate an introduced management program in clinical practice is substantial. If over half the population of asthmatic patients have already been exposed to the asthma management plan in part or in full, how can this be done? Small intensive clinical trials with objective outcomes such as peak flow measurements, or case-control studies comparing asthmatic patients with and without good quality of life, could be performed, but would have the disadvantage of not being generalisable to the population at large. Large population studies with specific outcome measures would rely on the outcome measures being validated against accepted criteria of asthma control. A national project that used specific health outcomes, such as prescriptions of reliever or preventer agents, and monitored hospital admissions for asthma could be used to evaluate interventions introduced on a State or regional basis. To coordinate and cooperate in such a project would present a challenge to organisations involved in asthma management. There is current interest in coordinated care programs for chronic diseases and the time is right to introduce an evaluation strategy for different interventions in asthma. References Campbell D, Ruffin R, McEvoy RD, Crockett AJ. South Australian asthma symptoms prevalence survey [abstract]. Paper presented at the Annual Scientific Meeting of The Thoracic Society of Australia and New Zealand. 1991 7-11 Apr; Lorne, Vic. Aust N Z J Med 1991; 21: 658. Jenkins WA, Hurley SF, et al. Trends in Australian mortality of asthma 1979-1985. Med J Aust 1988; 149: 620-624. National Asthma Campaign. Report on the cost of asthma in Australia 1994. Melbourne: National Asthma Campaign, 1994. National Health Survey 1989/90. Canberra: Australian Bureau of Statistics, 1991. Robertson CF, Heycock E, Bishop J, et al. Prevalence of asthma in Melbourne school children: change over 26 years. BMJ 1991; 302: 1116-1118. Bauman A, Young L, Peat J, et al. Asthma under-recognition and under-treatment in an Australian Community. Aust N Z J Med 1992; 22: 36-40. Woolcock A, Rubinfield A, Seale P, et al. Asthma management plan, 1989. Med J Aust 1989; 151: 650-652. Wilson D, Wakefield M, Taylor A. The South Australian Health Omnibus Survey. Health Promotion J Aust 1992; 2: 47-49. Nornsis MJ. SPSS for Windows. Advanced statistics release 6.0. Chicago: SPSS Inc, 1993. Comino E, Mitchell C, Bauman A, et al. Asthma management in eastern Australia, 1990 and 1993. Med J Aust 1996; 164: 403-406. Tse M, Bridges-Webb C, Bauman A. The impact of a mass communication campaign on the reported management of asthma by general practitioners. Fam Pract 1993; 10: 263-267. Abramson M, Kutin J, Bowes G. The prevalence of asthma in Victorian adults. Aust N Z J Med 1992; 22: 358-363. Armstrong D, Fry J, Armstrong P. General practitioners' views of clinical guidelines for the management of asthma. Int J Qual Health Care 1994; 6: 199-202. Bauman A, McKenzie D, Young L, Yoon R. Asthma education: the perception of family physicians. J Asthma 1990; 27: 385-392. Coates J, Steven I, Beilby J, et al. Knowledge and reported asthma management among South Australian General Practitioners. Br J Gen Pract 1994; 44: 123-126. Ruffin R, Pierce R. Peak flow monitoring -- which asthmatics, when and how? Aust N Z J Med 1994; 24: 519-520. Gibson P, Wlodarczyk J, Hensley M, et al. Using quality-control analysis of peak expiratory flow recordings to guide therapy for asthma. Ann Intern Med 1995; 123: 488-492. Charlton I, Charlton G, Broomfield J, Rullee M. 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. Charlton I, Charlton G, Broomfield J, Campbell M. An evaluation of a nurse-run asthma-clinic in general practice using an attitudes and morbidity questionnaire. Fam Pract 1992; 9: 154-160. Wilson S, German D, Sulochina L, et al. A controlled trial of two forms of self-management education for adults with asthma. Am J Med 1993; 94: 564-576. Bolton M, Tilley B, Kuder J, et al. The cost and effectiveness of an education program for adults who have asthma. J Gen Intern Med 1991; 6: 401-407. Guidelines for the diagnosis and management of asthma. Bethesda, Md.: United States Department of Health and Human Services, August 1991. (Publication No. 91-3042.) International consensus report on diagnosis and managment of Asthma. Bethesda, Md.: United States Department of Health and Human Services. June 1992. (Publication No. 92-3091.) Thompson P, Lavender M, Madhok R. How to ensure that guidelines are effective. BMJ 1995; 311: 237-242. Delamothe T. Wanted: guidelines that doctors will follow. Implementation is the problem. BMJ 1993; 307: 218. Parmley W. Clinical practice guidelines. Does the cookbook have enough recipes? JAMA 1994; 272: 1374-1375. (Received 17 Apr, accepted 11 Nov, 1996) Authors' details Research & Health Promotion Unit, Royal Australian College of General Practitioners, Adelaide, SA. Justin J Beilby, MPH, FRACGP, Director. Behavioural Epidemiology Unit, South Australian Health Commission, Adelaide, SA. Melanie A Wakefield, MA, PhD, Senior Behavioural Scientist. Department of Thoracic Medicine, The Queen Elizabeth Hospital, Adelaide, SA. Richard E Ruffin, MD, FRACP, Director. No reprints will be available. Correspondence: Dr J J Beilby, Department of General Practice, University of Adelaide, Adelaide, SA 5005. - - To top of article - ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Justin J Beilby · Melanie A Wakefield · Richard E Ruffin

Caring for adolescents with asthma: do we know how to? What is needed now is research based on an understanding of adolescents MJA 1996; 165: 463 Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright 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/>". - - ©MJA1996 Australian data show that the prevalence of asthma among teenagers is approximately 20%. 1 Estimated conservatively, at least half a million young adolescent Australians aged 10-19 years suffer from asthma. In Australian children the prevalence of asthma has increased substantially in the past three decades, 1,2 but most children with mild asthma do not have asthma in adolescence and adulthood. 3 However, for many, their childhood asthma per sists through adolescence into adult life. 4 Identified risk factors for this persistence of asthma into adult life include female sex, onset after two years of age, more than 10 attacks throughout childhood, lower peak flow rates in childhood, and parental atopy. 3 Personal atopy is also a major determinant of outcome. 2 Objective measurement of the physiological disturbances of asthma are well accepted as part of medical care for acute asthma. In addition, various asthma management plans imply that measurement of airflow obstruction has a role in ongoing interval asthma management. Indeed, in specialist practice this is a routine component of care. In this issue of the Journal, Hewson et al. ( page 469 ) provide firm evidence to support this view in a general practice setting. They found unexpectedly low values for forced expiratory volume in one second (FE V 1 ) and/or forced mid expiratory flow (FEF 25%-75% ), both calculated as a percentage of normal values, in patients in whom clinical and personal assessment had indicated no need to change asthma treatment. This occurred at 30% of assessment opportunities in general practice in adolescents undergoing review or attending for acute exacerbation of asthma. Presumably, had these results been available to their treating doctors, drug therapy would have been altered. That measurement of airflow obstruction by spirometry in general practice has the potential to contribute to fine tuning of asthma therapy is of substantial significance. Ambulatory monitoring of peak flow rate is promoted as assisting in diagnosing asthma, measuring its severity, assessing response to treatment and recognising any deterioration. 5 The limitations of peak flow rate monitoring are also well known, 5 and incidentally highlighted in the article by Hewson et al. While use of a peak flow monitor at home (70% of the study population) may have resulted in patients attending their general practitioner for assessment (reasons for consultation are stated only as acute deterioration or asthma management review), it did not result in appropriate medication change. Just as there are limitations in the testing of peak flow rate, there are also limitations in the use of spirometry. Training in the performance and interpretation of spirometry, as completed by the physiotherapist who performed the tests in the study by Hewson et al., is vital to the achievement of valid and reproducible results. 6 Although measurement of disease severity is an important factor in the management of adolescents with asthma, it is becoming increasingly apparent that assessment of the broad health status of adolescents with asthma is equally important. The evidence is only just emerging that the prevalence of smoking in young people with asthma appears to be the same as their peers without asthma. 7 Adolescence is a critical period for determining future smoking behaviour -- over 90% of adult smokers begin smoking by 19 years 8 -- and achieving an effective early intervention during adolescence has the potential to have an immense impact. Moreover, what is less well understood is that smoking in young people is more than just an exacer bating factor in asthma or a major risk factor for heart d isease and cancer. It is an important symptom of, or marker for, other adolescent health problems. Specifically, symptoms of anxiety and depression are strongly associated with smoking in adolescents, 9 and heavy tobacco use is a feature of concurrent abuse of drugs such as alcohol and marijuana. 10 Monitoring the health status of the adolescent process is of itself an important component in assessing the health status of young people. 11 A young person's development involves physical, cognitive and psychosocial maturation. Medically, we are well trained to assess the physical changes of adolescence, but we receive far less training in other aspects of adolescent maturation. How independent of their parents are these young people? How personally and socially responsible is their behaviour? What are their educational and vocational goals? What activities do they enjoy? In comparison with measuring airflow obstruction by spirometry, a suitable method of measuring adolescent developmental progress is less well defined. Frameworks have been promulgated to assist practitioners to obtain a psycho social history sensitively, 12 but it is only by placing these frameworks into the broader context of adolescent development that we can start to address adolescents' health needs. It is important that this lack of knowledge and competence in adolescent health, well recognised by general practitioners, 13 is redressed by improved training in adolescent medicine. Specific behaviours, such as smoking, or poor adherence to medication regimens or medical review appointments, are important factors because of their detrimental effect on asthma management in adolescents. However, they are also important as potential "beacons of distress". Putting these behaviours into the context of adolescent development can be more helpful in the development of key strategies to improve asthma management than the typical medical "disease-perspective" model. Research in asthma epidemiology has increased our understanding of the extent of asthma, and guided the development of major public health interventions for disease management. What is now needed is research based on an understanding of adolescents themselves. For adolescents with asthma, we need to define more clearly the problems they face as adolescents, not simply the problems they face because they have asthma. For example, research is required to determine the extent and nature of adherence to asthma medication regimens, and to identify young people's understanding of the effect of smoking on asthma. This may then be used to develop strategies that better engage young people in regular medical care and better target smoking. Appropriately, the recent National Asthma Week (6-12 October) targeted asthma and adolescents. We have a good understanding of the management of asthma. What we need now is an accompanying understanding of how best to care for adolescents with asthma. Susan Sawyer Senior Lecturer Glenn Bowes Professor Centre for Adolescent Health, University of Melbourne Royal Children's Hospital, Melbourne, VIC Robertson CF, Heycock E, Bishop J, et al. Prevalence of asthma in Melbourne schoolchildren: changes over 26 years. BMJ 1991; 302: 1116-1118. Peat JK, van den Berg RH, Green WF, et al. Changing prevalence of asthma in Australian children. BMJ 1993; 308: 1600-1604. Jenkins M, Hopper JL, Bowes G, et al. Factors in childhood as predictors of asthma in adult life. BMJ 1994; 309: 90-93. Oswald H, Phelan PD, Lanigan A, et al. Outcome of childhood asthma in mid-adult life. BMJ 1994; 309: 95-96. The Thoracic Society of Australia and New Zealand. Peak flow meter use in asthma management. Med J Aust 1996; 164: 727-730. American Thoracic Society. Pulmonary function laboratory personnel qualifications. Am Rev Respir Dis 1986; 134: 623-624. Wakefield M, Ruffin R, Campbell D, et al. Smoking-related beliefs and behaviour among adults with asthma in a representative sample. Aust N Z J Med 1995; 25: 12-17. Miller SK, Slap GB. Adolescent smoking. A review of prevalence and prevention. J Adolesc Health Care 1989; 10: 129-135. Patton GC, Hibbert M, Rosier MJ, et al. Is smoking associated with depression and anxiety in teenagers? Am J Public Health 1996; 86: 225-230. Patton GC, Hibbert M, Rosier J, et al. Patterns of common drug use in teenagers. Aust J Public Health 1995; 19: 393-399. Blum RW. Transition to adult health care: setting the stage. J Adolesc Health 1995; 17: 3-5. Goldenring JM, Cohen E. Getting into adolescent heads. Contemp Paediat 1988; July: 75-90. Veit FC, Sanci LA, Young DY, Bowes G. Adolescent health care: perspectives of Victorian general practitioners. Med J Aust 1995; 163: 16-18. - - To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Susan Sawyer · Glenn Bowes

Routine pulmonary function tests in young adolescents with asthma in general practice Peter H Hewson, Elizabeth A Tippett, Danny M Jones, Justin P Madden and Peter Higgs For editorial comment, see Sawyer and Bowes Readers may print a single copy for personal use. No further reproduction or distribution of the articles in whole or in part should proceed without the permission of the publisher. For copyright 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/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - ©MJA1996 Abstract Objective: To assess the value of performing routine pulmonary function tests by flow-loop spirometry in young adolescents with asthma. Design: A prospective clinical study comparing clinical assessment and patients' self- reporting of asthma severity with the results of pulmonary function tests. Setting: General practice in a small rural community of about 30 000 people. Patients: Young adolescents with asthma, aged 10-15 years, were enrolled in the study over a two-year period from July 1993 to June 1995 when they presented for either elective, interval assessments or with an acute exacerbation of asthma. Main outcome measures: Discrepancy between (i) the doctor's and the patient's perception of asthma control (six scale measures) and the consequent management plans, and (ii) the results of pulmonary function tests that indicated less than adequate airway function (i.e., forced expiratory volume in one second as a percentage of predicted vital capacity for height and sex [FEV 1 %] less than 65% or average flow rate over the middle 50% of forced vital capacity as a percentage of predicted normal value [FEF 25%-75% ] less than 65%). Results: Twenty-seven adolescents with asthma were assessed on a total of 37 occasions. The results of pulmonary function tests did not correlate with asthma symptoms and treatment in 11 of the 37 assessments (30%; 95% confidence interval [CI], 16%-47%). The 11 assessments were performed on eight patients. Conclusions: This small community-based study of adolescents with asthma supports the view that pulmonary function testing by flow-loop spirometry should be part of the routine assessment of acute and chronic asthmatics. Further study in a larger community is needed to clarify the frequency of over- and underestimation of asthma severity in this difficult age group. MJA 1996; 165: 469-472 Introduction Older children and adolescents often have difficulty assessing the severity of their asthma, 1 and consequently pulmonary function tests have been recommended for those with frequent or chronic asthma who are able to perform spirometry adequately. 2-4 Pulmonary function testing by flow-loop spirometry allows measurement of forced expiratory volume in one second as a percentage of the predicted vital capacity for height and sex (FEV 1 %), and forced mid expiratory flow (FEF 25%-75% : the average flow rate over the middle 50% of forced vital capacity). While peak flow monitoring and FEV 1 % have been used for decades as a measure of pulmonary function, forced mid expiratory flow is not as well known a measure, but is more sensitive than FEV 1 in detecting small airways obstruction. 2 Pulmonary function tests have been shown to be useful in adults, but there are few studies of their useful ness in children and young adolescents with asthma. One study found that 17% of apparently well children with asthma had a low forced expiratory volume in one second / vital capacity ratio (FEV 1 /FVC) and 54% had low forced mid expiratory flow (FEF 25%-75% ), suggesting that, without these tests, both patients and doctors were unable to detect mild degrees of broncho constriction, especially of the smaller airways. 5 To date, no study has described the use of pulmonary function tests as part of routine community medical practice in young adolescents. In fact, in some centres, spirometry tests are not yet done routinely in chronic asthmatics in this age group. We performed pulmon ary function tests in adolescents with asthma in an Australian country setting, comparing patients' and doctors' clinical assessment of asthma severity with the results of routinely performed pulmonary function tests. Methods This two-year study took place in Colac, Victoria (population, 14 000; regional population, 30 000) between July 1993 and June 1995. All young adolescents with asthma (recurrent wheeze responsive to bronchodilators) between the ages of 10 and 15 years pre senting to their general practitioner Monday to Friday either for an elective asthma management review, or because of an acute exacerbation of their asthma, were assessed by the general practitioner and included in the study. No adolescents were excluded from the study or refused to participate. Appointments for elective management reviews (interval assessments) had been made weeks in advance. An acute exacerbation of asthma was defined as an appreciably more severe wheeze and cough than usual (as assessed by the general practitioner). The severity of symptoms and the perception of asthma control were assessed by the general practitioner, giving day and night symptom scores (0-5), and a wheeze description, based on questioning of the patient. The doctor and the patient then separately graded asthma control as excellent, very good, fair, poor, or very poor. (The scoring system is given in the footnote to the Table). Forced expir atory volume in one second (FEV 1 ) and forced mid expiratory flow (FEF 25%-75% ) were measured -- on the same day if it was a daytime presentation (usually immediately after the clinical assessment) or the morning after if it was an evening presentation. An Alpha Vitalograph spirometer (Fisher & Paykel, Melbourne, Vic.) was used and the tests were conducted by the senior physiotherapist at Colac Hospital (E A T), who had attended the spirometry technician's course run by the Department of Respiratory Medicine, Alfred Hospital, Melbourne. The tests were repeated if the assessment was judged to be inadequate by the physiotherapist. The effect of bronchodilators on pulmonary function tests was determined in all patients, with recordings being taken 20 minutes (in one patient 25 minutes) after bronchodilator therapy. The pulmonary function tests were done without knowledge of the clinical status of the patient and the results were made available to the treating doctor if requested. The patients' previous home peak expiratory flow measurements were also recorded, as was peak flow measured with the spirometer. The results of the pulmonary function tests were considered not to correlate with asthma symptoms and treatment, and to be likely to lead to a change in asthma management, if: During an interval assessment: The patient complained of no, few or only moderate symptoms, the doctor felt asthma control was excellent, very good or reasonable, respectively, and did not change treatment, but FEV 1 % (normal, > >80%) or FEF 25%-75% (normal, > >65%) was less than 65%. The patient and the doctor thought control was poor, the dose of maintenance asthma therapy was increased, but pulmonary function tests revealed no evidence of bronchospasm. During assessment of an acute exacerbation: The patient and the doctor felt current asthma control was excellent or very good, no increase in dose of inhaled steroids was suggested and no oral corticosteroids were prescribed, but FEV 1 % or FEF 25%-75% was less than 65%. Results Twenty-seven adolescents with asthma (male : female ratio, 2 : 1) were assessed on a total of 37 occasions. On 22 occasions they were elective interval assessments and 15 were for an acute asthma exacerbation. Nineteen patients (70%) were monitoring peak flow at home. Twenty-nine (78%) of the pulmonary function tests were within two hours, four (11%) between two and four hours and four (11%) between four and 14 hours after the clinical assessment. Satisfactory spirometry measurements were achieved in all patients without difficulty (fewer than four repeats). Of the 22 interval assessments, 16 (73%) were in patients taking inhaled corticosteroids (in 11 of these the patients were taking more than 700 µg inhaled corticosteroids per day, and in five FEF 25%-75% values were less than 65%). In two (9%) interval assessments peak expiratory flows were less than 300 L/min (in only one of the assessments with FEF 25%-75% less than 65% were peak flows less than 300 L/min). Of the 15 acute exacerbation assessments, eight (53%) were in patients taking inhaled corticosteroids (in three of these the patients were taking more than 700 µg inhaled corticosteroids per day). In five (45%) acute exacerbation assessments peak expiratory flows were less than 300 L/min (four were unavailable). Details of the patients whose pulmonary function tests did not correlate with asthma symptoms and treatment are given in the Table. Overall, pulmonary function tests not correlating with clinical and patient assessment of asthma severity were found in 11 of 37 assessments (30%; 95% confidence interval [CI], 16%-47%). If only those tests performed within four hours of the clinical assessment are included, pulmonary function tests in 10 of 33 assessments (30%; 95% CI, 15%-46%) did not correlate with asthma severity. Pulmonary function tests in six of the 22 interval assessments (27%; 95% CI, 11%-50%) showed FEV 1 % or FEF 25%-75% to be less than 65% when management had not been changed after clinical assessment (Cases 1-6). During acute exacerbations, four of 15 assessments (27%; 95% CI, 8%-55%) showed FEV 1 % or FEF 25%-75% values to be less than 65% when no change in treatment had been made on clinical grounds (Cases 8-11). Tests in one patient (Case 7) showed normal pulmonary function after clinical assessment had suggested poor asthma control. Her pulmonary function tests were carried out within two hours of the clinical evaluation; her inhaled cortico steroid dose had been doubled. Discussion This community-based study of all young adolescent asthmatics presenting to their general practitioners in a country town found that in 30% of assessment opportunities the results of pulmonary function tests were likely to change management. This proportion was maintained even if slightly delayed pulmonary function tests (4-14 hours) were excluded. This result is comparable with previously published findings that 54% of apparently well asthmatics had lower than expected FEF 25%-75% values at follow-up, despite being asymptomatic. 5 At interval assessments in which management had not been changed and the results of pulmonary function tests were low, three of five adolescents (Table: assessments 1, 3-6) reported frequent wheeze. The other two thought their asthma was well controlled; however, their FEF 25%-75% values were 62% and 42%, respectively. In these patients peak flows, measured at home and by spirometry, were all above 300 L/min and this may have accounted for ALIGN=TOP the reluctance to change therapy. However, it has been shown previously that peak flow results can be misleading, and widely varying optimal values can be expected. 3 A low expectation of what can be achieved in frequently symptomatic patients may contribute to a less aggressive approach in adolescents with asthma. The rather frequent use of inhaled corticosteroids in relatively high doses in this small sample of asthmatics suggests that a more objective measure of asthma status should be used. Potential overuse of inhaled corticosteroids in these growing young people may not always safeguard those at risk of more severe asthma. Six of 11 patients (55%) taking more than 700 µg inhaled corticosteroids had FEF 25%-75% values less than 60%, suggesting that in these patients an even higher dose of inhaled corticosteroid may be required. More specific alterations to long term inhaled steroid use would be possible if pulmonary function tests were performed regularly. During assessments for acute exacerbation the rate of pulmonary function tests not correlating with symptoms was still high (27%) and the FEF 25%-75% was worryingly low in three patients in whom management was not altered (Table: assessments 8, 9, 10, and 11). These three adolescents all had frequent wheeze, but presumably were not distressed, with peak flows (measured at home and by spirometry) above 320 L/min. Pulmonary function tests gave an indication of small airways disease which they were not aware of or was not revealed by their peak flow measurements. Our study involved a small number of patients and the confidence intervals calculated suggest a larger study is necessary. Nevertheless, data on mortality in asthma indicate that underestimation of asthma severity can be extremely important. Robertson et al. found that about 35% of possibly preventable asthma deaths may have been related to medical practitioner underestimation of asthma severity. 6 The full implications of FEF 25%-75% values in the 55%-65% range is not yet certain. A long term follow-up of asymptomatic patients with values in this range has not yet been done. Most of our patients with low FEF 25%-75% values not correlating with symptoms had values below 55% (Table: 7 of 10 assessments). Thus, even if the implications of an FEF 25%-75% value between 55% and 65% is disputed, the frequency of the lower results suggests more aggressive treatment is required. This relatively small study of asthmatic adolescents in a small country town strongly supports the view that pulmonary function tests need to be part of the routine assessment of acute and chronic asthmatics. Acknowledgements We thank Professor P D Phelan, Department of Paediatrics, University of Melbourne, for his provocation, encouragement and support; and Mr Ross Gollan, Senior Lecturer, Department Mathematics and Statistics, Deakin University. References Sly PD, Landau LI, Weymouth R. Home recording of peak expiratory flow rates and perception of asthma. Am J Dis Child 1985; 139: 479-482. Landau LI. The value of lung function in guiding drug therapy in childhood asthma. Eur Respir Rev 1994; 4: 10-14. Phelan PD, Olinsky A, Robertson CF. Respiratory illness in children, 4th edition. Cambridge: Blackwell Scientific Publications, 1994; 152-156. Milner AD. Childhood asthma: diagnosis, treatment and management. London: Martin Dunitz, 1987; 18-38. Bye MR, Kerstein D, Barsh E. The importance of spirometry in the assessment of childhood asthma. Am J Dis Child 1992; 146: 977-981. Robertson CF, Rubinfeld AR, Bowes G. Deaths from asthma in Victoria: a 12-month survey. Med J Aust 1990; 152: 511-517.(Received 19 Sep 1995, accepted 4 Jul 1996) Authors' details 106 McKillop Street, Geelong, VIC 3220. Peter H Hewson, MD, FRACP, Consultant Paediatrician. Colac Hospital, Corangamite Street, Colac, VIC. Elizabeth A Tippett, DipPhys, Senior Physiotherapist. 2 Connor Street, Colac, VIC. Danny M Jones, MB BS, DA, DipRACOG, General Practitioner; Justin P Madden, MB BS, DA, DRCOG, General Practitioner; Peter Higgs, MB BS, General Practitioner. No reprints will be available. Correspondence: Dr P H Hewson. - - To top of article - ©MJA 1996 <URL: http://www.mja.com.au/> © 1996 Medical Journal of Australia.

Peter H Hewson · Elizabeth A Tippett · Danny M Jones · Justin P Madden · Peter Higgs

Position Statement Asthma in pregnancy and lactation A position paper for the Thoracic Society of Australia and New Zealand Christine F McDonald and Jonathan G W Burdon MJA 1996; 165: 485-488 Introduction - Literature search - Effects of pregnancy on asthma - Effects of asthma on pregnancy - Management of asthma in pregnancy - Pharmacological therapy - Labour - Breastfeeding - Patient education - Monitoring - References - Author's Details - - More articles on Respiratory medicine This position statement was developed as a consensus view between the two authors and was subsequently reviewed by the Education and Research Sub-Committee of the Thoracic Society of Australia and New Zealand, whose membership comprises six respiratory physicians with a broad range of interests in research and clinical respiratory medicine. This Committee also sought the opinion of an external reviewer with expertise in the subject. The following conclusions were reached: Physiological changes which occur during pregnancy may affect asthma control. Regular monitoring (monthly or every six weeks) of asthmatic women should occur throughout pregnancy. Regular therapy, including the use of inhaled steroids, is recommended. Well-controlled asthma should have no adverse effects on pregnancy, labour or breastfeeding. Medicines used to control asthma carry less risk to the mother and baby than a severe attack of asthma. Good asthma management will result in a birth outcome similar to that experienced by women without asthma. Introduction Pregnant women with asthma should be reassured that their asthma medication carries less risk to the fetus than a severe asthma attack. Inadequately treated asthma can cause maternal and fetal hypoxaemia, which leads to complications during pregnancy and poorer birth outcomes. Here, we outline the effects of asthma on pregnancy (and vice versa) and the management of asthma during pregnancy and the postpartum period. Literature search We searched the literature, using the MEDLINE database, for the period 1985-1995 and the keywords "asthma" and "pregnancy". Standard textbooks on asthma were also reviewed. A total of 146 papers were identified and other papers contained within their references were also reviewed. Thirty-three papers were found suitable. Effects of pregnancy on asthma Although bronchial hyperresponsiveness lessens during mid-pregnancy,1 studies reporting changes in asthma severity during pregnancy show widely differing results.2-5 Overall, the data indicate that the clinical severity of asthma during pregnancy improves in about 30% of women, remains stable in about 50% and worsens in about 20%.6Factors responsible for the variation in asthma severity during pregnancy include an increase in circulating free cortisol,7,8 a decrease in bronchomotor tone and an increase in serum concentrations of cyclic adenosine monophosphate.8 These changes would normally improve the asthma, but in pregnancy other competing factors, including exposure to fetal antigens and alterations in cell-mediated immunity, may worsen asthma symptoms.8 Asthma may be further complicated by sinusitis and rhinitis, which occur in about 35% of pregnant women, but vascular dilatation and congestion of the mucosa of the upper respiratory tract (vasomotor rhinitis of pregnancy) does not involve the lower airways.9 The physiological respiratory changes which occur during pregnancy may affect asthma control (Box). Changes in blood gases secondary to acute asthma will be superimposed on the physiological respiratory alkalosis of pregnancy. Therefore, a normal or elevated PCO2 associated with acute asthma will indicate respiratory compromise of greater severity in pregnancy than in the non-pregnant state. The dyspnoea of pregnancy must be differentiated from dyspnoea caused by asthma. Indeed, patients who develop asthma during pregnancy may wrongly attribute dyspnoea to the pregnancy, which can lead to undermedication and severe maternal and fetal hypoxaemia. It is difficult to predict which women will experience worsening of their asthma during pregnancy, but the severity of the condition before pregnancy,2,8 and an absence of the expected decrease in IgE concentration during pregnancy,8,13 should alert the clinician to this possibility. If asthma is going to worsen, it will usually do so between 24 and 36 weeks' gestation. Symptoms are likely to be less troublesome in the peripartum period. In most women, asthma severity returns to the prepregnant state within three months of delivery,1,5 but in rare cases it may be worse than before the pregnancy. Effects of asthma on pregnancy The fetus exists in a precarious state of oxygenation and is dependent for its oxygen supply on maternal arterial oxygen content, venous return and cardiac output, and uterine artery and placental bloodflow. Compensating mechanisms of the fetus to combat potentially adverse conditions of oxygenation include a haemoglobin level of at least 16 g/dL and a P50 of 22 mmHg (indicating a left shift in the oxyhaemoglobin dissociation curve). Poorly controlled asthma or severe asthma attacks further threaten the fetus because of increased maternal hypoxaemia and diminution of uterine artery bloodflow secondary to hypocapnic vasoconstriction. These women have an increased incidence of low birthweight and premature babies, neonatal hypoxia, complications during labour, and perinatal and maternal mortality.14-17 Hyperemesis gravidarum, maternal haemorrhage and pre-eclampsia are more common in this group.14 For these reasons, it has been argued that a pregnancy complicated by asthma should be regarded as a high risk pregnancy.16 However, the babies of most asthmatic women (i.e., those with well controlled asthma) show no difference in birthweight, Apgar scores or rates of congenital malformation when compared with those of non-asthmatic mothers.5,15,16 Management of asthma in pregnancy The management of asthma during pregnancy is similar to that at any other time: treatment should be aggressive, with the aim of eliminating symptoms and restoring and maintaining normal lung function. Guidelines for asthma management have been published by the National Asthma Campaign and are highly recommended.18 Cooperation between the respiratory physician and obstetrician is important throughout pregnancy for women with severe asthma. Pharmacological therapy Care should be taken with pharmacological therapy during pregnancy, particularly in the first trimester, when the risk of congenital defects is greatest. Fortunately, the medicines currently used in the treatment of asthma have been found in practice to have a good safety profile during pregnancy. The drug categories listed here are those of the Australian Drug Evaluation Committee's categorisation of risk of drug use in pregnancy.19 Bronchospasm relaxants β2-Agonists (category A): There is no evidence of a teratogenic risk with the commonly used inhaled β2-agonists salbutamol, terbutaline and fenoterol. Intravenous salbutamol may be used to delay the onset of labour in some circumstances and there is a theoretical risk that oral β2-agonists could also have this effect. Delayed labour does not occur with bronchodilators administered by metered-dose inhaler or wet nebulisation. Ipratropium bromide (category B1): Although there is less experience with this drug, it appears to be safe for use during pregnancy, as it is poorly absorbed when administered by the inhaled route and has not been identified as imparting an increased risk of fetal malformations. Salmeterol (category B3): These newer long-acting agents have not been tested extensively in pregnant women. Theopyllines (category A): The use of theophyllines remains controversial. They may aggravate the nausea and reflux suffered by some pregnant women and can cause transient neonatal tachycardia and irritability.20,21 Teratogenicity has been shown in animals,22,23 and there are occasional case reports of cardiovascular abnormalities in humans.24 However, larger human studies have not shown any significant increase in fetal abnormalities.25,26 It has been suggested that theophyllines be withheld during the first trimester.26 If they are used, serum theophylline levels should be measured as drug metabolism may alter during pregnancy. Preventive inhalations and aerosols Sodium cromoglycate (category A): This drug appears to have no adverse fetal effects. Nedocromil sodium (category B1): Animal studies have not shown any teratogenic effects, but, as with all new drugs, care should be exercised, especially in the first trimester. Inhaled corticosteroids Beclomethasone and budesonide (category B3): These are the mainstay of treatment in moderate to severe asthma and both appear to have a good safety profile in pregnancy. Although beclomethasone is a known animal teratogen, its use in pregnant women has not been associated with teratogenicity. The largest human experience of inhaled corticosteroids is with beclomethasone and it is therefore the inhaled steroid of choice in pregnancy.9 Less information is available on the use of budesonide in pregnancy as it is a newer drug. If moderate to severe asthma is well controlled with budesonide, the risks of destabilising the condition by changing from budesonide to beclomethasone must be weighed against the potential benefits of using a medicine which has been more extensively studied. Fluticasone (category B3): Experience with this drug in pregnancy is more limited. Oral corticosteroids (Category A) These are sometimes necessary for severe asthma in pregnancy but usually only for short periods. An increased risk of cleft palate and placental abnormalities has been reported in animals given huge doses of oral steroids.27,28 These abnormalities have not been reported in humans, and the results of animal studies should not deter the practising clinician from using oral corticosteroids if required. Methotrexate and other steroid-sparing agents have an occasional role in the treatment of some individuals with severe resistant asthma. However, these drugs are contraindicated in women of childbearing age who are trying to conceive or who are pregnant. Labour There is no increase in the induction of labour, use of forceps or emergency caesarean sections in women with asthma, but elective caesarean sections are more common. Women with very severe asthma may be advised to have an elective caesarean section at a time when their asthma control is good. Close cooperation between the respiratory physician, obstetrician and anaesthetist is particularly important at this time. Symptoms of asthma during labour are generally easily controlled with standard asthma therapy. Acute asthma attacks in labour are rare, but prostaglandin F2alpha (Dinoprost, UpJohn) and ergometrine cause bronchoconstriction. Their use in the induction of labour, the initiation of the third stage of labour and for placental separation should be avoided.29 There is no evidence that oxytocin causes bronchoconstriction. Breastfeeding Breastfeeding should be continued in women with asthma as breast milk confers some immunity to infection to the baby, especially to respiratory and gastrointestinal infections. Breast milk may contain very small amounts of the drugs used to treat asthma, but, in general, these are not known to be harmful to the infant. Corticosteroids are about 90% protein bound in the blood and are not secreted into breast milk in any significant quantity. However, the manufacturers of budesonide have recommended discontinuation of this drug during lactation because of an absence of information regarding its transmission into breast milk. The decision to alter a successful medication regimen that is controlling the mother's asthma must be weighed against any potential detrimental effects to the infant from continuation of the drug. Although less than 1% of maternal theophylline is transferred to the infant,30 it has been suggested that women breastfeed their baby before taking this drug to minimise its side effects.31 It is recommended that tetracycline antibiotics and iodine-containing mixtures be avoided in pregnant and lactating women as they may cause dental discoloration and goitre in the baby. Patient education Environmental trigger factors which cause deterioration in asthma control or may lead to acute asthma attacks must be avoided and pregnant women should be urged to stop smoking. Mothers should be advised about the importance of avoiding exposure to allergens and environmental tobacco smoke in the first years of their child's life to reduce the potential for later asthma development.32 Monitoring Women with asthma should be reviewed at least every four to six weeks (and more frequently if needed) so that early changes in respiratory function can be detected and treated expeditiously. Although formal spirometry may be indicated from time to time, lung function can be easily monitored at home with a peak flow meter.33 The doctor should formulate an asthma action plan with the patient, to be put into effect if her condition deteriorates.33If a woman with asthma is closely monitored, pregnancy outcomes approaching those of the general population can be expected.34 Well-controlled asthma should have no adverse effect on pregnancy, labour or breastfeeding. References Juniper EF, Daniel EE, Roberts RS, et al. Improvement in airway responsiveness and asthma severity during pregnancy. A prospective study. Am Rev Respir Dis 1989; 140: 924-931. Williams DA. Asthma and pregnancy. Acta Allergol 1967; 22: 311-323. Turner ES, Greenberger PA, Patterson R. Management of the pregnant asthmatic patient. Ann Intern Med 1980; 93: 905-919. Greenberger PA, Patterson R. Management of asthma during pregnancy. N Engl J Med 1985; 312: 897-902. Schatz M, Harden K, Forsythe A, et al. The course of asthma during pregnancy, post-partum and with successive pregnancies: a prospective analysis. J Allergy Clin Immunol 1988; 81: 509-517. Burdon JGW, Goss G. Asthma and pregnancy. Aust N Z J Med 1994; 24: 3-4. Nolten WE, Rueckert PA. Elevated free cortisol index in pregnancy: possible regulatory mechanisms. Am J Obstet Gynecol 1981; 139: 492-498. Gluck JC, Gluck PA. The effects of pregnancy on asthma: a prospective study. Ann Allergy 1976; 37: 164-168. National Heart, Lung and Blood Institute. Report of the Working Group on Asthma and Pregnancy. Executive Summary: Management of asthma during pregnancy. J Allergy Clin Immunol 1994; 93: 139-162. Prowse CM, Gaensler EA. Respiratory and acid-base changes during pregnancy. Anesthesiology 1965; 26: 381-392. Rees GB, Pipkin KB, Symonds EM, et al. A longitudinal study of respiratory changes in normal human pregnancy with cross sectional data on subjects with pregnancy-induced hypertension. Am J Obstet Gynecol 1990; 162: 826-830. Gee JBL, Packer BS, Millen JE, et al. Pulmonary mechanics in pregnancy. J Clin Invest 1967; 46: 945-952. Gazioglu K, Kaltreider NL, Rosen M, et al. Pulmonary function during pregnancy in normal women and patients with cardiopulmonary disease. Thorax 1970; 25: 445-450. Hernandez E, Angell CS, Johnson JW. Asthma in pregnancy: current concepts. Obstet Gynecol 1980; 55: 739-743. Gordon M, Niswander KR, Berendes H, et al. Fetal morbidity following potentially anoxigenic obstetric conditions. VII. Bronchial asthma. Am J Obstet Gynecol 1970; 106: 421-429. Bahna SL, Bjerkedal T. The course and outcome of pregnancy in women with bronchial asthma. Acta Allergol 1972; 27: 397-406. Fitzsimons R, Greenberger PA, Patterson R. Outcome of pregnancy in women requiring corticosteroids for severe asthma. J Allergy Clin Immunol 1986; 78: 349-353. National Asthma Campaign. Asthma Management Handbook. Melbourne: National Asthma Campaign Ltd, 1993. Australian Drug Evaluation Committee. Medicines in Pregnancy. 3rd ed. Commonwealth Department of Health and Family Services, 1996. 20. Yeh TF, Pildes RS. Transplacental aminophylline toxicity in a neonate [letter]. Lancet 1977; 1: 910. Labovitz E, Spector S. Placental theophylline transfer in pregnant asthmatics. JAMA 1982; 247: 786-788. Gilbert EF, Bruyere HJ, Ishikawa S, et al. The effect of methylxanthines on catecholamine-stimulated and normal chick embryos. Teratology 1977; 16: 47-52. Ishikawa S, Gilbert EF, Bruyere HJ, et al. Aortic aneurysms associated with cardiac defects in theophylline-stimulated chick embryos. Teratology 1978; 18: 23-30. Park JM, Schmer V, Myers TM. Cardiovascular anomalies associated with prenatal exposure to theophylline. South Med J 1990; 83: 1487-1488. Schatz M. Asthma during pregnancy: interrelationships and management. Ann Allergy 1992; 68: 123-133. Stenius-Aarniala B, Riikonen S, Teramo K. Slow-release theophylline in pregnant asthmatics. Chest 1995; 107: 642-647. Fainstat T. Cortisone-induced congenital cleft palate in rabbits. Endocrinology 1954; 55: 502-508. Blackburn WR, Kaplan HS, McKay DG. Morphologic changes in the developing rat placenta following prednisolone administration. Am J Obstet Gynecol 1963; 92: 234-246. Math AA, Hedqvist P. Effect of prostaglandins F2 and E2 on airway conductance in healthy subjects and asthmatic patients. Am Rev Respir Dis 1975; 111: 313-320. Yurchak AM, Jusko WJ. Theophylline secretion into breast milk. Pediatrics 1979; 57: 518-525. Berkowitz R, Coustan DR, Mochizuki TK. Handbook for prescribing medications during pregnancy. 2nd ed. Boston: Little, Brown and Co, 1986. Peak JK. Prevention of asthma. Eur Respir J 1996; 9: 1545-1555. The Thoracic Society of Australia and New Zealand. Peak flow meter use in asthma management. Med J Aust 1996; 164: 727-730. Stenius-Aarniala B, Piilrila P, Teramo K. Asthma and pregnancy: a prospective study of 198 pregnancies. Thorax 1988; 43: 12-18. Authors' details Department of Respiratory Medicine, Austin and Repatriation Medical Centre, Heidelberg, VIC. Christine F McDonald, PhD, FRACP, Consultant Respiratory Physician. Department of Respiratory Medicine, St Vincent's Hospital, Melbourne, VIC. Jonathan G W Burdon, MD, FRACP, Consultant Respiratory Physician. Reprints: Dr J G W Burdon, Director, Department of Respiratory Medicine, St Vincent's Hospital, 41 Victoria Parade, Fitzroy, VIC 3065. 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/> Physiological respiratory changes in pregnancy Dyspnoea Dyspnoea is experienced by 60%-70% of women at some time during pregnancy,10 most commonly in the first or second trimester. Mechanical factors do not seem to play a major role in its pathogenesis because it frequently occurs before any increase in abdominal girth. Early pregnancy: Dyspnoea may be caused by rising circulating maternal progesterone levels, which result in a progressive increase in minute ventilation of up to 40% by the end of the first trimester, largely as a result of increases in tidal volume.11 Late pregnancy: Dyspnoea later in pregnancy is (likely to be) caused by a combination of the hyperventilation of pregnancy and restriction due to uterine enlargement. The latter leads to a small reduction in both residual volume and functional residual capacity, while total lung capacity is maintained by an increase in inspiratory capacity.12,13 Changes in peak flow rates and forced expiratory volume in one second (FEV1) are small and of no clinical significance.1,13 Respiratory alkalosis Maternal gas exchange is mildly disordered as a result of the increase in minute ventilation.11 A slight rise in arterial oxygen tension, a change in carbon dioxide tension and pH changes are common and indicate a mild respiratory alkalosis. The changes in arterial blood gas tensions occur despite increases in oxygen consumption and carbon dioxide production in the last few months of pregnancy.11 Back to text

Christine F McDonald

Approximately one-quarter of adult Australians are "active" smokers, but almost everyone is a "passive" smoker at some time. The right of adults to make a fully informed decision to begin or to continue smoking is not in question, but there is widespread concern about the risks carried by non-smokers who breathe environmental tobacco smoke (ETS) from others' cigarettes. If passive smoking really does harm health, then a strong case can be made for limiting the places and situations in which smoking is permitted. In November 1995, the National Health and Medical Research Council (NHMRC) released for public comment a new report on the effects of passive smoking on health.1 It reviewed the scientific evidence on the risks to health from exposure to ETS, gave an estimate of the total burden of illness attributable to passive smoking in Australia, and gave 25 recommendations for measures to reduce this burden. (The main recommendations are shown in the Box.) The report concluded that the evidence relating ETS to several important categories of illness had strengthened considerably since the last NHMRC review in 1986.2 It found that ETS is firmly linked, as a likely causal factor, to lower respiratory tract illness in young children, asthma, lung cancer and cardiovascular disease, and provided detailed calculations of the numbers and costs of additional cases of these conditions attributable to passive smoking in Australia. Evidence since 1986 implicates exposure to ETS as a cause of sudden infant death syndrome, "glue ear" in childhood, acute irritation of the respiratory tract, and low birth weight (as a consequence of non-smoking mothers being exposed to ETS during pregnancy). However, the report found insufficient evidence concerning these conditions to include them in estimates of the burden of illness. Each year, according to the NHMRC report, passive smoking leads to more than 5400 extra hospital admissions in Australia and costs the country about $21 million. The brunt of this excess morbidity -- 51 600 episodes of asthma (about 9% of all cases) in people aged less than 15 years, and about 2000 admissions to hospital in the first 18 months of life because of chest illness -- is borne by children. There are approximately 10 attributable cases of lung cancer among adults who have never smoked and 100 deaths from coronary disease. These figures are likely to be underestimates. The effects of passive smoking on current and ex-smokers have not been included, any effects of low levels of exposure in causing or exacerbating asthma have been ignored, and it has been assumed that passive smoking does not cause other respiratory problems in children over 18 months of age. Evidence from overseas indicates that the burden of adult illness from exposure outside the home is likely to be at least as great as that from domestic exposure,3 but the NHMRC estimates include domestic exposure only. The term "passive smoking" was coined 25 years ago,4 but scientific and public interest in the issue accelerated sharply in 1981 when Hirayama published evidence that exposure to ETS went beyond being a source of annoyance to non-smokers and actually caused lung cancer.5 The NHMRC working party was able to find 31 separate studies of ETS and lung cancer in non-smokers published before 1995, as well as 41 investigations of the impact of passive smoking on various respiratory complaints in childhood. As the report by Doyle et al. in this issue of the Journal shows, the evidence linking ETS with impairment and illness continues to grow. This prospective study of a cohort of very low birthweight children found that those who had been exposed to tobacco smoke since birth had worse respiratory function than their non-exposed peers when tested at 11 years of age. The findings exhibit a dose-response relationship, despite a somewhat crude assessment of exposure to ETS, and cannot be explained by differences in the socioeconomic circumstances. The results are based on small numbers of children, but are consistent with other published studies. It should be noted also that active smokers never regain the decrement in respiratory function that they accumulate, even if they give up smoking.6 There is a clear message to doctors and parents: passive smoking is the most readily preventable cause of respiratory impairment in childhood. Vulnerable groups in society -- infants, children and adults with asthma and other respiratory conditions, and individuals with established cardiac disease -- are most affected by exposure to ETS. Workplaces where smoking is still allowed, including hotels and restaurants, are also a special case because the passive smoking by employees in these enterprises is often involuntary. Progress has been made in the provision of smoke-free workplaces, but about 40% of Australian indoor workers are still exposed to tobacco smoke at work.7 What is now the appropriate public policy response to more than two decades of careful scientific research into the risks associated with passive smoking? We probably can do little better than be guided by John Stuart Mill's oft-quoted essay On liberty:8 "The only purpose for which power can be rightfully exercised over any member of a civilised community, against his will, is to prevent harm to others." Alistair Woodward Professor of Public Health Wellington School of Medicine, New Zealand Konrad Jamrozik Associate Professor, Department of Public Health University of Western Australia References National Health and Medical Research Council. The health effects of passive smoking: The draft report of the NHMRC Working Party, November 1995. Canberra: NHMRC, 1995. National Health and Medical Research Council. Effects of passive smoking on health. Canberra: AGPS, 1987. United States Environmental Protection Agency. Respiratory health effects of passive smoking: lung cancer and other disorders. Washington DC: Office of Research and Development, 1992. Harke HP. Zum problem des "passiv-rauchens". Munch Med Wochenschr 1970; 51: 2328-2334. Hirayama T. Nonsmoking wives of heavy smokers have a higher risk of lung cancer: a study from Japan. BMJ 1981; 282: 183-185. Fletcher CM, Peto R. The natural history of chronic airflow obstruction. BMJ 1977; 1: 1645-1648. Borland R, Mullins R. The increasing prevalence of workplace smoking bans in Victoria, 1994. J Occup Health Safety Aust N Z 1994; 10: 35-40. Mill JS. On liberty. London: Watts & Co., 1941: 11.

Alistair Woodward · Konrad Jamrozik

Passive smoking and respiratory function in very low birthweight children Lex W Doyle, Geoffrey W Ford, Anthony Olinsky, Annette M L Knoches and Catherine Callanan For editorial comment see Woodward & Jamrozik 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/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - ©MJA1997 Abstract Aim: To determine if an adverse relationship exists between passive smoking and respiratory function in very low birthweight (VLBW) children at 11 years of age. Setting: The Royal Women's Hospital, Melbourne. Patients: 154 consecutive surviving children of less than 1501 g birthweight born during the 18 months from 1 October 1980. Methods: Respiratory function of 120 of the 154 children (77.9%) at 11 years of age was measured. Exposure to passive smoking was established by history; no children were known to be actively smoking. The relationships between various respiratory function variables and the estimated number of cigarettes smoked by household members per day were analysed by linear regression. Results: Most respiratory function variables reflecting airflow were significantly diminished with increasing exposure to passive smoking. In addition, variables indicative of air-trapping rose significantly with increasing exposure to passive smoking. Conclusions: Passive smoking is associated with adverse respiratory function in surviving VLBW children at 11 years of age. Continued exposure to passive smoking, or active smoking, beyond 11 years may lead to further deterioration in respiratory function in these children. MJA 1996; 164: 266-269 Introduction Passive smoking is associated with several adverse health outcomes in children, including higher rates of asthma,1 and infections of the upper2 and lower3 respiratory tract. Further, respiratory function is reduced with passive smoking in children who have no lung disease,4 as well as those with lung diseases such as asthma5 and cystic fibrosis.6 To survive the neonatal period, many very low birthweight (VLBW) children (less than 1500 g at birth) require prolonged periods of assisted ventilation, and some may develop bronchopulmonary dysplasia (BPD) and suffer from ongoing respiratory problems as a consequence. We have previously reported the respiratory health to eight years of age of cohorts of children of birthweight 500-999 g (n = 83), 1000-1500 g (n = 114) and > > 2500 g (n = 51).7 Passive smoking was significantly related to the duration of hospitalisation for respiratory problems up to two years of age for all children in that study, but was not associated with changes in respiratory function at eight years of age. In contrast, in another recent cohort study of respiratory function at seven years of age in children of birthweight less than 2000 g Chan et al.8 reported reduced air-flow rates with maternal smoking, but not with smoking by other household members. Because the effects of passive smoking could increase with increasing duration of exposure, the aim of this study was to determine if an adverse relationship exists between passive smoking and respiratory function at 11 years of age in VLBW children. Methods We studied 154 consecutive surviving children of less than 1501 g birthweight born during the 18 months from 1 October 1980 at the Royal Women's Hospital, Melbourne, the largest of the three tertiary-level perinatal centres in Victoria. Details of the survival rate and early neonatal care of this cohort have been described.9,10 Bronchopulmonary dysplasia (BPD) was diagnosed in children who had required intermittent positive pressure ventilation in the neonatal period, who had respiratory distress and were still having oxygen therapy at 28 days of age, and who had an abnormal chest x-ray consistent with stage III or IV disease (as defined by Northway et al.11 ) at or after 28 days. A previous report of the respiratory function of this cohort at eight years of age7 included data for some children with birthweights of less than 1000 g born before 1 October 1980. We did not have the resources to measure respiratory function at 11 years of age of the children born before October 1980. Respiratory health was determined by history and examination, and measurement of respiratory function. Children who had required bronchodilators within the previous year for attacks of wheezing were considered to have asthma. Data on passive smoking were obtained by asking the parents about the daily consumption of cigarettes by members of the household. We did not distinguish between mothers and other smokers, or between smoking inside or outside the home. Some data on maternal smoking in pregnancy had been collected in the perinatal period, but were obtained for only one-third of mothers. Children were questioned about active smoking in their parents' absence. As some children had changed households in their lifetimes, we considered those who had lived in any household with smokers over the 11-year period to have been passively smoking during childhood. Two categories of social class were determined -- unskilled or unemployed, and other (professional, skilled or semi-skilled) -- based on the occupation of the family breadwinner. Respiratory function was measured in the Department of Thoracic Medicine at the Royal Children's Hospital, Melbourne, as described previously,7 by personnel blinded to the exposure of individual children to passive smoking. Maximum expiratory flow rates were recorded with a pneumotachograph (Fleisch No. 3, Switzerland) and plotted against volume by integrating flow on an X-Y recorder to obtain flow-volume loops. Maximum flow rates at 75% (VEmax75%), 50% (VEmax50%) and 25% (VEmax25%) of forced vital capacity (FVC), and forced expiratory flow between 25% and 75% of FVC (FEF25%-75%), were measured from the loops. Flow rates were corrected for body size by dividing by vital capacity (VC). Vital capacity, FVC and forced expiratory volume in one second (FEV1) were measured with a water-filled spirometer (Godart Expirograph, Bilthoven, Netherlands) in accordance with standard guidelines, and results at body temperature and pressure saturated with water vapour were expressed as a percentage of the predicted value for age, height and sex.12 Total lung capacity (TLC) and residual volume (RV) were measured in a body plethysmograph (Jaeger Bodyscreen 2, Wurzburg, Germany). Children were not subjected to bronchial provocation tests as these are poorly tolerated, and we were eager to maintain a high degree of cooperation with these and with future respiratory function tests. Not all children could complete all respiratory function tests, either because of poor cooperation, or unavailability or malfunction of equipment on the day of testing. Data were edited and analysed using SPSS.13 Dichotomous variables were contrasted by chi-squared analysis, and continuous variables by t test, or Mann-Whitney U test if the data were skewed. The dose-response relationship between the estimated daily number of cigarettes consumed by members of the household and various respiratory function variables was established by linear regression; linear and quadratic relationships were tested. Data were then analysed by linear regression to adjust for the potentially confounding variables of birthweight, gestational age, birthweight ratio (child's birthweight divided by median birthweight for gestational age14 ), sex, BPD, and asthma; all variables were entered simultaneously, even if they were not statistically significant. Durations of intermittent positive pressure ventilation and oxygen therapy were not included as they were strongly related to BPD. For all analyses, P values of less than 0.05 for any test were regarded as statistically significant. Results We measured the respiratory function of 120 of the 154 (77.9%) children at 11 years of age. Of the 34 children not tested, 15 lived in another State, four lived in another country, 10 refused the tests, three were lost to follow-up, and two were too disabled to complete the tests. There were no substantial differences in perinatal variables between children who did and did not have respiratory function tests at 11 years of age. Eighty of the 120 children (66.7%) had been exposed to passive smoking in the household. The only substantial differences in perinatal or subsequent variables between children who were and were not exposed to passive smoking were a significantly longer duration of oxygen therapy and a lower proportion of unskilled or unemployed families in the group not exposed (Table 1). For children exposed to passive smoking, the median number of cigarettes consumed in the household per day was 21 (interquartile range, 15-25). Of the 15 children tested who had developed BPD in the newborn period, three (20%) had asthma at 11 years of age; this proportion was similar for children with asthma at 11 who did not have BPD (22 of 105; 21%). For variables expressed as a percentage of predicted values (FEV1, FVC, RV, TLC), the means of the measured values were all close to their expected values of 100% (Table 2). For all respiratory function variables significantly associated with the dose of passive smoking, a quadratic relationship was more significant than a linear relationship (Table 2, Figures 1 and 2). Most respiratory function variables reflecting airflow (VEmax75%/VC, VEmax50%/VC, FEF25%-75%/VC, FEV1 and FEV1/FVC) were significantly diminished by increasing exposure to passive smoking (Table 2 [below], Figures 1a and 1b). In addition, RV, TLC and RV/TLC rose significantly (consistent with progressive air trapping) with increasing exposure to passive smoking (Table 2 [below], Figure 1c). One child was exposed to 115 cigarettes per day, and the next highest exposure was only 70 cigarettes per day. When the child exposed to 115 cigarettes per day was excluded, most of the statistically significant relationships disappeared, except for the increases in RV and RV/TLC (Figure 2). From the multiple linear regression analyses, some variables reflecting flow (VEmax75%/VC, VEmax50%/VC, VEmax25%/VC, FEF25%-75%/VC and FEV1/FVC) were significantly higher in girls. BPD was significantly associated with reductions in some variables reflecting air-flow (VEmax50%/VC, FEF25%-75%/VC, FEV1 and FEV1/FVC), as was asthma (with significant reductions in FEF25%-75%/VC, FEV1 and FEV1/FVC). FVC was significantly lower and VEmax25%/VC significantly higher with lower social class. Birthweight ratio, birthweight and gestational age were not significantly associated with any lung function variable. None of the statistical conclusions relating respiratory function variables with passive smoking were altered by adjusting for all potentially confounding variables, except that the reduction in VEmax50%/VC was no longer statistically significant. Discussion Passive smoking was associated with reduced airflow and air-trapping in VLBW children at 11 years of age, which is consistent with observations in non-preterm children free of lung disease.4 However, this finding was different from our observations of these children at eight years of age,7 when passive smoking was unassociated with any lung function variable. Chan et al.8 reported reduced flow rates with smoking by mothers in children of less than 2000 g birthweight at seven years of age, but they did not measure variables reflecting air-trapping. We did not distinguish between mothers and other smokers in the household. The association between passive smoking and adverse respiratory function in our VLBW children at 11, but not at eight, years of age suggests that the harmful effects of passive smoking take time to become obvious in VLBW children. Moreover, the adverse response seems to accelerate with increasing dose of passive smoking (Figures 1 and 2). We are concerned that continued exposure to passive smoking, or, even worse, active smoking, beyond 11 years will lead to not only further, but also to an accelerating rate of, deterioration in respiratory function. Our results should not be overinterpreted. They were not substantially altered by adjusting for potentially confounding perinatal or other variables, but we did not have data on a wide range of confounding variables. Moreover, they were heavily influenced by one child who lived in a household whose members consumed 115 cigarettes per day. Excluding this child from the analysis, the only remaining statistically significant associations indicated air-trapping with increasing exposure to passive smoking. However, we consider that this child's data should not be excluded just on the basis of heavier-than-average exposure to passive smoking. To remove any doubt about the association between passive smoking and adverse lung function in VLBW children, lung function could be measured in another cohort of VLBW children, or the same cohort when they are older. Parents of VLBW children, particularly those of children who have received assisted ventilation, frequently ask about long-term lung problems. Many variables, such as family history or duration of assisted ventilation and oxygen therapy, may be related to long-term lung problems, but most cannot be altered by the parents. Exposure to passive smoking is one variable associated with poorer respiratory function in VLBW children they can influence. Until there is evidence to the contrary, families of VLBW children should be encouraged to stop exposing their children to cigarette smoke in the household. As there appears to be a dose-response relationship, those who cannot stop smoking should at least reduce their children's exposure to passive smoking. Acknowledgement This study was supported in part by a grant from the Royal Women's Hospital-3AW Community Services Trust. References Landau L. Smoking and childhood asthma. Med J Aust 1991; 154: 715-716. Wright AL, Holberg C, Martinez FD, et al. Relationship of parental smoking to wheezing and nonwheezing lower respiratory tract illnesses in infancy. J Pediatr 1991; 118: 207-214. Etzel RA, Pattishall EN, Haley NJ, et al. Passive smoking and middle ear effusion among children in day care. Pediatrics 1992; 90: 228-232. Cook DG, Whincup PH, Papacosta O, et al. Relation of passive smoking as assessed by salivary cotinine concentration and questionnaire to spirometric indices in children. Thorax 1993; 48: 14-20. Chilmonczyk BA, Salmon LM, Megathlin KN, et al. Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. N Engl J Med 1993; 328: 1665-1669. Smyth A, O'Hea U, Williams G, et al. Passive smoking and impaired lung function in cystic fibrosis. Arch Dis Child 1994; 71: 353-354. Kitchen WH, Olinsky A, Doyle LW, et al. Respiratory health and lung function in 8-year-old children of very low birth weight: a cohort study. Pediatrics 1992; 89: 1151-1158. Chan KN, Noble-Jamieson CM, Elliman A, et al. Lung function in children of low birth weight. Arch Dis Child 1989; 64: 1284-1293. Kitchen WH, Ford GW, Murton LJ, et al. Mortality and two year outcome of infants of birthweight 500-1500 g: relationship with neonatal cerebral ultrasound data. Aust Paediatr J 1985; 21: 253-259. Kitchen WH, Yu VYH, Lissenden JV, Bajuk B. Collaborative study of very-low-birthweight infants: techniques of perinatal care and mortality. Lancet 1982; i: 1 454-1457. Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline-membrane disease: bronchopulmonary dysplasia. N Engl J Med 1967; 276: 357-368. Hibbert ME, Lanigan A, Landau LI, Phelan PD. Lung function values from a longitudinal study of healthy children and adolescents. Pediatr Pulmonol 1989; 7: 101-109. SPSS for Windows [computer program]. Version 6.1. Chicago, Ill: SPSS Inc, 1994. Kitchen WH, Robinson H, Dickinson AJ. Revised intrauterine growth curves for an Australian hospital population. Aust Paediatr J 1983; 19: 157-161. (Received 8 Jun, accepted 18 Nov 1995) Authors' details Division of Paediatrics, the Royal Women's Hospital, Melbourne, VIC. Lex W Doyle, MD, FRACP, Paediatrician; and Associate Professor, Departments of Obstetrics and Gynaecology, and Paediatrics, the University of Melbourne. Geoffrey W Ford, MB BS, FRACP, Paediatrician. Annette M L Knoches, MB BS, FRCP(C), Paediatrician. Catherine Callanan, RN, Research Nurse. Department of Thoracic Medicine, the Royal Children's Hospital, Melbourne, VIC. Anthony Olinsky, FRACP, Respiratory Physician. No reprints will be available. Correspondence: Associate Professor L W Doyle, Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, VIC 3052. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Lex W Doyle · Geoffery W Ford · Anthony Olinsky · Catherine Callanan

Editorial Oily fish and asthma - a fishy story? Further studies are required before claims can be made of a beneficial effect of oily fish consumption on asthma Interest in the possible health benefits of dietary fish lipids followed observations that populations with a high dietary intake of fish, such as Greenland Inuit and the Japanese, had low incidences of atherosclerotic disorders and of inflammatory conditions such as rheumatoid arthritis. Our recent understanding of asthma as a chronic inflammatory airway disease has led to speculation that a diet rich in fish oil may also ameliorate asthma. The potential anti-inflammatory effect of fish oil stems from its active ingredient, eicosapentaenoic acid (EPA), which is a competitive substrate with arachidonic acid for the generation of inflammatory mediators. The derivatives of arachidonic acid (an n-6 fatty acid) are leukotriene B4 (LTB4), a potent neutrophil chemoattractant and pro- inflammatory mediator, and the cysteinyl series of leukotrienes (LTC4, LTD4 and LTE4), which produce potent smooth muscle contraction and bronchoconstriction. In contrast, EPA (an n-3 fatty acid), as well as inhibiting arachidonic acid metabolism, is a substrate for the less active prostanoids (e.g., thromboxane A3) and leukotrienes (e.g., LTB5), and so has the potential to reduce airway inflammation and reverse bronchoconstriction. As the most profound anti-inflammatory actions of fish oil are on neutrophil function and mediator generation, it is not surprising that clinical trials of dietary fish oil have been beneficial in diseases where there is a neutrophilic inflammation, such as rheumatoid arthritis, psoriasis, cystic fibrosis and inflammatory bowel disease. However, in asthma the role of neutrophils is much less certain. Eosinophils and mast cells are thought to be the predominant effector cells in asthma (through the release of mediators), with T lymphocytes, macrophages and, possibly, mast cells having initiating and immunomodulatory roles through cytokine secretion. Placebo-controlled interventional studies of high dose fish oil supplementation in patients with asthma have been disappointing. Early short term trials (eight weeks) of up to 4 g/day of EPA in severe asthmatics showed no clinical benefit, despite demonstrating profound suppression of neutrophil chemotaxis and mediator generation.1 In a study in aspirin-intolerant subjects asthma control worsened after six weeks of 3 g/day of EPA, 2 consistent with the known aspirin-like effect of cyclooxygenase inhibition by EPA. Further studies in milder asthmatics with 3.2 g/day for 10 weeks showed no benefit in either clinical symptoms or bronchial hyperresponsiveness,3 despite demonstrating attenuation of allergen-induced late-phase bronchoconstriction induced in the laboratory.4 A more prolonged trial for six months with 3.2 g/day of EPA also showed no clinical benefit in patients with pollen-induced asthma and seasonal hayfever.5 These disappointing results are consistent with in-vitro evidence that EPA does not inhibit eosinophils and mast cells. In contrast to its dampening effect on neutrophils, EPA incubated with cultured murine mast cells produced a marked increase in production of platelet-activating factor, without an effect on histamine release.6 Similarly, stimulated human eosinophils incubated with EPA generated significantly greater amounts of leukotrienes than those incubated with arachidonic acid.7 Furthermore, in asthma there is a complex interaction between cells, cytokines, nerves and lipid and other mediators. Although of the lipid mediators leukotrienes may have the most influential role in asthma, modulating any one group of inflammatory mediators alone may not be sufficient to produce clinical improvement. The only interventional study which has shown positive results was a small placebo-controlled trial of low-dose EPA (1 g/day) for 12 months in 12 adult asthmatic subjects (six taking fish oil and six taking placebo). After nine months a small but significant improvement was found in forced expiratory volume at one second (FEV1).8 However, no details were given of concurrent medication use or assessment of compliance with therapy by leukocyte membrane phospholipid analysis, and there have been no follow-up data since 1991. The question of fish diet and respiratory health has also been investigated from an epidemiological perspective in recent American studies. In a survey of 2526 adult subjects aged 30-70 years, the first National Health and Nutrition Survey found eating fish more than once a week, compared with less than once a week, was associated with a higher level of lung function. However, only 2.9% of subjects in this survey were asthmatic, so no conclusion could be drawn about the effect of fish consumption on asthma.9 The Atherosclerosis Risk in Communities (ARIC) study surveyed 8960 adult current and former smokers10 and reported that a high dietary intake of n-3 fatty acids was inversely related to the risk of chronic obstructive pulmonary disease (COPD). This apparent protective effect is biologically plausible as neutrophilic inflammation is a feature of COPD. The Nurses' Health Study, possibly the largest prospective study of its type, reporting the incidence of adult-onset asthma in 77 866 women aged 34-68 years, found no relationship between dietary intake of fatty acids and the incidence of doctor-diagnosed asthma over a 10-year period.11 With this background, what interpretation can be put on the study by Hodge et al. in this issue of the Journal (page 137)? The novel aspects of this epidemiological survey are that the study population consisted of Australian children aged 8-11, and that the diagnosis of asthma was based both on symptoms and measurement of bronchial hyperresponsiveness. The investigators found an inverse relationship between weekly oily fish intake and prevalence of asthma in 574 schoolchildren. A number of salient points may be made. Firstly, the investigators previously reported an inverse relationship between weekly total fish intake and asthma, which is not evident in this study. This may reflect the inherent variability of food frequency questionnaire data or the different sample sizes of the two studies, but it does raise doubts about the primary hypothesis being tested. Secondly, the estimated mean intake of EPA from a weekly serve of fish10 is about 0.2-0.8 g, which is much lower than the amount that would be expected to have anti-inflammatory effects on leukocyte mediator and cytokine generation. It is possible that it is not the oil in the fish per se but some other dietary or social component associated with families who eat fish which is responsible for these results. Thirdly, a much larger prospective study in adults did not find a similar relationship between dietary fish intake and asthma prevalence.11 Can this discrepancy be explained by subtle effects of low-dose fish oil on the immunological development of asthma in childhood, which are no longer relevant in adulthood? There is currently insufficient understanding of the mechanisms involved to put forward a biologically plausible hypothesis. Finally, the study of Hodge et al. is a cross-sectional study, and thus cannot establish a temporal relationship between oily fish intake and asthma. Nevertheless, these are very interesting data but they need to be confirmed in larger studies. Placebo-controlled prospective intervention studies with dietary manipulation for prolonged periods in childhood are also required before any claim can be substantiated. Until then, unwarranted speculation about the relationship between dietary fats and asthma12 should be avoided as this may have a negative impact on other health outcomes, cause even more confusion about diet and health in the general population and undermine an evidence-based approach to public health initiatives. Francis C K Thien Senior Lecturer Rosalie K Woods Research Fellow E Haydn WaltersProfessor/Director Department of Respiratory Medicine, Alfred Healthcare Group Melbourne, VIC (©MJA 1996; 164: 135-136) Kirsch CM, Payan DG, Wong MYS, et al. Effect of eicosapentaenoic acid in asthma. Clin Allergy 1988; 18: 177-187. Picado C, Castillo JA, Schinca N, et al. Effects of a fish oil enriched diet on aspirin intolerant asthmatic patients: a pilot study. Thorax 1988; 43: 93-97. Arm JP, Horton CE, Mencia-Huerta J-M, et al. Effect of dietary supplementation with fish oil lipids on mild asthma. Thorax 1988; 43: 84-92. Arm JP, Horton CE, Spur BW, et al. The effects of dietary supplementation with fish oil lipids on the airways response to inhaled allergen in bronchial asthma. Am Rev Respir Dis 1989; 139: 1395-1400. Thien FCK, Mencia-Huerta J-M, Lee TH. Dietary fish oil effects on seasonal hay fever and asthma in pollen-sensitive subjects. Am Rev Respir Dis 1993; 147: 1138-1143. Triggiani M, Connell TR, Chilton FH. Evidence that increasing the cellular content of eicosapentaenoic acid does not reduce the biosynthesis of platelet-activating factor. J Immunol 1990; 145: 2241-2248. Thien FCK, Hallsworth MP, Soh C, Lee TH. Effects of exogenous eicosapentaenoic acid on generation of leukotriene C4 and leukotriene C5 by calcium ionophore-activated human eosinophils in vitro. J Immunol 1993; 150: 3546-3552. Dry J, Vincent D. Effect of a fish oil diet on asthma: results of a 1-year double-blind study. Int Arch Allergy Appl Immunol 1991; 95: 156-157. Schwartz J, Weiss ST. The relationship of dietary fish intake to level of pulmonary function in the first National Health and Nutrition Survey (NHANES I). Eur Resp J 1994; 7: 1821-1824. Shahar E, Folsom AR, Melnick SL, et al. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. N Engl J Med 1994; 331: 228-233. Troisi RJ, Willett WC, Weiss ST, et al. A prospective study of diet and adult-onset asthma. Am J Respir Crit Care Med 1995; 151: 1401-1408. Hodge L, Peat JK, Salome C. Increased consumption of polyunsaturated oils may be a cause of increased prevalence of childhood asthma. Aust N Z J Med 1994; 24: 727. (©MJA 1996; 164: 135-136)

Rosalie K Woods

Research Consumption of oily fish and childhood asthma risk Linda Hodge, Cheryl M Salome, Jennifer K Peat, Michelle M Haby, Wei Xuan and Ann J Woolcock For editorial comment, see Thien et al. Abstract - Authors' details - Introduction - Methods - Results - Discussion - Appendix - Acknowledgements - References - Box 1 - Box 2 - Box 3 - Figure - © MJA 1996 - Abstract Objective: To investigate the association between diet and airway disease in children in the light of epidemiological studies suggesting that consumption of fish more than once a week reduces the risk of developing airway hyperresponsiveness (AHR). Design: Diet was assessed by a detailed food frequency questionnaire and airway disease by respiratory symptoms or airway responsiveness to exercise. Methods: A questionnaire, containing questions about the frequency of eating more than 200 foods, was sent to the parents of 574 children in whom we had measured recent wheeze (by questionnaire), AHR (by exercise) and atopy (by skin prick tests) six months before this study. We defined current asthma as the presence of both recent wheeze and AHR. Results: Response rate to the questionnaire was 81.5% (n = 468). After adjusting for confounders such as sex, ethnicity, country of birth, atopy, respiratory infection in the first two years of life and a parental history of asthma or smoking, children who ate fresh, oily fish (> 2% fat) had a significantly reduced risk of current asthma (odds ratio, 0.26; 95% confidence interval, 0.09-0.72; P < 0.01). No other food groups or nutrients were significantly associated with either an increased or reduced risk of current asthma. Conclusion: These data suggest that consumption of oily fish may protect against asthma in childhood. MJA 1996; 164: 137-140 Introduction The substantial increase in the prevalence of childhood asthma in the past 20 years has affected both rural and urban communities of westernised countries,1,2 suggesting that local environmental factors, such as exposure to allergens or industrial air pollutants, are not the cause. However, the widespread changes in diet may be responsible. Seaton et al.3 have postulated that increases in the prevalence of asthma may be due to a reduced intake of antioxidant vitamins (beta-carotene, vitamins A, C and E) and mineral cofactors essential for antioxidant defence mechanisms (selenium, zinc and copper) as a result of reduced consumption of meat, fresh fish, fruit and vegetables in Western diets. Reduced consumption of magnesium4 and increased consumption of salt5 have been implicated as risk factors for airway hyperresponsiveness (AHR). Our own epidemiological studies of Australian schoolchildren have shown that children who eat fish more than once a week have a third the risk of AHR of children who do not eat fish regularly.6 However, these studies did not include other dietary questions, so that fish consumption may have been a marker for another dietary characteristic. Here, we investigate the association between diet, as assessed by a detailed dietary questionnaire, and airway disease, assessed by respiratory symptoms or airway responsiveness to exercise. Methods Subjects In June 1993, a cross-section of 808 children aged 8-11 years from schools randomly selected from all schools within a 10 km radius of Sydney General Post Office had airway responsiveness to exercise, respiratory symptoms and atopy measured and frequency of fish consumption assessed.7 In October 1993, 584 children were selected from this group in a stratified case-control design and their parents were asked to complete a detailed food frequency questionnaire about their child's eating habits. The selection criteria included all children with AHR, all children who had had wheeze in the last 12 months (recent wheeze) and a three-in-five sample of children with normal airways (no AHR or recent wheeze), who were chosen by excluding two children after every three from numerically ordered lists of children identified by number. The study coordinator who collected the food frequency questionnaires was blind to the respiratory symptom and AHR status of the subjects. Ethical approval for the study was obtained from the Ethics Review Committee of the University of Sydney. Permission to approach schools was obtained from the New South Wales Department of School Education and the Catholic Education Office. Respiratory questionnaire In June 1993 the parents or guardians of the children completed a standard respiratory questionnaire, with questions on age, sex, ethnicity, country of birth, history of asthma or wheeze in the last 12 months, medication use, and also parents' occupations, history of asthma and smoking. The questionnaire included the question used in previous studies about the dietary consumption of fish - "How often does your child eat a meal that contains fish?" - with the options of replying "never or rarely", "once a week", or "more than once a week". Dietary questionnaire In October 1993, a food frequency questionnaire (adapted from that developed and validated by the Commonwealth Scientific and Industrial Research Organisation [CSIRO], Division of Human Nutrition, South Australia8,9) was distributed to the selected children, whose parents were asked to complete this for their child's usual eating habits over the last year. The questionnaire identified consumption patterns (daily, weekly, monthly, rarely or never) of more than two hundred foods commonly consumed in Australia. Additional questions on the type of fresh fish consumed and regular consumption of vitamin, mineral or herbal supplements were included. Estimates of sodium intake included naturally occurring sodium in foods, salt added in cooking, at the table and from processed foods. If questionnaires were not returned after one month the parents were contacted by telephone and offers were made to replace the questionnaires, or to provide assistance. In 11 cases, where neither parent spoke fluent English, an interpreter was commissioned to complete the questionnaire with the parents over the telephone. Returned dietary questionnaires were checked for missing or obviously erroneous information. Parents were contacted by telephone to complete omitted sections or to clarify erroneous information. Each food in the dietary questionnaire was allocated to one of 23 different food groups (see Appendix). Diets were analysed for energy, fibre and 39 nutrients (see Appendix). Definitions of respiratory categories, atopy, and categories of fish, plus a list of fish with more than 2% fat, are given in Box 1. Statistical analyses The questionnaires were analysed by the Division of Human Nutrition, CSIRO, South Australia, using Australian tables of nutrient composition12 for energy, protein, fat, carbohydrates, vitamins and minerals. The total quantity of food in each food group for every child was converted to a common base of weekly serves with Clinical Reporting Systems software.13 Data were analysed with the statistical package SAS.14The association between fish, food or nutrient intake and respiratory category was analysed categorically using chi-squared tests, and continuously using Student's t tests and analysis of variance. Some values obtained from the nutrient analysis were well outside what could reasonably be expected in children of this age group. These outliers were excluded from the statistical analysis. The number of exclusions never exceeded nine subjects in any analysis and were not significantly associated with any of the respiratory groups. Logistic regression was used to adjust estimates for the effects of known confounders for the effect of fish consumption on AHR and symptoms of asthma (e.g., sex, race, country of birth, atopy, early respiratory infection, parental smoking and parental asthma). Only those confounding factors found to be significant or approaching significance (P < 0.1) (atopy, parental asthma, early respiratory infection, country of birth) were included in the model. Results Of the 584 children selected 574 received the dietary questionnaire and 468 completed questionnaires were returned (81.5%). Non-responders were not significantly different from responders in the prevalence of AHR (26.0% v. 27.1%) or fish consumption (46.2% v. 52.1%). Box 2 shows details of the children studied. Children with current asthma did not differ significantly from children with normal airways in the consumption of any nutrient or food group. (Tables showing mean weekly intake in standard serves of food groups and mean daily intake [SD] of nutrients for children with normal airways and children with current asthma are available from the authors.) Children with wheeze only had a significantly higher intake of red meat (P < 0.05), offal meat (P < 0.001) and vitamin B12 (P < 0.03) and a significantly lower intake of mixed vegetables (P < 0.05) than children with normal airways. Children with AHR only consumed significantly more offal meat (P = 0.001) and high fat/high sugar foods (P < 0.001) than children with normal airways. They also had higher intakes of nitrogen, protein, total sugar, cholesterol, potassium nicotinamide, total nicotinamide, calcium, copper, zinc, vitamin B12 (P < 0.05) and refined sugar (P < 0.01). Total fish intake per week did not differ significantly between children with normal airways (1.2 serves per week; 95% confidence interval [CI], 1.0-1.3), AHR only (1.2 serves; CI, 0.9-1.5), wheeze only (1.2 serves; CI, 0.8-1.5) and current asthma (1.0 serve; CI, 0.8-1.2). Fresh fish was eaten by 84% (CI, 79.6%-88.4%) of children with normal airways, and by 72% (CI, 61.6%-82.4%) of children with current asthma. When fresh fish was divided into oily and non-oily types, significantly fewer children with current asthma (15.5%; CI, 7.1%-23.9%) included oily fish in their diet than did children with normal airways (30.8%; CI, 25.2%-36.4%; P < 0.05). There were no significant differences in the proportions of children with current asthma (56.3%; CI, 44.8%-67.8%) and normal children (52.9%; CI, 46.9%-58.9%) who ate exclusively non-oily fish. Neither fresh fish consumption nor respiratory disease was significantly associated with socioeconomic status, as defined by the father's occupation, or with the consumption of vitamin, mineral or other dietary supplements (including fish oil). The unadjusted risk (odds ratio) for children having current asthma was significantly lower in those who consumed any fresh fish or oily fresh fish (Box 3). Current asthma was found in only 8.8% (CI, 3.8%-13.8%) of children who ate oily fish, but in 15.6% (CI, 11.2%-20.0%) of those who ate non-oily fish only and 23% (CI, 14.2%-31.8%) of those who never ate fresh fish (Figure). When the results were adjusted for the effects of other known risk factors such as atopy, parental asthma, parental smoking, ethnicity, country of birth, early respiratory illness and sex, only children who ate oily fresh fish had a significantly reduced risk of current asthma. In these children, the risk was almost a quarter that of children who did not eat oily fish (odds ratio, 0.26; CI, 0.09-0.72) (Box 3). Consumption of any fresh fish, whether or not it was separated into oily fresh fish and non-oily fresh fish, did not significantly reduce the risk of AHR only or wheeze only either before or after adjustment for other risk factors. Discussion Our study shows that regular consumption of fresh, oily fish is associated with a reduced risk of current asthma. This reduced risk remained significant after adjustment for other known risk factors for asthma, including sex, atopy, parental asthma, parental smoking, early respiratory infection, ethnicity and place of birth. The subjects were selected from a random cross-sectional sample of children which was stratified (on the basis of recent respiratory symptoms and AHR to exercise) to increase the proportion of cases in the study group. The response rate was high (81.5%) and non-responders were not different from responders with respect to AHR or fish consumption. Socioeconomic status was not a confounder for either respiratory illness or fish consumption. Current asthma was defined as recent wheeze plus AHR to exercise. We have shown previously that current asthma, defined as recent wheeze plus AHR to histamine, identifies a group with severe, ongoing respiratory impairment, while those with AHR only and wheeze only have a milder condition which differs only slightly from the normal group.15 The diets of children with current asthma differed from those of the normal group only in the consumption of fresh, oily fish. In our previous study, more than one serve of fish per week was associated with a reduced risk of asthma,6 but in that study it was not possible to distinguish the effects of oily and non-oily fish. In the study reported here we were unable to detect differences in total fish consumption, possibly because of the smaller sample size. There were no significant differences between respiratory groups in the consumption of non-oily fish, suggesting that parents had not selectively withheld fish from the diets of asthmatic children. It is unclear why consumption of canned and processed fish was not associated with reduced risk of asthma. Processing may alter the integrity or activity of the fatty acids in fish oils. Several foods and nutrients in the diets of children with AHR only and wheeze only differed significantly from those of the normal group. However, none of these factors differed between the asthmatic and normal groups, suggesting that they are unlikely to have an aetiological role. Intake of offal meats was higher in both the AHR-only and wheeze-only groups, but, as offal meats are eaten by very few children, this may be a type I error. Vitamin B12 intake was also higher in both the AHR-only and wheeze-only groups, but the mechanism by which this could affect respiratory symptoms or AHR is unclear. There were no significant differences between any of the respiratory groups in consumption of sodium, vitamin C, vitamin E, selenium or magnesium. These findings do not support previous evidence that these dietary factors are important in the aetiology of asthma.4,5,16 Reduced risk of current asthma was associated with the consumption of oily fish, but not with non-oily fish. Fish oil contains the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which have anti-inflammatory effects.17 Theoretically, EPA could either prevent the development of asthma or reduce its severity by altering two of the cardinal features of asthma, namely airway inflammation and AHR. Supplementation with EPA reduces production of leukotriene B4,18 a chemical mediator responsible for the recruitment of inflammatory cells, such as neutrophils, into the airways. It also reduces production of the cytokine tumour necrosis factor (TNF),19 which increases airway responsiveness.20 Fish oil supplements given over 6-10 weeks cause a substantial uptake of EPA in neutrophil membrane phospholipids.18,21 In asthmatics, this may reduce the allergen-induced late asthmatic response,22 but does not change severity of asthma.21,22 However, a recent study suggests that a longer period of supplementation may be required to reduce asthma severity.23 Data of recent fish consumption (during the last 12 months) were used in our study, but may also reflect lifetime dietary habits. In conclusion, we have shown that consumption of oily fish is associated with a reduced risk of asthma in childhood. Although further studies are required to confirm these benefits, public health interventions to increase the consumption of oily fish may reduce the morbidity and prevalence of asthma in children. Appendix The 23 food groups were: cereals; dairy products; eggs; red, white, preserved meat and offal; seafood, fried, steamed, canned fish and fish fingers; red, green, white, mixed and other vegetables; legumes; high and low vitamin C fruit and other fruit; high sugar or fat content; and other. The 39 nutrients were: nitrogen; protein; starch; refined, natural and total sugar; total carbohydrate; saturated, monounsaturated, polyunsaturated and total fat; cholesterol; carotene; retinol; vitamin A; thiamine; riboflavin; potassium nicotinic acid and total nicotinic acid; niacin; vitamins B6 and B12; pantothenic acid; biotin; free and total folate; vitamins C, D, E; calcium; copper; iron; magnesium; manganese; phosphorus; potassium; selenium; sodium; and zinc. Acknowledgements This study was supported by the Fisheries Research and Development Corporation, Australia. The authors thank Dr Katrine Baghurst for allowing us to use the dietary questionnaire, Sally Record and Kay Pender for their help with the nutritional analyses, Elena Belooussova for data organisation and Suzanne Gray for her assistance with collecting the questionnaires. We are grateful for the support of the New South Wales Department of School Education, the Catholic Education Office and the Principals and teachers of all the schools involved. We are especially grateful to the parents and the children who participated in the survey. (©MJA 1996; 164: 137-140) References Robertson CF, Bishop J, Sennhauser FH, Mallol J. International comparison of asthma prevalence in children: Australia, Switzerland, Chile. Pediatr Pulmonol 1993; 16: 219-226. Burney P, Chinn S, Rona RJ. Has the prevalence of asthma increased in children? Evidence from the national study of health and growth 1973-86. BMJ 1990; 300: 1306-1310. Seaton A, Godden DJ, Brown K. Increase in asthma: a more toxic environment or a more susceptible population? Thorax 1994; 49: 171-174. Britton J, Pavord I, Richards K, et al. Dietary magnesium, lung function, wheezing, and airway hyperreactivity in a random adult population sample. Lancet 1994; 344: 357-362. Burney PG, Neild JE, Twort CHC, et al. Effect of changing dietary sodium on the airway response to histamine. Thorax 1989; 44: 36-41. Peat JK, Salome CM, Woolcock AJ. Factors associated with bronchial hyperresponsiveness in Australian adults and children. Eur Respir J 1992; 5: 921-929. Haby MM, Peat JK, Mellis CM, et al. An exercise challenge for epidemiological studies of childhood asthma: validity and repeatability. Eur Respir J 1995; 8: 729-736. Baghurst KI, Record SJ. Intake and sources in selected Australian subpopulations of dietary constituents implicated in the etiology of chronic diseases. J Food Nutr 1983; 40: 1-15. Rohan TE, Record SJ, Cook MG. Repeatability of estimates of nutrient and energy intake: the quantitative food frequency approach. Nutr Res 1987; 7: 125-137. Analyses of NSW fish and shellfish. Sydney: Australian Government Analytical Laboratory, 1989. Sinclair A, Dunstan GA, Naughton JM, et al. The lipid content and fatty acid composition of commercial marine and freshwater fish and molluscs from temperate Australian waters. Aust J Nutr Diet 1992; 49: 77-83. English R, Lewis J. Composition of foods Australia. 1st ed. Vols 1-5. Canberra: AGPS, 1989-1990. Clinical Reporting Systems [computer program], version 3.0. Sydney: Clinical Reporting Systems Pty Ltd. 1992. SAS [computer program], version 5. Cary, NC: SAS Institute, 1984. Toelle BG, Peat JK, Salome CM, et al. Toward a definition of asthma for epidemiology. Am Rev Respir Dis 1992; 146: 633-637. Stone J, Hinks LJ, Beasley R, et al. Reduced selenium status of patients with asthma. Clin Sci 1989; 77: 495-500. Kremer JM, Jubiz W, Michalek A, et al. Fish-oil fatty acid supplementation in active rheumatoid arthritis. Ann Intern Med 1987; 106: 497-503. Lee TH, Hoover RL, Williams JD, et al. Effect of dietary enrichment with eicosapentaenoic and docosahexaenoic acids on in vitro neutrophil and monocyte leukotriene generation and neutrophil function. N Engl J Med 1985; 312: 1217-1224. Endres S, Ghorbani R, Kelley VE, et al. The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the synthesis of interleukin-1 and tumor necrosis factor by mononuclear cells. N Engl J Med 1989; 320: 265-271. Thomas PS, Yates DH, Barnes PJ. Tumor necrosis factor-alpha increases airway responsiveness and sputum neutrophilia in normal human subjects. Am J Respir Crit Care Med 1995; 152: 76-80. Arm JP, Horton CE, Mencia-Huerta J-M, et al. Effect of dietary supplementation with fish oil lipids on mild asthma. Thorax 1988; 43: 84-92. Arm JP, Horton CE, Spur BW, et al. The effects of dietary supplementation with fish oil lipids on the airways response to inhaled allergen in bronchial asthma. Am Rev Respir Dis 1989; 139: 1395-1400. Dry J, Vincent D. Effects of fish oil diet on asthma: results of a 1-year double blind study. Int Arch Appl Immunol 1991; 95: 156-157. (Received 31 May, accepted 28 Nov 1995) Authors' details Institute of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Linda Hodge, MSc(Med), GradDipNutr&Diet, Dietitian. Department of Medicine, University of Sydney, Sydney, NSW. Cheryl M Salome, BSc, Senior Research Officer. Jennifer K Peat, PhD, Senior Research Officer. Michelle M Haby, MSc, Research Assistant. Wei Xuan, MSc, MApplStat, Statistician. Ann J Woolcock, MD, FRACP, Professor in Respiratory Medicine. Reprints: Professor A J Woolcock, Institute of Respiratory Medicine, Royal Prince Alfred Hospital, Camperdown, NSW 2050. (©MJA 1996; 164: 137-140)

Linda Hodge · Cheryl M Salome · Jennifer K Peat · Michelle M Haby · Wei Xuan · Ann J Woolcock