Volume 168 Issue 1

Breast cancer mortality trends in Australia: 1921 to 1994 Catherine L Smith, Anne Kricker, Bruce K Armstrong MJA 1998; 168: 11-14 Abstract - Introduction - Methods - Results - Discussion - Conclusions - Acknowledgements - References - Authors' details - - ©MJA1997 Abstract Objective: To analyse breast cancer mortality trends in Australia and to see if mammographic screening has yet led to a reduction in mortality. Design: Retrospective analysis of trends in mortality rates from breast cancer in Australian women between 1921 and 1994, and in potentially explanatory variables such as fertility, body size, age at menarche, and screening. Results: Changes in breast cancer mortality in Australian women could not be explained by chance variation alone. Mortality rose steadily (average annual increase, 1.0%) to 1940-1944, fell to the 1960s and early 1970s, and rose (average annual increase, 0.3%) to the late 1980s. Between 1985-1989 and 1990-1994, breast cancer mortality fell by 3.2% in women 50-69 years of age (the target age group for mammographic screening) and by 4.2% in women 25-49 years of age. There was almost no change ( - 0.2%) in breast cancer mortality in older women in this period. The proportion of women screened in all age groups increased substantially between 1988 and 1994; nearly 65% of women in the target age group had had at least one mammogram by 1994. Decreases in fertility were followed by increases in mortality, and vice versa. Conclusions: Trends in breast cancer mortality have probably been influenced by changing fertility, nutrition and body-size increases among Australian women. Improvements in stage at diagnosis and treatment have probably moderated the upwards pressure on mortality caused by an increasing incidence. Recent falls in mortality could be expected to continue as more women participate in the mammographic screening program. This trend should be more clearly evident in the second half of the 1990s. Introduction Breast cancer mortality in women in most developed countries, including Australia, has levelled off or fallen in recent years.1 In Britain, an important fall in mortality since 1989, considered too early to be the result of mammographic screening, is thought to be the result of improved treatment.2 Similar observations have been made in the United States.3 We examined trends in breast cancer mortality and breast cancer risk factors in Australia between 1921 and 1994 to see if we could explain recent mortality changes and, in particular, to see if mammographic screening has yet led to decreased breast cancer mortality in the target age group for screening (50-69 years). Methods Age-specific and age-standardised mortality rates from breast cancer per 100 000 woman-years, standardised to the world population, were calculated for one four-year period (1921-1924) and 14 five-year periods (1925-1929 to 1990-1994) from annual mortality and population data from the Australian Bureau of Statistics. Rates for 1995 have subsequently been released. Estimates of the number of women who had had at least one mammogram by the end of each year from 1984 to 1994 were obtained as follows: Annual numbers of women by age having a first or subsequent bilateral mammogram (bilateral mammograms being most likely for screening purposes) under Medicare from 1984 to 1994 were estimated from data of the Commonwealth Department of Health and Family Services; Annual numbers of first screens in 10 pilot projects of the national screening program were estimated by age from 1 January 1988 to 30 June 19914-7 (BreastScreen Australia, personal communication) on the assumption, where necessary, that all screens were initial and that rates were constant within and over time periods and age groups; and Similar estimates were made for BreastScreen Australia from 1 July 1991 to December 1994 by applying the age distribution for all screens, initial and subsequent, in Victoria8 (BreastScreen Australia, personal communication) and New South Wales9 to published national screening estimates,9 and by estimating the fraction that were initial screens from State-based proportions of initial screens. These three sets of estimates were totalled to estimate numbers of women who had had at least one mammogram by the end of each year from 1984 to 1994. Total fertility rates by age in Australian women were obtained by year from 1921 to 1994.10,11 Rates of first births by age and year, available only for married women, showed patterns similar to those for total fertility. Results Mortality Breast cancer mortality (Box 1a) increased in Australia between the periods 1921-1924 and 1940-1944 (average annual increase, 1.0%), fell to a post-war low around 1960, and increased slowly again to a peak in 1985-1989. The average annual increase in rates from 1970-1974 to 1985-1989 was 0.3%. Thereafter, rates fell by 0.5% a year between 1985-1989 and 1990-1994. The recent fall in annual age-standardised rates has been from 20.7 per 100 000 woman-years in 1990 and 1991, to 19.6 per 100 000 in 1992, 1993 and 1995, and 19.2 in 1996; in 1994 the mortality rate was 20.3 per 100 000 woman-years. Age-specific mortality rates for women aged 25-49 years showed little change between 1921 and 1994 (Box 2). In women 50 years of age and older, breast cancer mortality rose steadily to reach initial peaks at different times between 1935-1939 and 1950-1954. These peaks occurred in women born between 1865 and 1885. Mortality in women 50 years and older then fell to a post-war low between 1950-1954 and 1985-1989 depending on age group and occurring in women born around 1890 to 1905. Thereafter, mortality rates again rose and appeared to peak in 1980-1984 or 1985-1989 for each age group of women from 50-54 years to 70-79 years. There was little evidence of this later mortality rise in women older than 80 years. In the target age group for mammographic screening (50-69 years), the age-standardised mortality rate increased by 4.0% (95% CI, - 0.1 to 8.3) from 1980-1984 to 1985-1989 and then fell by 3.2% (95% CI, - 6.9 to 0.6) to 1990-1994. In women 25-49 years of age, rates increased by 7.5% (95% CI, 0.4-15.0) from 1980-1984 to 1985-1989 and then fell by 4.2% (95% CI, - 9.9 to 1.9) to 1990-1994. Women 70 years of age and older showed only weak evidence of change from the early to the late 1980s (1.3%; 95% CI, - 3.1 to 6.0) and almost no evidence of a fall in the 1990s ( 2 0.2%; 95% CI, - 4.2 to 4.0). Mammographic screening Our analysis of mammographic screening data is summarised in Box 3. The percentages of women screened between 1988 and 1994 increased in all age groups, most notably in women aged 50-69 years. The beginning of most pilot projects in late 1988 and early 1989 and of the National Program in 1991 led to a substantial change in the age distribution of screening mammograms. There was a nearly sevenfold increase in the cumulative numbers of women in the target age group who had been screened once or more, from around 138 000 in 1988 to nearly one million by 1994. The estimated number of women under 50 years of age who had been screened (which was twice the number in the target group in 1988) increased only 3.7 times (to an estimated 1 140 000) by 1994. By 1994, about 70% of women in their 50s and 58% of women in their 60s had had an initial screen. In all, 54% of women in their 40s and 22% of women younger than 40 were estimated to have been screened once by 1994. In older women, the proportion screened reached 25% at 70-74 years of age and 6% at 80 years and older. Fertility Fertility fell at all ages from 1921-1924 or 1925-1929, to reach a minimum in most age groups in 1930-1934 or 1935-1939 (Box 1b), and then rose to reach a peak between 1945-1949 and 1970-1974. Rates again fell from these peaks. Minima were reached in 1975-1979 or 1980-1984 in those aged between 30 and 44 years, with subsequent rises to 1990-1994. There was little evidence that any of these trends related better to cohort of birth than time period. Discussion Compared with many other countries, breast cancer mortality in Australia has varied little over the past 75 years.1 However, the clear trends we found cannot be explained by chance fluctuation. The recent fall in the early 1990s, while apparently quite definite in women aged 40-69 years, could be a chance occurrence and will need to be shown for several more years for it to be declared a "real" trend. There are three broad classes of explanation for these trends, represented under the subheadings below. Changes in how cause of death is registered and coded can influence reported cause-specific mortality rates, but no substantial changes of this kind are known to have occurred in Australia.1,12 We have specified "real" incidence (below) because recent apparent increases in breast cancer incidence have probably been the result of increased screening.3,13 These increases will not cause increases in mortality because they reflect either earlier diagnosis of breast cancers, or the diagnosis of lesions that would otherwise never have been detected.13 Changes in determinants of real incidence Incidence trends: Whether changes in incidence caused changes in mortality would be most easily determined by comparing incidence and mortality trends. Incidence of breast cancer in New South Wales (representing about one-third of Australian women) changed little from 1972 to 1983, but increased steadily from 1984, and by 1995 was nearly 50% higher than it was in 1983.14 The greatest increase was in women in the target age group for mammographic screening (50-69 years). As there was no parallel increase in mortality during that period, the observed increase in incidence has probably been caused by screening. Incidence was not measured in Australia before 1972. However, it is most likely that incidence rates in Australia, as in several other countries,15-17 were increasing and thus underlie the steady increase in mortality from 1921 to the peak of the mid 1940s. Incidence rates in Australia were probably also increasing in the post-war period, as in other populations of European origin,18,19 when Australian mortality rates were falling or stable. Fertility: Breast cancer is associated with late age at first birth, childlessness and low parity.13 Box 1 shows that Australian trends in rates of mortality from breast cancer moved in the opposite direction from those of fertility rates, with changes in mortality occurring a few years after those in fertility. Australian women born in the 1840s were at the forefront of a transition to lower family sizes in English-speaking countries.10 This falling fertility could have produced the increasing mortality from breast cancer from 1921 onwards. The peak breast cancer mortality in the 1940s occurred in women born before 1885; the highest proportions of unmarried and childless women seen in Australia up to the 1940s were among those born in 1871 to 1876.10 The upward trend in fertility after 1935, which peaked in 1955-1964, started about 10 years before mortality began to fall in the mid 1940s. Fertility again fell in the late 1960s and 1970s to a new low in the 1980s, with a pronounced shift during that period to later childbearing; mortality began to rise again in the 1980s. Body size and age at menarche: Each 5-cm increase in average height in adult women has been estimated to increase breast cancer risk by 10%.13 From the early 1900s to about 1980, net increases of 8-9 cm in height and 10 kg in weight20,21 could have contributed appreciably to increases in mortality in women born from about 1895 to 1935 (evident in overall mortality from breast cancer between 1970-1974 and 1985-1989). A fall in age at menarche is also associated with an increase in breast cancer incidence.13,22 Trends in Australia, probably similar to the 2-3 months' fall per calendar decade seen in the United Kingdom and United States in the 100 years to about 1950,13,22,23 would have been expected to increase breast cancer rates. Younger age at menarche is very likely caused by increased height and body mass index, perhaps because menarche depends on attainment of a critical body mass.22,24 Diet: Dietary changes may have affected breast cancer rates by way of changes in body size, and possibly by other means.25 Alcohol consumption is associated with increased risk of breast cancer, being 35% higher in women who have 2-4 drinks and 67% higher in those who have more than four drinks a day compared with women who drink little or no alcohol.26 The high alcohol consumption among Australian women of the early 1800s was not equalled again until 1989, when more than 50% of women over 18-20 years were consuming up to two drinks a day.26,27 However, it has been estimated that no more than 3% of breast cancers in Australia in 1990 were the result of drinking more than two drinks of alcohol a day.26 Physical activity may reduce risk of breast cancer.27 The proportion of Australian women who participate in any recreational exercise (around 70%) appears not to have changed in recent times.28 Changes over time in the physical activity associated with running a household and in paid employment have not been measured. Migration: Breast cancer rates vary six-fold internationally.29 Migration of women from countries of higher (UK) and lower (eastern Europe, southern Europe, Asia) breast cancer mortality than in Australia has varied, but the net effect of migration on breast cancer mortality rates has probably been small. Oestrogen use: Use of the oral contraceptive pill increased rapidly in Australia after its introduction in 1961.30 If the Pill has caused an increase in breast cancer mortality, it would have done so mainly in younger women who were current or recent users.31 The increase in mortality in the late 1980s, however, was mostly in women over 50 years of age. Falling mortality from breast cancer in the generations of women who first used oral contraceptives in the US, UK and Sweden also suggests no major effects of the Pill on breast cancer rates.32,33 The use of oestrogen replacement therapy, which may increase breast cancer risk, has probably not affected breast cancer incidence appreciably as long term use has been uncommon in Australia. Changes in determinants of stage at diagnosis Trends to smaller breast cancers and fewer axillary node metastases over nearly 100 years34-36 are probably the results of increased access to and use of care. The trend to more localised disease is probably continuing because of increased screening.3,13,37 Such trends would have caused downward pressure on breast cancer mortality. Mortality from breast cancer in Australian women in the target age group for screening (50-69 years) fell by 3.2% between 1985-1989 and 1990-1994. This may be the result of screening, although the same or larger falls in mortality also occurred in younger women, for whom there is little evidence that mammographic screening reduces breast cancer mortality.38 Changes in determinants of probability of survival after diagnosis at a particular stage The effectiveness of radical mastectomy as the primary treatment for breast cancer has probably changed little in the past 100 years. However, advances in anaesthetics and operating conditions38 as well as the recent use of adjuvant chemotherapy and hormonal therapy3,39 have almost certainly increased survival. Conclusions While no certain conclusions can be drawn about the causes of changes in breast cancer mortality since 1921, it is probable that the increase to the mid 1940s was caused mainly by rapidly falling fertility in the latter part of the 19th and the early 20th centuries. Subsequent increased fertility, and earlier diagnosis, may have contributed to the fall in mortality from 1940-1944 to 1960-1964. The increasing mortality in women born between 1895 and 1935 was probably caused by nutritional factors leading to increases in body size and resultant earlier age at menarche. However, this incidence-driven increase in mortality was probably moderated by increasing survival with earlier diagnosis and, more recently, improved treatment. Improved treatment is probably the reason for cross-sectional falls in mortality between 1985-1989 and 1990-1994 in women up to 69 years of age. Early effects of mammographic screening may have contributed to these falls, but should be more clearly evident in the second half of the 1990s. Acknowledgements Australian Bureau of Statistics data on mortality from breast cancer from 1921 to 1994 were supplied by Mr Paul Jelfs from the national mortality database at the Australian Institute of Health and Welfare, Canberra. References Hermon C, Beral V. Breast cancer mortality rates are levelling off or beginning to decline in many western countries: analysis of time trends, age-cohort and age-period models of breast cancer mortality in 20 countries. Br J Cancer 1996; 73: 955-960. Beral V, Hermon C, Reeves G, Peto R. Sudden fall in breast cancer death rates in England and Wales [letter]. Lancet 1995; 345: 1642-1643. Chu KC, Tarone RE, Kessler LG, et al. Recent trends in US breast cancer incidence, survival, and mortality rates. J Natl Cancer Inst 1996; 88: 1571-1579. Essendon Breast X-Ray Program Collaborative Group. A mammographic screening pilot project in Victoria 1988-1990. Med J Aust 1992; 157: 670-673. Rickard MT, Lee W, Read JW, et al. Breast cancer diagnosis by screening mammography: early results of the Central Sydney Area Health Service Breast X-ray Programme. Med J Aust 1991; 154: 126-131. Robinson JI, Crane CEB, King JM, et al. The South Australian Breast X-Ray Service: results from a statewide mammographic screening programme. Br J Cancer 1996; 73: 837-842. Australian Health Ministers' Advisory Council. Breast Cancer Screening Evaluation Committee. Breast cancer screening in Australia: future directions. Canberra: AGPS, 1990. Victorian Breast Screening Program. Annual statistical report 1994. Melbourne: Victorian Breast Screening Program, 1996. Smith D, Oudod V, Supramaniam R, et al. BreastScreen NSW Statistical Report 1991 to 1995. Sydney: NSW Cancer Council, 1996. McDonald P, Ruzicka L, Pyne P. Marriage, fertility and mortality. In: Vamplew W, editor. Australians: historical statistics. Sydney: Fairfax, Syme and Weldon, 1987: 44-61. Australian Bureau of Statistics. Births, Australia. Canberra: AGPS, 1995. (Catalogue No. 3301.0.) Fleming NT, Armstrong BK, Sheiner HJ, James IR. Occurrence of breast cancer in Australian women. Med J Aust 1981; 1: 289-293. Ursin G, Bernstein L, Pike MC. Breast cancer. Cancer Surv 1994; 19-20: 241-264. Cancer Control Information Centre. Breast cancer incidence, 1995. Sydney: NSW Cancer Council, 1996. Wigle DT. Breast cancer and fertility trends in Canada. Am J Epidemiol 1977; 105: 428-438. Stevens RG, Moolgavkar SH, Lee JA. Temporal trends in breast cancer. Am J Epidemiol 1982; 115: 759-777. Ewertz M, Carstensen B. Trends in breast cancer incidence and mortality in Denmark, 1943-1982. Int J Cancer 1988; 41: 46-51. Tulinius H, Sigvaldason H. Trends in incidence of female breast cancer in the Nordic countries. In: Magnus K, editor. Trends in cancer incidence. Washington: McGraw-Hill, 1982: 235-247. Nab HW, Mulder PG, Crommelin MA, et al. Is the peak in breast cancer incidence in sight? A study conducted in the southeastern Netherlands. Eur J Cancer 1994; 30A: 50-52. May GM, O'Hara VM, Dugdale AE. Patterns of growth in Queensland schoolchildren, 1911 to 1976. Med J Aust 1979; 2: 610-614. Hitchcock NE, Maller RA, Gilmour AI. Body size of young Australians aged five to 16 years. Med J Aust 1986; 145: 368-372. Henderson BE, Bernstein L. The international variation in breast cancer rates: an epidemiological assessment. Breast Cancer Res Treat 1991; 18 Suppl 1: S11-S17. Frisch RE. Body weight, body fat, and ovulation. Trends Endocrinol Metab 1991; 5: 191-197. Petridou E, Syrigou E, Toupadaki N, et al. Determinants of age at menarche as early life predictors of breast cancer risk. Int J Cancer 1996; 68: 193-198. Prentice RL, Sheppard L. Dietary fat and cancer: consistency of the epidemiologic data, and disease prevention that may follow from a practical reduction in fat consumption. Cancer Causes Control 1990; 1: 81-97. English DR, Holman CDJ, Milne E, et al. The quantification of drug caused morbidity and mortality in Australia, 1995 edition. Canberra: AGPS, 1995. Willett WC, Trichopoulos D. Nutrition and cancer: a summary of the evidence. Cancer Causes Control 1996; 7: 178-180. Bennett SA, Magnus P. Trends in cardiovascular risk factors in Australia. Results from the National Heart Foundation's Risk Factor Prevalence Study, 1980-1989. Med J Aust 1994; 161: 519-527. Parkin DM, Muir CS, Whelan SL, et al. Cancer incidence in five continents. Vol. VI. Lyon: International Agency for Research on Cancer, 1992. (IARC Scientific Publications No. 120.) Santow G. Trends in contraception and sterilization in Australia. Aust N Z J Obstet Gynaecol 1991; 31: 201-208. Collaborative group on hormonal factors in breast cancer. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies. Lancet 1996; 347: 1713-1727. Beral V, Hermon C, Reeves G, et al. Breast cancer trends in women in Sweden, the UK, and the USA in relation to their past use of oral contraceptives. In: Proceedings of the Second International Symposium on Hormonal Carcinogenesis. Berlin: Springer Verlag, 1996: 99-106. dos Santos Silva I, Swerdlow AJ. Recent trends in incidence of and mortality from breast, ovarian and endometrial cancers in England and Wales and their relation to changing fertility and oral contraceptive use. Br J Cancer 1995; 72: 485-492. Snaedal G. Cancer of the breast. A clinical study of treated and untreated patients in Iceland 1911-1955. Acta Chir Scand 1964; Suppl 338. Joensuu H, Toikkanen S. Comparison of breast carcinomas diagnosed in the 1980s with those diagnosed in the 1940s to 1960s. BMJ 1991; 303: 155-158. Buchanan EB. A century of breast cancer surgery. Cancer Invest 1996; 14: 371-377. Kricker A, H¿yer AP, McCredie M, Porter LA. Breast cancer in NSW women: a shift in tumour size. Med J Aust 1995; 163: 79-81. Glasziou PP, Woodward AJ, Mahon CM. Mammographic screening trials for women aged under 50. A quality assessment and meta-analysis. Med J Aust 1995; 162: 625-629. Early Breast Cancer Trialists' Collaborative Group. Systemic treatment of early breast cancer by hormonal, cytotoxic, or immune therapy. Lancet 1992; 339: 1-15. (Received 29 Jan, accepted 21 Jul, 1997) Authors' details National Health and Medical Research Council National Breast Cancer Centre, Sydney, NSW. Catherine L Smith, MPH, Statistician; Anne Kricker, PhD, Epidemiologist. Cancer Control Information Centre, NSW Cancer Council, Sydney, NSW. Bruce K Armstrong, DPhil, FRACP, Director. Reprints will not be available from the authors. Correspondence: Dr A Kricker, NHMRC National Breast Cancer Centre, PO Box 572, Kings Cross, NSW 2011. 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.

Catherine L Smith · Anne Kricker · Bruce K Armstrong

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