Environmental health

Despite well publicised claims of the therapeutic value of dietary supplements and other new treatments, the evidence for their effectiveness is modest The distinction between conventional and alternative medicine is often based on the presence or absence of scientific evidence. However, this evidence is expensive to gather, and often difficult to interpret and reduce to practical advice. Age-related macular degeneration (ARMD), the dominant and rapidly increasing cause of permanent visual loss in Australia, is an important case in point. Its prevalence rises from 0.7% in the 65–74-years age group to 5.4% at 75–84 years and 18.5% in people over 85.1 Definitive treatment does not yet exist. While we have some knowledge of risk factors, this knowledge is imperfect and has recently been muddied by well publicised claims (discussed below) that, although evidence-based, are preliminary and need to be interpreted with caution. The early signs of ARMD include hypo- or hyperpigmentation of the retina and large yellow drusen (> 63 μm) or soft drusen with indistinct margins.2 A few small hard drusen can be found in almost everyone over 50 years of age, and, in contrast to large or soft drusen, do not appear to progress with age.1 Loss of vision from ARMD occurs either as a result of choroidal neovascularisation with exudation and haemorrhage (the “wet” form) or by slow atrophy of the retinal-pigment epithelium and overlying receptors (the “dry” form). Wet ARMD is twice as common as the dry type and causes rapid vision loss. About 10% of patients with wet ARMD who present early with distorted vision and an eccentric neovascular lesion can be treated successfully with laser photocoagulation.3 However, the recurrence rate is over 60%, and further vision is then usually lost. Another small proportion of patients can be treated with photodynamic therapy (involving low-intensity red laser treatment after intravenous verteporfin infusion), but the functional benefit is usually modest.4 There is no treatment yet for the dry form of ARMD. Elderly people fear blindness and the loss of independence greatly, and the prevalence of ARMD is rising dramatically. It is no surprise that recent studies of possible risk factors have attracted a lot of public interest. People with an ARMD-affected first-degree relative have a 50% lifetime risk of experiencing advanced ARMD and vision loss, and tend to develop it earlier.5 Smoking is associated with a fourfold increase in the risk of ARMD and visual loss and, again, tends to promote earlier occurrence.6 Weaker associations have been found with obesity, hypertension, macro-vascular disease, raised cholesterol and fibrinogen levels, cumulative light exposure and cataract surgery. Dietary associations have also been found both with the signs of ARMD and with progression to vision loss.7-9 In a well conducted, prospective study, dietary fat intake was systematically analysed after correcting for other risk factors.9 Vegetable fat intake had the strongest relationship with ARMD progression, with a relative risk of 3.82 for the highest fat-intake quartile compared with the lowest quartile. Higher intakes of total fat and of saturated, monounsaturated, polyunsaturated and transunsaturated fats all raised the relative risk of ARMD progression about twofold. Weekly fish intake and eating nuts two to three times a week were mildly protective. The implication is that a large shift away from vegetable oils, margarine and fat-containing processed foods might reduce this epidemic of blindness in the elderly. Some of these measures conflict with conventional advice on controlling cardiovascular conditions and need further research.10 Definitive evidence for the effectiveness of certain interventions might be obtained by randomly assigning those in the top quartile of risk to receive either a diet with low vegetable fat, fish, nuts and fruit, or a normal diet. There is also evidence from a randomised controlled trial that high-dose dietary supplements of the antioxidants vitamin C, vitamin E, beta-carotene and zinc can reduce the risk of progression from large or soft drusen to advanced ARMD and visual loss by about 20% compared with controls over 6 years.11 However, high-dose zinc can cause gastric irritation or anaemia, and beta-carotene may possibly be associated with an increased risk of lung cancer among smokers. Uncontrolled studies suggest the antioxidants selenium, lutein and zeaxanthin, which localise in the normal macula, may also help. There are as yet no studies to show whether dietary supplements are protective in patients with only small drusen or in the 20% of patients who are at genetic risk. It is not yet known whether major dietary adjustment and/or introduction of dietary supplements for large numbers of elderly people will be justified in terms of preventing blindness. On present evidence, we should identify people at increased risk of ARMD (ie, those with a family history, large or soft drusen, or vision loss in one eye from ARMD), encourage them to stop smoking, and promote a diet that includes vegetables, fish and nuts and reduces fatty foods laced with vegetable oils. Antioxidant supplements should be recommended if a fresh diet is impractical and if retinal signs of progression are present. For people of advanced age with a lower risk of ARMD, we might compliment them on reaching seniority and note that, in the dietary supplement study mentioned above,11 only 1.3% of patients with small drusen experienced ARMD progression over a 6-year period. Retinal images showing age-related macular degeneration (ARMD) A. “Dry” ARMD. Large soft macular drusen, signifying a high risk of progressive visual loss. B. “Wet” ARMD. Arrowed area delineates advanced wet macular degeneration with subretinal exudation and neovascular scar tissue. These changes result in blindness.

Ian J Constable FRANZCO, FRACS, FRCS

Objective: To describe the impact of a hepatitis A vaccination program for Indigenous children in north Queensland.Design: Enhanced surveillance of all notified cases of hepatitis A in north Queensland from 1996 to 2003.Setting: North Queensland; population, 596 500 people, including about 6900 Indigenous children aged under five years.Interventions: Hepatitis A vaccine was provided to Indigenous children in north Queensland from February 1999; two doses were recommended (at 18 months and 2 years of age), as was catch-up vaccination up to the sixth birthday.Results: In the 4 years 1996–1999, 787 cases of hepatitis A were notified in north Queensland, 237 (30%) of which were in Indigenous people. The average annual notification rates in Indigenous and non-Indigenous people during this period were 110 and 25 cases per 100 000 persons, respectively. In the first 4 years after introduction of the vaccination program (2000–2003), 66 cases of hepatitis A were notified. Only nine of the 66 (14%) were in Indigenous people. The average annual notification rates in Indigenous and non-Indigenous people in 2000–2003 were 4 and 2.5 cases per 100 000 persons, respectively.Conclusion: Hepatitis A seems to have been eradicated from Indigenous communities in north Queensland very soon after the vaccination program began. The rapid decline in notifications in non-Indigenous as well as Indigenous people suggests the program quickly interrupted chains of transmission from Indigenous children to the broader community. To our knowledge this is the first evidence that a hepatitis A vaccination program targeting a high-risk population within a community can reduce disease in the broader community. Hepatitis A vaccine should be provided to other high-risk Indigenous children elsewhere in Australia.

Jeffrey N Hanna MPH, FAFPHM · Susan L Hills MTH, FAFPHM · Jan L Humphreys

Recent data from Australia, the United States and Europe show increased self-reported energy intake associated with obesity, in contrast to earlier suggestions that the obesity epidemic has occurred despite minimal or no increase in per capita energy intake from food. The effect of increased energy intake is compounded by sedentary lifestyles. Both physical activity and nutrition must be addressed to reduce the prevalence of obesity and improve the health of Australians. During the past decade, several authors from the United States and the United Kingdom have suggested that the obesity epidemic has occurred despite minimal or no increase in per capita energy intake and/or energy from the food supply.1,2 This has been described as the “American paradox”,2 and cited as evidence that the obesity epidemic is due to decreased physical activity and not to changes in eating patterns.3 There are dangers inherent in this viewpoint. According to the International Obesity Taskforce (IOTF), the food industry seeks to focus on inactivity and promote sports to divert attention from the role of foods and drinks.4,5 The IOTF asserts that the causes of the obesity epidemic are twofold: an abundance of energy-dense foods and drinks, leading to a pervasive “passive over-consumption” of energy; and an environment that limits opportunities for physical activity, leading to an almost universal sedentary state.4 Energy intakeTrends in energy consumption are difficult to establish because of a variety of measurement issues. People under-report their energy intake, and higher BMI is associated with a greater degree of under-reporting.6 This introduces a systematic bias, resulting in the paradoxical observation that obese individuals appear to eat less than lean people. Techniques have been developed to reduce this bias by excluding the most blatant under-reporters. The Australian Food and Nutrition Monitoring Unit undertook a bridging study to compare the food and nutrient intake data from the 1983 and 1995 Australian national nutrition surveys and the 1985 Australian Council for Health, Physical Education and Recreation (ACHPER) study.7 For these studies, energy intake was estimated from 24-hour intake and food frequency data, collected by dietitians at in-home interviews. After adjusting for differences in the food composition databases and demographic changes in the Australian population, the study found that mean energy consumption of Australian adults living in capital cities increased significantly by around 3%–4% (about 350 kJ/day) between 1983 and 1995.7 Between 1985 and 1995, mean energy intake increased greatly and significantly by 11% for girls and 15% for boys aged 10–15 years. The major source of increased energy intake was carbohydrate. Absolute fat intake did not increase among children, and declined slightly among adults.7 Fat as a percentage of energy decreased because of the increase in energy intake. An energy imbalance of 3%–4% in adults (about 350 kJ/day, equivalent to a slice of bread, or 30 minutes of sitting instead of brisk walking) would produce weight gain of about 1 kg per year until equilibrium is again reached, when the higher energy expenditure at a higher body mass equals energy intake. The Australian intake data are supported by recent data from the US. A significant increase in total energy intake between 1971 and 2000, particularly from carbohydrate, has been reported in the US, based on intake data from the National Health and Nutrition Examination Survey (NHANES).8 Data on food supply in the US and Europe also indicate that energy supply has increased.9,10 In Europe, data from the MONICA study indicate that per capita energy supply correlates with prevalence of obesity.10 In that study, trends in total energy supply per capita explained 41% of the between-population trends in BMI. Energy supply combined with prevalence of ex-smokers (who are more likely to be overweight) explained 69% of the between-country differences in change of prevalence of overweight. An economic analysis of factors underlying the trends in obesity in the US found that the per capita increase in the numbers of restaurants accounted for 61% of the increase in BMI and 65% of the increase in the percentage of the population who are obese.11 Energy expenditureAlthough it is not possible to measure energy expenditure at a population level, it has been suggested that population Total Daily Energy Expenditure (see Box) has declined.1,2,12 However, all of these reviews rely on the argument, based on the UK data,1 that energy intake has not increased and therefore energy expenditure must have decreased. Objective analysis of Total Daily Energy Expenditure and Activity Energy Expenditure in free-living individuals is possible using doubly-labelled water techniques. A large review of objective studies of energy expenditure found that Resting Energy Expenditure, Activity Energy Expenditure and Total Daily Energy Expenditure are all substantially and progressively higher with obesity. For BMI categories ranging from < 25 to > 35 kg/m2, Total Daily Energy Expenditure ranges from 9.5 to 13.5 MJ/day for women and from 12.9 to 17.5 MJ/day for men.13 This contradicts the popular view that obesity is due to “low metabolism” and is maintained despite a low level of food intake. After adjustment for body size, energy expenditure of obese individuals is similar to that of lean individuals. Population body mass has increased, so population per capita Total Daily Energy Expenditure must have increased. Clearly, energy intake must also have increased to maintain energy balance. The recent studies quoted above, based on both food supply and self-reported intake data in the US, Australia and Europe, confirm this. Physical activityAt an individual level, physical activity is clearly important for weight control. Physical activity is an effective adjunct to dietary management for weight loss and maintenance.14 However, at a population level, measurement of physical activity relies on self-report and suffers from methodological difficulties similar to those for determining nutrition. Prospective observational population studies of the effect on body weight of physical activity measured at baseline are few and the results are inconsistent.15-17 Physical inactivity appears to be both a cause and a consequence of obesity. Many studies have shown that television viewing is associated with obesity, although this is independent of physical activity level.18 However, it is very clear that a sedentary lifestyle is almost universal in developed societies, and that this is related to physical, technological and economic environmental conditions.19 In Australia, population surveys suggest that the proportion of the population reporting undertaking 30 minutes of moderate physical activity daily has declined from 62% in 1997 to 57% in 2000.20 However, there is now consensus that 45–60 minutes of moderate physical activity may be required for some people to prevent weight gain in the current environment of abundant energy-dense food.15,17 Relative contributions to obesityTwo longitudinal studies using objective measures of energy expenditure have attempted to determine the relative contribution of energy intake and expenditure to subsequent risk of obesity. In the first study, involving infants, measured energy intake determined weight gain between 3 months and 12 months, but measured energy expenditure did not.21 The other study showed that, among Pima Indian adults, baseline total energy intake (calculated from energy expenditure measured by using doubly-labelled water) is a predictor of weight gain over 4 months or more.22 However, baseline Activity Energy Expenditure and physical activity were not related to weight gain. As in many other studies, the physical activity level was lower in obese subjects, and the authors concluded that this was secondary to obesity. ConclusionAn increase in energy supply and consumption has made a major contribution to the obesity epidemic. It is probable that population physical activity level has also decreased, as both a cause and a consequence of the obesity epidemic. There are many other benefits of physical activity and healthy eating besides weight management, and both physical activity and nutrition must be addressed together to improve the health of all Australians. This requires multistrategy interventions across a range of sectors, including food producers, manufacturers, wholesalers, retailers, restaurateurs, caterers, transporters, advertisers, urban planners, employers, sporting associations, the fitness industry, community groups, the media, and policymakers at all levels of government, in addition to interventions in schools. A national, coordinated, systematic approach to monitoring overweight and obesity, dietary intake and physical activity is essential to both inform and evaluate interventions. Key evidence-based interventions to address childhood obesity through improved nutrition and increased physical activity are outlined in the National Obesity Taskforce report Healthy weight 2008 — Australia’s future.23 Energy expenditure terminology Total Daily Energy Expenditure is the amount of energy expended by an individual in one day. This is made up of Resting Energy Expenditure and Activity Energy Expenditure. Resting Energy Expenditure is the energy expended by the body in the resting state to maintain itself and digest food. This is made up of Basal Metabolic Rate (energy expended in the rested and fasted state) plus the Thermic Effect of Food (the energy used in digesting food — estimated at ~10% of Total Energy Expenditure). Activity Energy Expenditure is the energy expended by the body in movement, and is the only aspect of energy expenditure that is under conscious control. Activity Energy Expenditure makes up 20%–40% of Total Energy Expenditure, depending on activity level. Physical Activity Level is expressed as the ratio of Total Daily Energy Expenditure divided by Basal Metabolic Rate.

Christina O Stubbs BSc, GradDipDiet, APD · Amanda J Lee BSc, GradDipDiet, PhD

Gordon R W Davies Psychiatrist, 33 Smith St, Wollongong, NSW 2500. alienistATihug.com.au To the Editor: The recent article on obesity by Proietto and Baur in the Journal1 coincided with another by Campos in New Scientist,2 in which he criticised the conventional view of the risks of obesity and the norms usually accepted. Campos quoted evidence suggesting that, in fact, the group in the overweight range (body mass index [BMI], 25–30 kg/m2) are healthier than those with a BMI below 25 kg/m2. He also noted that between 1990 and 2002, despite a further increase in the prevalence of obesity in the United States, the incidence of type 2 diabetes hardly changed, while cardiovascular death rates fell. According to Campos, similar claims about the risks of obesity have been repeated over the past 50 years and relate more to cultural and political factors than to reliable scientific evidence. Clearly, this view is inconsistent with that articulated by Proietto and Baur. While Campos’ view obviously does not apply to the grossly obese, there is a strong suggestion that the overall evidence base is inconsistent. This may be because the assumption of a linear relationship between excess weight and illness is false. It is further likely that there is confounding of variables, with weight a proxy for lack of exercise. As Campos points out, large-scale observational studies are inevitably poorly controlled. If this is so, then it may well be more useful for the medical profession to emphasise exercise and lifestyle rather than weight loss. It may be much easier to obtain and reinforce behavioural change in these areas, and avoid the common feeling of hopelessness (“why bother”) expressed by people who find it hard to diet and to lose weight.

Gordon R W Davies

Ray C McHenry,* Richard W Gilhome,* Chris Hensman* * General Surgeon, Eastern Surgical, Suite 7529, Police Road, Mulgrave, VIC 3170. To the Editor: We take issue with the recommendations on treatment of morbid obesity in the otherwise excellent article on obesity management by Proietto and Baur.1 Like most non-surgical clinicians involved in the management of obesity, they fail to differentiate between the treatment of obesity (body mass index [BMI], 30–35 kg/m2) and morbid obesity (BMI > 35 kg/m2). The literature is crystal clear — non-surgical treatments are unsuccessful in achieving and maintaining weight loss in morbid obesity.2,3 We are unaware of any branch of medicine, other than morbid obesity management, where respected clinicians routinely recommend treatments (drugs, diet and lifestyle modification) which have been proven not to be effective. We challenge all clinicians to accept what the evidence clearly shows, that: the only known effective treatment for morbid obesity is surgery;2,3 and laparoscopic adjustable gastric banding is much safer than bypass/diversion surgery4 and just as effective; it is the treatment of choice for morbid obesity.

Ray C McHenry · Richard W Gilhome · Chris Hensman

Huy A Tran Director of Clinical Chemistry, John Hunter Hospital, Hunter Region Mail Centre, Locked Bag No 1, New Lambton Heights, NSW 2310. huy.tranAThunter.health.nsw.gov.au To the Editor: I read with interest the recent article on obesity in Australia by Proietto and Baur1 and would like to comment on the issue of proteinuria and measurement of insulin level in obese patients. Proteinuria in obesity, commonly referred to as obesity-related glomerulopathy, is a clinical syndrome with an estimated incidence of about 2% in obese subjects.2 With a fifth of the population being obese,1 the sheer number suspected to have this condition will create an enormous management and cost burden. Furthermore, the incidence of this condition appears to have increased disproportionately to the incidence of obesity.2 The syndrome of obesity-related glomerulopathy comprises the triad of morbid obesity, marked proteinuria without oedema, and normal serum albumin concentration. It can occur in any degree of obesity but is more common in the morbidly obese group (body mass index > 40 kg/m2; Class III obesity). It often presents as proteinuria on urinary dipstick testing, with marked proteinuria seen on confirmatory testing (up to 32 g/day).2 Other features of the nephrotic syndrome do not occur, and the cholesterol level is often lower than that in patients with nephrotic syndrome. However, glomerular filtration rate is raised, and glomerulosclerosis is seen on biopsy. The pathogenesis is unknown. Obesity-related glomerulopathy is a diagnosis of exclusion: secondary causes of proteinuria should be fully eliminated, including hypertensive renal disease and undetected type 2 diabetic renal disease. More often than not, biopsy will be required to guide management, with cost implications. Although the condition is said to be benign, in a small proportion of patients it progresses to end-stage renal failure requiring replacement therapy, further adding to the cost of management. Fortunately, the condition is readily reversible with weight loss, which is an important emphasis in management. 3 My second comment relates to the case of the overweight adolescent described by Proietto and Baur. In this patient, measurement of insulin level is not indicated.4 There is no standardised insulin immunoassay, the sample has to be collected and processed correctly to produce a valid result, and the result would not add to or alter the management of the condition. It is doubtful if normative data exist for adolescents, but the clinical picture suggests the insulin resistance syndrome. As the primary goal would be to detect disordered glucose metabolism, appropriate testing of glucose level is all that is required.

Huy A Tran

Joseph Proietto,* Louise A Baur† * Endocrinologist, Department of Medicine, Repatriation Hospital, Heidelberg, VIC 3081; † Paediatrician, Children's Hospital at Westmead Clinical School, Sydney, NSW. j.proiettoATunimelb.edu.au In reply: We agree with McHenry and colleagues that, until very recently, surgery was the only effective treatment for morbid obesity. However, the development of effective pharmacotherapy that targets the underlying cause — increased hunger — may well change this situation, as evidenced by the effect of leptin treatment in leptin-deficient children.1 In the not-too-distant future, a medical alternative may be possible. The issue of the relative merits of surgery to insert a foreign body (gastric band) or permanently alter the anatomy of the gastrointestinal tract versus lifelong pharmacotherapy will need to be considered. However, economic as well as health issues may be important, and, as McHenry and colleagues suggest, may still favour surgery as the preferred therapy. We thank Davies for bringing to our attention Campos’ book The obesity myth, in which he claims that overweight individuals are in fact healthier than those of normal weight.2 While many of the book’s other claims can be challenged (such as the statements that the prevalence of type 2 diabetes is not rising in the United States, and that bald men have higher testosterone levels), the fact that there is no simple linear relationship between body mass index (BMI) and illness is correct. Sex, race and fat distribution can all influence the relationship. Moderately overweight women with gynoid (hip and thigh) fat are not at increased risk of illness.3 In contrast, South Asian people have an increased risk of developing diabetes at lower BMI values than people of European background. We agree with Davies that maintaining fitness through regular exercise is very important in minimising the health consequences of obesity. Tran raises the issue of whether it is useful to measure insulin levels in children. It is not unreasonable to assume that insulin levels are raised in most obese children, but this is not always the case. The National Health and Medical Research Council clinical practice guidelines for management of overweight and obesity in children and adolescents state that: “Fasting insulin and glucose should be considered in obese children or adolescents, particularly those with a family history of type 2 diabetes, those with acanthosis nigricans and those from certain ethnic backgrounds”.4 In the presence of insulin resistance, serum glucose level remains normal because of high insulin levels. Thus, glycaemia cannot be used to monitor improvement in insulin sensitivity.

Joseph Proietto · Louise A Baur

We need a national tobacco act to regulate all aspects of tobacco manufacturing and marketing “Fire safe” cigarettes are those which self-extinguish when they are not being smoked, as opposed to regular cigarettes which continue to burn. For nearly two decades there has been opposition from the tobacco industry to proposals for legislation that would mandate fire-safe, or “reduced ignition propensity”, cigarettes. And this is despite the fact that smoking is the leading cause of residential and total fire deaths in at least eight countries, including Australia.1 The good news is that two jurisdictions in North America have now legislated to require all cigarettes to pass a “fire-safe” standard. Around 14 people in Australia die from cigarette-caused fires annually, and infants are over-represented in these deaths . . . The evidence that cigarettes cause fires is extensive. Data from the Australasian Fire Authorities Council (Mr C Donnelly, Director Corporate Strategy, New South Wales Fire Brigades, on behalf of the Australasian Fire Authorities Council, personal communication 5 February 2004) show that, annually, at least 4574 fires are caused directly by cigarettes and smokers’ materials around Australia (excluding the Northern Territory and South Australia, for which no data were available). In addition, an unknown proportion of another 78 894 fires of indeterminate origin could be associated with smoking. Determining the exact ignition source of a fire is often difficult because the evidence is generally destroyed. Cigarette butts are easily destroyed in fires, and conclusions about their role in causing fires are therefore deduced from a combination of evidence about the location and ignition point of fires (eg, beds, furniture, roadsides) and the elimination of other possible causes. The costs of cigarette-caused fires in terms of lives lost and property damaged are high. Around 14 people in Australia die from cigarette-caused fires annually,2 and infants are over-represented in these deaths, often dying in household fires resulting from cigarettes igniting bedding or furniture.3 In 1998–99, smoking-related fires throughout Australia cost some $52.1 million in tangible costs — health costs, private property damage and fire service costs — plus an estimated $28.5 million in intangible costs (such as the value of lives lost in such fires). This estimate is highly conservative, as it excludes valuations of public property damage, such as national parks, loss of animals, and of amenity while bushland regenerates.4 In Australia, particular focus has fallen on the role of discarded cigarettes as one cause of our infamous bushfires. Conservatively, it is estimated that about 7% of bushfires are caused by discarded cigarettes,5 and all states and territories now have laws for prosecuting people who discard lighted butts. A recent study has confirmed the ability of cigarettes to ignite bush litter. In outdoor conditions, with wind speed about 40 km/h, grassy fuel moisture content about 12% of oven dry weight, and humidity 14%, cigarette butts caused three ignitions in 75 trials (4%). If 1000 smouldering butts were discarded in comparable conditions, 40 fires might result.6 The same 2003 study examined butt discard rates on median strips next to two traffic lights on two of Sydney’s major arterial roads. Everyone’s daily experience of seeing people discarding glowing butts hardly needed confirmation, and the study found 426 discarded butts in a 3-week period.6 Education, fines, and talkback radio vilification of butt-throwers would thus appear to have minimal impact on this practice. Australian fire investigators report that hundreds of fire officers are often unnecessarily exposed to physical and psychological harm from cigarette-caused fires. Fire-cause investigators and other fire industry leaders unanimously support the introduction of regulations to reduce the fire risk of cigarettes.7 Tobacco companies commonly add burn accelerants, such as sodium and potassium citrate, to cigarette paper.8 However, in the United States, tobacco companies have patented many reduced ignition propensity cigarettes,9 and their own market research has shown them to be acceptable to smokers.10 To date only one such brand has been released (Philip Morris’s Merit, which is available in the USA and New Zealand). A recent comparative study of self-extinguishment showed that all regular manufactured cigarettes, 73% of Merit cigarettes, but no hand-rolled cigarettes (wrapped in virtually citrate-free paper), burnt full length.11 The hand-rolled cigarettes were wrapped in a brand of cigarette paper containing only trace levels of impregnated citrate. The elimination of citrate and other burning agents in cigarette paper thus appears to be a simple and effective means of dramatically reducing the ignition propensity of cigarettes. Now, after decades of advocacy from paediatricians, trauma physicians and fire authorities, both the state of New York and Canada have passed legislation on “fire-safe” cigarettes. From July this year, all cigarettes sold in the state of New York must pass a performance standard requiring that no more than 25% of cigarettes tested shall exhibit full-length burns on a bed of filter paper specified in the test method.12 (Merit would thus fail the New York standard.) Canada’s similar legislation was passed in March 2004, to take effect from October 2005.13 It would appear ethically inconceivable that the tobacco industry, knowing that it can produce products that will greatly reduce the potential to cause fires, should refuse to release them onto the market. Why, then, does it continue to do this, given the potential for saving lives, property and the likely public relations benefits to that beleaguered industry that would almost certainly follow? Evidence from internal tobacco company documents shows that the industry’s principal concerns appear to be legal — they are concerned about litigation relating to people burnt in fires caused by cigarettes that the industry could have made less combustive. As a 1983 British American Tobacco document stated: In view, however, of their recent decision taken by the Tobacco Institute not to work actively in the development of self-extinguishing cigarettes (for product liability reasons) it will be necessary for B&W management to define its wishes . . . [emphasis added].14 A major impediment to regulating fire-safe cigarettes in Australia is that the constituents of tobacco products are totally unregulated.15 Their ingredients and “quality” are not controlled by any food, pharmaceutical or poisons legislation, allowing the industry to avoid the sort of regulatory standards that could require cigarettes with reduced ignition propensity to conform to a standard. Instead, the industry enters into self-regulatory agreements with government, such as the current arrangement to list additives on industry websites. This agreement allows local manufacturers to avoid listing any ingredients they do not wish to reveal by designating them as generic “processing aids” or declaring them commercial-in-confidence.15 This regulatory “no-man’s land” should be replaced by a national tobacco act,16 which would allow complete regulation of all aspects of tobacco manufacturing and marketing. Such regulation, in mandating reduced ignition propensity cigarettes, would save lives, millions of dollars in damage and contribute to bushfire reduction. In the event that a national tobacco act was opposed by one or both of the major political parties, interim cigarette reduced ignition propensity regulations should be introduced, in line with those introduced in the Canadian and New York State jurisdictions.

Simon Chapman PhD · Antony Balmain

Joshua P Hanson,* Carmel T Taylor,† Ann R Richards,‡ Ina L Smith,§ Craig S Boutlis¶ *Registrar, ¶ Physician, Cairns Base Hospital, PO Box 902, Cairns, QLD 4870; † Scientist, § Research and Development Coordinator, Public Health Virology, Queensland Health Scientific Services; ‡ Public Health Nurse, Tropical Public Health Unit, Cairns, QLD. joshua_hansonAThealth.qld.gov.au To the Editor: The Japanese encephalitis flavivirus is the most common cause of encephalitis in Asia. Death occurs in 25% of clinical cases, and permanent neurological deficits occur in up to 50% of survivors.1 Infection is transmitted from amplifying hosts (primarily waterbirds and pigs) by Culex mosquitoes. Although the virus has been isolated in the Western Province of Papua New Guinea,2 and clinical cases have been described in the Western Province and suspected in the Milne Bay region,3 to our knowledge cases have not been reported from around Port Moresby. In January 2004, a 66-year-old man of European background was evacuated to our hospital with a 7-day history of fever and confusion. On examination, he had generalised upper motor neurone signs and a Glasgow coma score fluctuating between 6 and 10. Computed tomography and magnetic resonance imaging showed multiple non-specific white-matter lesions bilaterally. An electroencephalogram (EEG) demonstrated diffuse slowing in the delta to theta range in both hemispheres, with preserved response to painful stimulation. Lumbar puncture showed clear cerebrospinal fluid (CSF), with a leukocyte count of 65 × 106 cells/L (81% mononuclear) (reference range [RR], < 5 × 106 cells/L), normal erythrocyte count, raised protein level of 0.79 g/L (RR, 150–500 mg/L); glucose level of 4.3 mmol/L (RR, 2.8–4.0 mmol/L) and negative bacterial and fungal cultures. The CSF was also negative for cryptococcal antigen and by polymerase chain reaction (PCR) testing for enterovirus and herpes simplex, Japanese encephalitis, Murray Valley encephalitis and Kunjin viruses. Serological tests were negative for syphilis and human immunodeficiency virus infection. Paired sera from Days 2 and 19 of admission were tested in parallel against a panel of flaviviruses using a haemagglutination inhibition assay.4 This showed fourfold rises in antibody titre against dengue virus serotypes 1, 3 and 4, and Japanese encephalitis, Murray Valley encephalitis, Kunjin, Alfuy and Kokobera viruses, and twofold rises in titre against dengue virus serotype 2 and Stratford virus. Overall, these results were diagnostic of recent flavivirus infection but were non-specific. IgM antibody responses to the same flaviviruses were measured in sera and CSF using an in-house enzyme-linked immunosorbent assay (ELISA), with strongest reactivity demonstrated to Japanese encephalitis virus (Box). The patient had lived in Papua New Guinea since 1970, predominantly on a church-run farm at Bootless Bay, about 20 km from Port Moresby. He had not travelled outside this region in the month before his illness, and had no history of Japanese encephalitis vaccination or of dengue fever. The farm was situated about 150 metres from a piggery. The patient had no direct contact with this piggery. His accommodation was poorly screened against mosquitoes. After 3 weeks of primarily supportive intensive care, the patient was discharged to a general ward. His neurological recovery was slow. After 5 months, he was able to walk with assistance and required a tracheostomy to protect his airway. He was judged likely to experience permanent neurological deficits. The clinical, epidemiological, radiological, EEG and serological features of this case strongly support a diagnosis of Japanese encephalitis. Japanese encephalitis virus is difficult to detect in CSF by isolation or PCR because of neutralising antibodies and the limited duration of viraemia, which may have accounted for the negative PCR result in this case, despite the use of a highly sensitive method.5 This case highlights the desirability of further defining the epidemiology of Japanese encephalitis in the Port Moresby region, as well as reconsidering the current recommendation to vaccinate Australians only if they intend travelling to the Western Province of Papua New Guinea.1 IgM antibody levels, measured against a panel of flaviviruses by enzyme-linked immunosorbent assay (ELISA) JE = Japanese encephalitis. MVE = Murray Valley encephalitis. * IgM levels were measured as the P/N (positive/negative) ratio (ratio of the absorbance of the test sample to the absorbance of a negative control sample tested against the same antigen).

Joshua P Hanson · Carmel T Taylor · Ann R Richards · Ina L Smith · Craig S Boutlis

To the Editor: The Australian Technical Advisory Group on Immunisation (ATAGI) is responsible for maintaining and updating the Australian immunisation handbook, on behalf of the National Health and Medical Research Council (NHMRC).1 At its 25th meeting, in April 2004, ATAGI discussed data (then unpublished) presented by Hanson and colleagues on evidence for the spread of Japanese encephalitis virus beyond the Western Province of Papua New Guinea to the Port Moresby region.2 ATAGI believes it is probable the virus has spread to other parts of Papua New Guinea. The current (8th) edition of The Australian immunisation handbook states on page 179: “Current understanding of the ecology of the JE [Japanese encephalitis] virus elsewhere in Papua New Guinea is fragmentary and unsubstantiated. Therefore no definitive recommendations about JE vaccination for travellers to other parts of Papua New Guinea can be made at the current time.” ATAGI agreed that the evidence provided by Hanson and colleagues was compelling, and sufficient to warrant expanding the current recommendation for Japanese encephalitis vaccination. ATAGI is proposing the recommendation be changed to include travellers staying more than one month in all parts of Papua New Guinea, not just those planning to stay in the Western Province. A public consultation process to change this recommendation is being conducted as part of the requirements of the NHMRC Act 1992. A public consultation paper is available from the Immunise Australia Program website (www.immunise.health.gov.au). Submissions close on 17 September and can be directed to Ms Letitia Toms, Assistant Director, Immunisation Section, Department of Health and Ageing, MDP 14, GPO Box 9848, Canberra, ACT 2601 (letitia.tomsAThealth.gov.au).

on behalf of the Australian Technical Advisory Group on Immunisation (ATAGI)

It all depends on which studies you emphasise Four years ago in the Journal we posed the question of whether active and passive exposure to cigarette smoke could cause breast cancer. We concluded, at the time, that biological plausibility had been established, but that the epidemiological evidence was inconclusive.1 This was consistent with a 1997 report2 of the California Environmental Protection Agency (Cal/EPA), which found that the link between environmental tobacco smoke (ETS) and breast cancer was inconclusive. However, in a recent draft review of the health effects of ETS,3 the Cal/EPA stated that the evidence for a causal association between ETS and breast cancer is now conclusive. Its latest report was based on a systematic review of 15 studies, 11 of which had been published since the 1997 report. Is this new conclusion justified? Until the 1990s, most case–control and cohort studies examining the association between cigarette smoke exposure and breast cancer focused on active smoking. These studies did not adequately ascertain the whole-of-life ETS exposure of the participants.1,4,5 Notably, childhood exposure was usually ignored.6 This is of particular relevance, as chemical carcinogenesis studies of breast cancer in experimental animals, and other studies on the development of the mammalian breast, indicate that breast ductal cells would be most susceptible to chemical carcinogenesis during puberty and first pregnancy.5 Thus, it is possible that childhood, adolescent and adult exposure to cigarette smoke up until the delivery of a woman’s first child is a crucial component of lifetime exposure. If an association with ETS did exist, case–control and cohort studies on active smoking and breast cancer could have underestimated the effects by inadequate assessment of ETS exposure.1,4-6 The conclusion of the Cal/EPA report on ETS and breast cancer3 is based on a systematic review that gives prominence to the recent studies in which several sources of ETS exposure have been ascertained and to the clear dose–risk relationships seen in some studies. The meta-analysis used in the Cal/EPA’s review yielded a relative risk of 1.40 (95% CI, 1.17–1.68) — a significantly increased risk. However, a closer look at the studies reviewed in the latest Cal/EPA report raises some questions about its conclusion. Of the 15 studies in the review, five were cohort studies, of which none showed a statistically significant increase in breast cancer risk with ETS exposure. Several of these cohort studies had a very limited assessment of ETS — for example, defining exposure as simply being married to a smoker. However, one of the five cohort studies, which prospectively assessed childhood, adult and occupational ETS among US nurses,7 also showed no association. Moreover, another major cohort study8 published since the Cal/EPA review supports the conclusion of the US nurses’ study in regard to ETS. In this report of a 5-year follow-up of a cohort of 116 564 Californian teachers, 1150 new cases of invasive breast cancer were diagnosed among the 76 189 never-smoking women who provided data on ETS.8 The study aimed to ascertain total lifetime ETS exposure, although the published analysis is limited to household exposure throughout life. No significant association between ETS exposure and breast cancer was found for any age range of exposure or by menopausal status. However, a significant association was found between active smoking and breast cancer. The relative risks of acquiring breast cancer after ETS exposure in childhood, adulthood, or both childhood and adulthood, were 0.92, 0.93 and 0.93, respectively. Adding this new study to the Cal/EPA’s meta-analysis, the overall relative risk, based on the six cohort studies, is 1.01 (95% CI, 0.92–1.12) — that is, there is no significant effect. The strong association between ETS exposure and breast cancer emphasised in the Cal/EPA report3 is based on five case–control studies regarded as “unlikely to have missed important ETS exposures”. The summary odds ratio for these studies was 1.92 (95% CI, 1.54–2.39). The association was stronger in premenopausal women (summary odds ratio, 2.20; 95% CI, 1.70–2.85). However, if a true association exists, it is difficult to see why the two high-quality US cohort studies of nurses and teachers7,8 showed no association. In both studies, data on ETS exposure were collected before the diagnosis of breast cancer, thus avoiding recall bias, and both groups are likely to have given reasonably complete and valid information, including data on childhood exposures. Other research results add to the complexity of the issue. A 2002 systematic review, based largely on the same case–control studies as the Cal/EPA review,3 concluded that the strength of the association with breast cancer is similar for passive as for active smoking9 — a conclusion that others find implausible.7 One possible explanation for this seeming paradox could be that the association is linked mainly or exclusively to ETS exposure in childhood or early adolescence, as has also been suggested for active smoking, perhaps through hormonal mechanisms as well as the direct effects of carcinogens.10 The fact that p53-gene mutations in breast tumours are increased in smokers compared with non-smokers or ex-smokers suggests a genotoxic effect of smoking on breast tissue.11 Further complexities related to genotype may emerge: one case–control study12 showed that the association between passive smoking and breast cancer was stronger in rapid acetylators (ie, women who, owing to their specific NAT2 genotype, more rapidly metabolise carcinogenic compounds, such as aromative amines, in tobacco smoke). However, with regard to active smoking, slow acetylators were more at risk.12 Although many genotypes have been reported to affect the association between active or passive smoking and breast cancer,13 the results are inconsistent and do not explain the variable epidemiological results. Is a causal association between ETS exposure and breast cancer now certain, as the Cal/EPA draft report proposes? The jury would be wise to stay out on this one. If the emphasis is put on cohort studies, there appears to be no association between ETS exposure and breast cancer. If the emphasis is put on case–control studies with more detailed information on ETS exposure — but the possibility of recall bias — there appears to be an increased risk, especially in premenopausal women. An analysis focusing on childhood and adolescent ETS exposure may be the key to solving the current confusion. Such an analysis could be based on a pooled analysis of available studies with access to the original data, or on further assessment and follow-up of the ongoing cohort studies. In the interim, it is prudent to accept the possibility of an association, while also accepting the limitations of the available evidence. The International Agency for Research on Cancer has just released a major report on smoking, in which it states that the evidence does not support a causal link between either active or passive smoking and breast cancer.14 However, the report confirms a causal link between ETS and lung cancer, which, in itself, justifies efforts to restrict ETS.

J Mark Elwood MD, DSc · Robert C Burton MD, PhD

Jessica H Ford,* Annette J Dobson† * Research Assistant, † Professor of Biostatistics, School of Population Health, University of Queensland, Herston Road, Herston, QLD 4006. A. DobsonATsph.uq.edu.au To the Editor: Helping pregnant women to stop smoking and not to resume after their baby is born is a key target for smoking prevention. Pregnancy (or trying to become pregnant) is a time when women are motivated to stop smoking for the sake of the baby and they are in contact with healthcare professionals who can help them do so. We have calculated the impact of smoking during pregnancy in terms of deaths, hospital separations and costs to the healthcare system, and estimated the extent to which these effects could be reduced through interventions initiated by healthcare professionals as part of routine clinical contact. We considered the following conditions: pre-eclampsia (which is less common among smokers), low birthweight (including hospital costs for the mother and the baby, and infant deaths), premature rupture of membrane, spontaneous abortion, ectopic pregnancy, placenta praevia (including infant death), and sudden infant death syndrome (SIDS). We used estimates of relative risks (RRs) for these conditions for women who smoke during pregnancy (or, for ectopic pregnancy, for women who might become pregnant) from meta-analyses.1-3 We obtained data on deaths,4 hospital separations,5 and costs to the healthcare system6 for 2001–02. The prevalence of smoking among pregnant women of all ages in New South Wales since 1994 has been in the range 17% to 22%.7 The prevalence of smoking among all women of child-bearing age in 2001 was about 28%.8 From these data, we calculated attributable fractions1,2,9 for average values (using point estimates for RRs and 20% for prevalence of smoking in pregnancy) and extreme values (using the 95% confidence limits for RRs and 17% and 22% for smoking prevalence). In summary, the average number of adverse events attributable to smoking each year in Australia are: infant deaths, 78 (extreme values, 66–87); hospital separations, 6890 (extreme values, 4130–9450); costs to the healthcare system, $23 million (extreme values, $16–$29 million). A Cochrane review of behavioural (not pharmacological) interventions for stopping smoking in pregnancy showed an absolute reduction of 6% (95% CI, 4%–8%).10 Thus, if the prevalence of smoking during pregnancy were reduced from 20% to 14%, we calculate that there would be 20 fewer infant deaths, 1600 fewer hospital separations, and a saving of $5 million to the Australian healthcare system per year. (Details of the calculations can be obtained from the authors.) These gains could be realised by increasing community awareness of the risks of smoking in pregnancy and helping health professionals to use smoking prevention strategies in their routine encounters with pregnant women.

Jessica H Ford · Annette J Dobson

Marianne E Jauncey,* Paul K Armstrong,† Emily L Morgan,‡ Jeremy M McAnulty§ NSW Public Health Officer, Public Health Training and Development Branch; † Medical Epidemiologist, § Director, Communicable Diseases Branch; NSW Health, North Sydney, NSW. ‡ General Practitioner, Ballina West Medical Centre, Ballina, NSW. Marianne.jaunceyATyahoo.com.au To the Editor: In 2003, severe acute respiratory syndrome (SARS) became the first pandemic of the 21st century. Despite spreading to 29 countries, a rapid and coordinated international effort led to its containment. Here, we examine Australia’s only laboratory-confirmed case, and the investigation of possible subsequent transmission. In June 2003, the World Health Organization (WHO) notified Australian health authorities of a 26-year-old tourist in whom SARS-coronavirus-specific antibodies had recently been detected. She was part of a retrospective serological survey of people who stayed at the Hotel Metropole, Hong Kong, on 21 February,1 the same time a SARS source case infected at least 14 other hotel guests.2 On 22 February, the 26-year-old tourist travelled to Australia and 4 days later developed myalgia, lethargy and cough. On 6 March, 6 days before the first WHO global alert on SARS, she saw a general practitioner (GP) in northern New South Wales, to whom she also reported nausea, vomiting, nocturnal fever and pronounced lethargy. On examination she was afebrile, pale, unwell, with a cough and clear chest on auscultation. She declined further investigations and hospital admission; her condition gradually improved, and she left Australia 6 days later. She reported close contact with only three people during her Australian visit — her partner, the GP, and the GP’s surgery nurse. None reported subsequent illness and all tested negative for SARS-coronavirus antibody by direct immunofluorescence, a highly sensitive and specific method.3 Australia was fortunate that the tourist was not particularly infectious. The Hotel Metropole case was identified as the source case for four national and international clusters of SARS.2 The resulting human and economic cost was substantial.4 Without specific treatments, basic public health measures proved the only effective means to contain SARS. These included rapid case detection and isolation, contact tracing, handwashing and the correct use of personal protective equipment.5 Many GP practices and some hospitals in Australia do not have isolation facilities or infection control resources to effectively contain diseases like SARS. In the event of local transmission of SARS, infection may well have occurred in Australian healthcare workers. In the wake of SARS and, more recently, avian influenza, GPs must develop infection control plans to protect their own health as well as that of their patients. These should include obtaining a history of travel to outbreak-affected areas, reserving an area for patient isolation, and using appropriate infection control precautions during such outbreaks. Clinicians in other healthcare settings also need to review current infection control practices. If Australia is to remain the “lucky country” with regard to communicable diseases, basic public health measures aimed at preventing transmission of infection in healthcare settings is essential.

Marianne E Jauncey · Paul K Armstrong · Emily L Morgan · Jeremy M McAnulty

A more efficient system of governance is needed to safeguard individual privacy while allowing registries to operate for the public good The recent controversy about cancer registries and patient privacy in the United Kingdom highlights the need for more debate about the governance of medical registries.1 For 40 years, identified data from UK patients with cancer have been transmitted to cancer registries without the patients’ express knowledge or consent. Although many benefits have flowed from analysis of these data, societal conventions have now changed, and questions are being asked in the UK and other countries, including Australia, about the privacy issues involved in the governance of medical registries in particular2-4 and medical research in general.5,6 Medical registries were traditionally established by public health authorities to monitor trends in the incidence of conditions such as infectious diseases and cancer. However, registries have become increasingly important in monitoring outcomes after the implementation of disease-prevention and treatment programs. They are now vital to quality-improvement programs that assess the safety of new drugs and procedures, identify best clinical practice and compare healthcare systems. For example, the Australian Orthopaedic Association National Joint Replacement Register currently monitors the use and survivorship of artificial hip- and knee-replacement prostheses,7 while the Victorian State Trauma Registry (VSTR) was established largely to monitor the effects of changes to the state trauma system.8 For registries to be effective, they must include all eligible participants so as to avoid biases that would affect the applicability and generalisability of results, and they must collect patient-specific data so as to adjust outcomes for risk and management factors. Further, in the absence of a unique national identification number, registries require name-based identification if participants are to be contacted for follow-up, or if registry data are to be validated against those held in other databases. The need for identified data raises consent and privacy issues. Registries must be established and governed in compliance with both federal and state legislation on privacy. Current requirements of this legislation have necessitated the development of consent procedures that maintain the effectiveness of medical registries, while informing patients and protecting their personal medical information. However, obtaining patient consent before participation in broad-based registries is often impractical and results in poor enrolment rates.,4 A more practical approach is to inform participants of their registration but to allow them to opt out of the registry. This approach resulted in the loss of fewer than 0.5% of eligible participants from the VSTR (unpublished data). This both complies with privacy legislation and achieves enrolment levels sufficient to maintain the scientific integrity of registries. Privacy legislation also sets down the circumstances under which privacy principles may be waived. For example, a human research ethics committee (HREC) may determine that the public benefit in allowing access to identified data substantially outweighs individuals’ right to privacy. However, as broad-based registries collect identified data from many sources, they are currently required to seek approval from many individual HRECs. This process is both time consuming and expensive. Further, many local HRECs have insufficient resources or expertise to evaluate the scientific merit of epidemiological research or to interpret privacy legislation,4,8,9 and consequently may reject legitimate research proposals. Registries could be established by legislation that overrides privacy provisions, but this approach lacks flexibility. A more workable system is required for establishing and governing medical registries that both safeguards individual privacy and allows the registries to continue to provide the foundations for quality-improvement programs and epidemiological research. No general guidelines for establishing and governing registries have been published, either in Australia or overseas. However, the National Health and Medical Research Council (NHMRC) has produced guidelines for genetic registers,10 which complement the National Privacy Principles11 with respect to the collection, use and disclosure of sensitive information, data quality and security, and the use of unique identifiers. After further development by the NHMRC in conjunction with federal and state privacy commissions, this model might be applied to other medical registries. We also propose that the NHMRC acts as an accrediting authority for institutions maintaining medical registries. This would ensure that the institutions comply with privacy legislation, maintain independence from the agencies that directly manage participating patients’ healthcare, and have the personnel, facilities and funding to maintain the registry and achieve its purpose. Institutions could be encouraged to seek accreditation by linking it to ongoing funding for registries. Further, a centralised HREC with scientific, ethical and legal expertise might be better able than local HRECs to ensure that registries can achieve their public health aims while maintaining patient privacy. Such a centralised committee should include patient advocates, as well as experts in epidemiology, ethics and privacy law. It could also provide guidance to local HRECs, if current legislation requires that they make their own determination, to avoid unnecessary duplication of review processes. Good registry governance involves developing a structure that includes stakeholders in management of institutions that analyse personal medical information; has a management independent of the institutions that provide healthcare; provides a research environment that maximises scientific benefit to patients and the wider community; and receives adequate funding to ensure continuity of data collection and quality assurance. We hope that developing processes to ensure good registry governance will allay public concerns about privacy and allow registries to continue to underpin programs of healthcare quality improvement and epidemiological research.

Owen D Williamson GradDipClinEpi, FRACS · Peter A Cameron MD, FACEM · John J McNeil PhD, FRACP

The NHS was founded on the principle of access to adequate healthcare for all Roman society in Britain was highly classified. At the top were . . . the legions, the provincial administration, the government of towns and the wealthy traders and commercial classes who enjoyed legal privileges not generally accorded to the majority of the population. In 212 AD, the Emperor Caracalla extended citizenship to all free-born inhabitants of the empire, but social and legal distinctions remained rigidly set between the upper rank of citizens known as honestiores and the masses, known as humiliores. At the lowest end of the scale were the slaves . . .1 In the United Kingdom today, the widening gap between upper and lower “social classes” is regularly presented by politicians and health bureaucrats to professional and lay audiences alike, and used to justify the public health agenda. Health inequalities have become the driving force for public health initiatives. The government under Thatcher explored “variations” in health outcomes and in health service provision. Subsequently, the Blair government replaced “variations” with the more class-oriented “inequalities”. All too often, however, attempts to deal with the real and frequently demonstrated social gradient in disease and in health service provision is limited to “hand-wringing epidemiology”. In any case, discussion of a widening gap reflects a failure to understand the difference between relative and absolute risk, as well as demographic change and the type of outcomes amenable to prevention. . . . unless public health programs are based on sound theoretical bases, they will fail. The debate in Australia is rather more sophisticated: for example, in the report of the Chief Health Officer of New South Wales,2 trends over time in the social gradient are presented in terms of absolute risk, as well as for diseases in which social interventions are likely to be effective. Presented in this way, the social gradient persists, but does not necessarily appear to widen over time, and some improvement in the experience of the least affluent may also be apparent. Are we carping and nit-picking to criticise the UK approach? No, because unless public health programs are based on sound theoretical bases they will fail. Implausible and non-achievable targets aimed at “narrowing the gap” have been established. These include: reducing, by 10%, the difference in infant mortality between the children of manual workers and the whole population; and reducing, by 10%, the gap in life expectancy at birth between the quintile of local council areas with the lowest life expectancy and the whole population. Far better would be to aim at the more important goal of improving the health of the whole community, as well as the disadvantaged part. The NHS was founded on the principle of access to adequate healthcare for all. Selectivity, even well intentioned selectivity, not only flies in the face of this ideal, it ignores the late Geoffrey Rose’s astute observation3 that small changes in the average for the whole population can bring great benefits to those at greatest risk, provided the change involves the whole population. People in the UK still talk about, and measure, social class. Although the use of the term “socioeconomic status” may be an example of political correctness, the fact that “class” is still an acceptable form of scientific terminology in the UK reflects the underlying acceptance of its existence. People typically “know their place”. They measure themselves against a social standard. Those who are “working class” stoutly defend their place in the social hierarchy and are proud of it. Expectations of health and of access to healthcare are firmly rooted in the class system. It is “posh” to eat healthy food, and “posh” is a derogatory term. If men (and women) are born into such shackles of social convention, their freedom to improve their health is distinctly limited. The claim that Australian society is classless is oft made but open to challenge. The concept of social class, as developed by Weber and Marx, is a complex one that involves consciousness of social position and sharing of values and outlooks within the group. If Australia has social classes, they are probably blue collar, white collar, “squattocracy” and those on the dole, but ranged against this are the acknowledged rights of all to “have a go” and to “a fair go”. These maxims make attempts to improve everyone’s health possible, as well as socially and politically legitimate. Why should we care if socially entrenched self-denial of the chance for better health exists in the UK? The reason is that attempts to deal with health inequalities are doomed to failure in such a climate. The debate about equity and health is complex and wide-ranging, and has an international component — all countries have inequality and inequity. The ancient Romans introduced a rigid social class structure into Britain, but the current inhabitants of the British Isles have made its perpetuation an art form.

Richard F Heller MD, FRCP, FRACP, FAFPHM · David P Weller MPH, PhD, FRACGP, FAFPHM · Konrad Jamrozik DPhil, FAFPHM, MFPH

Objective: To conduct a systematic review of studies on clinically relevant digital mobile phone electromagnetic interference with medical equipment.Data sources: MEDLINE and SUMSEARCH were searched for the period 1966–2004. The Cochrane Library and Database of Abstracts of Reviews of Effects were also searched for systematic reviews.Study selection: Studies were eligible if published in a peer-reviewed journal in English, and if they included testing of digital mobile phones for clinically relevant interference with medical equipment used to monitor or treat patients, but not implantable medical devices.Data synthesis: As there was considerable heterogeneity in medical equipment studied and the conduct of testing, results were summarised rather than subjected to meta-analysis.Results: Clinically relevant electromagnetic interference (EMI) secondary to mobile phones potentially endangering patients occurred in 45 of 479 devices tested at 900 MHz and 14 of 457 devices tested at 1800 MHz. However, in the largest studies, the prevalence of clinically relevant EMI was low. Most clinically relevant EMI occurred when mobile phones were used within 1 m of medical equipment.Conclusions: Although testing was not standardised between studies and equipment tested was not identical, it is of concern that at least 4% of devices tested in any study were susceptible to clinically relevant EMI. All studies recommend some type of restriction of mobile phone use in hospitals, with use greater than 1 m from equipment and restrictions in clinical areas being the most common.

Nathan Lawrentschuk MB BS · Damien M Bolton FRACS, MD

Risks to the fetus make it imperative that revised guidelines for fish consumption are clear and reach those most likely to be affected Headlines such as “Mercury warning for children, pregnant women” and “Danger of too much fish” appeared in March throughout Australian newspapers. The media blitz was triggered by the release of revised advice from Food Standards Australia New Zealand (FSANZ) on health risks associated with consuming fish with high methylmercury (MeHg) content (Box).1 The warnings come after a Food and Agriculture Organisation of the United Nations/World Health Organization Expert Committee halved the “provisional tolerable weekly intake” of MeHg in pregnancy from 3.3 µg to 1.6 µg per kilogram bodyweight to protect fetal development.2 Fetal neurotoxicity of MeHg was discovered in the 1960s in Japan. It was named “fetal Minamata disease” after 25 cases of cerebral palsy were found in newborns whose mothers had high levels of MeHg exposure from eating fish contaminated by industrial pollution,3 while the expected number of cases in that population was less than one. Subsequent cohort studies following children from birth to 14 years in New Zealand4 and in the Faeroe Islands5 reported associations between maternal MeHg exposure from fish consumed during pregnancy and deficits in psychological performance or in neurophysiological testing. One prospective study in the Seychelles did not find such effects.6 The Minamata case and subsequent studies indicate that there may be a shift to the left in IQ distribution as a result of excessive MeHg exposure from fish, even at levels too low to produce overt mental retardation. However, a robust debate is continuing about the toxic level of exposure and the “safety margin” required to protect the fetus. The potential risk to children in Australia needs to be carefully considered. The new advice from FSANZ is welcome, as some commonly consumed ocean fish (such as shark) often have natural MeHg concentrations sufficient to cause high weekly exposures. Interestingly, no recommendation was made for tuna. Although canned tuna is usually sourced from smaller, younger fish and is relatively low in mercury, some tuna (albacore, bluefin) has higher concentrations. The United States Environmental Protection Agency advises vulnerable groups against consuming any fish with high mercury content.7 Fish is well established as a “healthy” food. Evidence for cardiovascular benefits from regular fish consumption emerged in the 1990s, as low rates of cardiovascular disease were found in populations with high levels of fish consumption. A number of studies indicate that omega-3 fatty acids reduce cardiovascular risk by improving lipid profiles, inhibiting atherosclerotic plaque, improving arrhythmia, improving vascular function, and reducing damage from ischaemia.8 Curiously, one study reported that high levels of MeHg exposure from fish increased the incidence of myocardial infarction.9 We are therefore faced with the difficult public health challenge of avoiding the health risks from MeHg intake in fish in vulnerable groups while taking advantage of the health benefits of fish consumption. The National Heart Foundation recommends fish be consumed at least twice a week, consistent with advice from FSANZ for most kinds of fish, but this is two to four times the latest recommendations for consumption of fish containing high levels of mercury. While some species of fish have high levels of MeHg, others, such as salmon and hake, have relatively low levels. Expecting consumers to change their understanding that “fish is good” to “some fish are good, sometimes”, and “some fish are not so good, sometimes” introduces a level of complexity into consumer health education that has rarely been seen. Parallels might be drawn with fats and oils, with important shifts in understandings from “all fats are bad” to “some fats are good”, or with alcohol consumption, where some patterns of moderate drinking might be more beneficial to health than abstinence.10 Patterns of fish consumption are highly variable, so ensuring advice reaches those most at risk is essential. For example, shark is frequently unintentional “by-catch”, often used in cheaper meals such as fish and chips and fishcakes, which are consumed fairly regularly by some groups. People more likely to rely on these products may also be less aware of, and less able to respond to, the health advice from FSANZ. While some relatively expensive fish are also high in mercury (swordfish, orange roughy), these are perhaps less likely to form a regular part of the diet. Mercury has a half-life of about 9 weeks, so that women who stop all consumption of fish on becoming pregnant may still be exposing their fetuses to high levels of mercury well into pregnancy. Therefore, we suggest that all healthcare professionals make women of child-bearing age aware of the revised FSANZ recommendations and the potential risks to the developing fetus associated with even moderate consumption of some types of fish during pregnancy. Standards of fish nomenclature should also be developed and enforced to reduce confusion and to ensure consumers are getting what they expect. Further, epidemiological research on actual levels of exposure and the efficacy of the FSANZ health advice is much needed. Revised Australian recommendations for fish consumption* One serve per week (no other fish that week)* One serve per fortnight (no other fish that fortnight)* Two or three serves per week Pregnant women, women intending to become pregnant, and children (up to 6 years) Orange roughy (sea perch), catfish OR Shark (flake), billfish (swordfish, broadbill, marlin) OR Any fish or seafood not listed to the left Rest of population Shark (flake), billfish (swordfish, broadbill, marlin) OR OR Any fish or seafood not listed to the left * Serving size = 150 g for adults and older children, 75 g for children aged up to 6 years.1

Hilary J Bambrick PhD · Tord E Kjellström MEng (Stockholm), MedDr (Stockholm)

Objective: To analyse cancer survival in New South Wales by geographic remoteness.Design, setting and participants: A survival analysis of all patients with cancers diagnosed in NSW between 1 January 1992 and 31 December 1996. Survival was determined to 31 December 1999.Main outcome measures: The relative excess risk (RER) of death over 5 years was estimated for each geographic remoteness category relative to the highly accessible category for 20 cancer types adjusted for age, sex, years since diagnosis and, subsequently, stage of cancer at diagnosis.Results: There were statistically significant differences in the RER of death across remoteness categories (P < 0.001) for cancers of the cervix and prostate and for all cancers. The RERs for the most remote categories (compared with the highly accessible category) before and after adjustment for stage were cervix, 3.22 (95% CI, 1.54–6.75) and 2.25 (95% CI, 1.06–4.77); prostate, 3.38 (95% CI, 2.21–5.16) and 2.53 (95% CI, 1.60–4.01); all cancers, 1.35 (95% CI, 1.20–1.51) and 1.25 (95% CI, 1.11–1.41). In addition, there were significant variations in RER of death by remoteness for head and neck, lung and colon cancers and cutaneous melanoma.Conclusion: Cancer survival varies by remoteness of residence in NSW for all cancers together and some cancers individually. Access to screening or early diagnosis probably contributes to this variation, but persistence after adjustment for stage suggests that treatment variation is also important.

Katharine E Jong MPH · David P Smith MPH · Xue Q Yu MPH · Dianne L O’Connell PhD · David Goldstein MB BS, MRCP, FRACP · Bruce K Armstrong PhD

Objective: To examine trends in hospital admission for hip fracture in New South Wales between July 1990 and June 2000.Design: Analysis of routinely collected hospital separation data.Setting: Public and private acute-care hospitals in NSW.Participants: Admissions of patients aged 50 years and over with a primary diagnosis of fracture of the neck of femur (International classification of diseases, 9th revision [ICD-9] code 820 or ICD-10 codes S72.0–S72.2).Main outcome measures: Number and rates of hospital admission for fracture of the neck of femur per 1000 population; inpatient mortality rates per 1000 admissions.Results: Between July 1990 and June 2000, the number of admissions to NSW acute-care hospitals for hip fracture increased by 41.9% in men (from 1059 to 1503 per year) and by 31.2% in women (from 3160 to 4145 per year). However, age-specific and age-adjusted rates remained practically unchanged. The average length of stay for admissions for hip fracture decreased significantly from 19.2 days (95% CI, 18.5–19.8 days) in 1990–1991 to 14.2 days (95% CI, 13.8–14.6 days) in 1999–2000. No significant change was observed in the overall inpatient death rates per 1000 admissions.Conclusions: The findings support recent reports that the increase in hip fracture rates during most of the past century may have ended. However, the number of admissions for hip fracture is still rising. Preventive measures to reduce the burden of this condition on the healthcare system and community need to be pursued and strengthened.

Soufiane Boufous BH(Hons), MPH(Hons) · Caroline F Finch BSc(Hons), MSc, PhD · Stephen R Lord BSc, MA, PhD

Clinical recordsOutbreak 1In January 2002, an outbreak of influenza A occurred at a Melbourne aged-care facility (ACF) housing 42 residents (median age, 86 years; range, 64–98 years). There were 29 staff working at the facility (median age, 46 years; range, 29–64 years) (Box 1). The index case (Visitor A) was an 86-year-old woman who regularly visited her husband (Resident A) at the ACF. Visitor A developed respiratory symptoms on 26 Dec 2001 (Day 0), was hospitalised with fever and respiratory symptoms on Day 2, and died of pneumonia on Day 17. Visitor A had a history of emphysema and had received the influenza vaccine in March 2001. On Day 5, Resident A developed respiratory symptoms, and between Days 8 and 13, 15 more residents developed respiratory illness, of whom nine were hospitalised. The hospitalisation of four residents on a single day (Day 13) with suspected pneumonia led to the emergency department manager notifying the Victorian Department of Human Services (DHS) of the outbreak. On Day 14, DHS staff visited the ACF and collected nose and throat swabs from symptomatic individuals whose onset of respiratory symptoms had occurred less than 5 days earlier (ideally, specimens should be collected within 72 hours of onset). Where possible, acute and convalescent sera were collected. The Victorian Infectious Diseases Reference Laboratory tested combined nose and throat swabs for influenza virus RNA using a respiratory multiplex polymerase chain reaction (PCR) assay, designed to detect RNA from respiratory syncytial virus; parainfluenza virus types 1, 2, and 3; influenza A virus (subtypes H3N2, H1N1); influenza B virus; and picornaviruses (rhinoviruses, enteroviruses). The reference laboratory also tested acute and convalescent sera for antibodies to influenza A virus, influenza B virus, Mycoplasma pneumoniae, Legionella spp., and Chlamydia pneumoniae antibodies. On Day 14, the DHS recommended that the ACF implement infection control measures (Box 2). The DHS also gave notification of the outbreak to attending general practitioners and infection control staff at hospitals where patients had previously been admitted. Thirty-eight of 42 residents, but only two of 29 staff, had received the 2001 influenza vaccine in either February or March 2001. As an outbreak control measure, 22 of 23 unvaccinated staff who were unaffected by illness were vaccinated (the four unvaccinated residents had already developed respiratory symptoms). On Day 15, 24 hours after collection, PCR test results showed that the samples were positive for influenza A (H3N2). The DHS then recommended antiviral therapy for all residents and all unvaccinated staff: amantadine for prophylaxis and zanamivir for therapy or prophylaxis. Oseltamivir was not recommended at the time, as it was not licensed for prophylaxis. Because of the perceived difficulties in administration and possible gastrointestinal and neurological side effects in elderly and chronically ill people, the facility elected not to use amantadine, and decided on zanamivir for treatment and prophylaxis. However, as the ACF was unable to obtain sufficient stock of zanamivir for these purposes, two residents and four staff members received zanamivir for treatment and 21 unaffected residents received prophylactic oseltamivir (despite its use being outside the licensed indications for the drug at the time). None of the residents who were given prophylactic oseltamivir developed influenza. The latest date of onset of respiratory illness occurred on Day 18 (13 January 2002). The World Health Organization (WHO) Collaborating Centre for Reference and Research on Influenza (Melbourne) identified the outbreak strain as influenza A/H3N2/Moscow-like and concluded that the H3N2-like strain in the 2001 vaccine protected against infection with this virus. Outbreak 2In March 2002, an outbreak of influenza A occurred at a Melbourne ACF housing 32 elderly residents (median age, 84 years; range, 55–91 years). There were 31 staff working at the facility (median age, 42 years; range, 20–55 years) (Box 1). The first two cases in the outbreak were residents who developed respiratory symptoms on 3 March 2002 (Day 0). Their infection could not be linked with a source case. Between Day 1 and Day 3, 22 more people associated with the ACF developed respiratory symptoms. The DHS was notified of the outbreak on Day 5 by an attending GP. On Day 5, the DHS recommended infection control measures (as with outbreak 1), and nose and throat swabs and acute and convalescent sera were collected. Infection with influenza A (H3N2) was confirmed on Day 8, but, by that stage, most affected individuals had recovered and antiviral therapy was not recommended. Although 30 out of 32 residents had received the 2001 influenza vaccine, only three of the 31 staff members had been vaccinated in 2001. Because the outbreak occurred in March, all staff and residents received the influenza vaccine as part of the 2002 influenza vaccination program. The WHO laboratory determined that the outbreak strain was influenza A/H3N2/Moscow-like and concluded that the H3N2-like strain in the 2001 vaccine protected against infection with this virus. However, the infecting viruses in outbreaks 1 and 2 were genetically different, suggesting they were not directly linked. Preventing and controlling influenza outbreaks in ACFsVaccinationIn Australia, influenza vaccination is recommended and funded annually for people aged 65 years and over and recommended, but not publicly funded, for healthcare workers in ACFs.1 Elderly residents may have an impaired response to the vaccine because of age or comorbidities.2,3 Outbreaks have been reported in ACFs, despite high vaccination coverage rates (> 85%) in residents using a vaccine that matches the circulating strain.4,5 This was the case in the outbreaks described here, in which at least 90% of residents had received the influenza vaccine. In view of this, the priority for preventing influenza outbreaks in ACFs should be to prevent individuals introducing the virus into the facility. The key way to do this is to ensure that ACF healthcare workers (including attending GPs) are vaccinated. Educating visitors about vaccination and instructing them to stay away from the ACF when unwell is less likely to be successful. In both outbreaks, there was low staff vaccination coverage, and in outbreak 2, staff appeared to contribute to ongoing transmission. Diagnosis and infection controlThe current non-systematic method of notification of influenza outbreaks in Melbourne ACFs is inadequate. Facilities should be encouraged to establish a sentinel surveillance system to recognise, notify and diagnose early cases of respiratory illness to allow timely outbreak control measures to be implemented.2,6 The response to influenza outbreaks in ACFs should be a collaborative effort between the ACF, the attending GPs and the DHS. The DHS is currently developing guidelines to manage outbreaks of respiratory virus infection in ACFs and will be piloting a system of ACF respiratory diseases surveillance for the 2004 respiratory virus season. Antiviral therapyAntiviral agents available in Australia include amantadine, zanamivir and oseltamivir. Amantadine has been shown to be 70%–90% effective in preventing illness caused by naturally occurring strains of influenza A virus7 and has been successful in controlling 60%–80% of influenza A outbreaks.8 In Australia, amantadine is approved for prophylaxis of influenza A virus but not treatment. Amantadine has several disadvantages, including lack of activity against influenza B, the potential for the occurrence of adverse side effects (despite individualised dosing based on renal function), and the rapid emergence of resistance to the drug.9 Spread of amantadine-resistant viral strains has been associated with simultaneous prophylaxis and treatment in the same facility.8 Zanamivir and oseltamivir are a newer class of antiviral agents (neuraminidase inhibitors) that are effective against both influenza A and B and have less serious side effects. Initial reports indicate that the frequency of emerging resistance to these agents is low during clinical use.9 In Australia, both agents have been recently licensed for prophylaxis. Neuraminidase inhibitors are 74% effective (95% CI, 50%–87%) in preventing illness caused by naturally occurring strains of influenza viruses in healthy adults.10 From the few available published reports of the use of these antiviral agents for chemoprophylaxis in outbreaks, both appear to be effective in stopping outbreaks in ACFs.9,11 When ACF staff and attending GPs are making decisions about antiviral treatment and prophylaxis in outbreak situations, they should take into account the influenza strain, the health status of the residents, the dosage schedules required, the potential side effects of the drug and the cost (antiviral drugs are not covered by the Pharmaceutical Benefits Scheme). The following recommendations for the use of antiviral agents to control influenza outbreaks will be detailed in guidelines being developed by the DHS: To be effective, treatment with zanamivir or oseltamivir must be started within 48 hours of symptom onset and continued for 5 days; Antiviral prophylaxis should be offered to all residents (whether vaccinated or unvaccinated) and to all unvaccinated staff members and should continue for 10 days or until the outbreak is declared over; If the outbreak is caused by a strain of influenza not covered by the vaccine, prophylaxis should be considered for all staff members, regardless of their vaccination status; To limit the potential transmission of drug-resistant virus during outbreaks, measures should be taken to reduce contact as much as possible between people taking antiviral drugs for treatment and those taking them for prophylaxis; and ACF staff should make arrangements with attending GPs to ensure residents can be prescribed antiviral treatment and prophylaxis rapidly and efficiently. Lessons from practice Even when vaccination coverage is high among residents, influenza outbreaks (with a strain covered by the vaccine) can still occur in aged-care facilities (ACFs), including during the summer months. Because of the poor health status of many residents, influenza outbreaks in ACFs can cause significant morbidity and mortality. When influenza vaccine coverage among residents is high, coverage in ACF healthcare workers is a priority for preventing outbreaks. If an influenza outbreak is suspected, this should be confirmed using nasopharyngeal aspirates or nose and throat swabs tested by a polymerase chain reaction assay. Serological testing may also be useful when symptoms have been established for longer than 72 hours. When influenza outbreaks occur in ACFs, antiviral therapy should be considered as an outbreak control measure. 1: Timeline for influenza A outbreaks in two aged-care facilities (confirmed and probable cases) Outbreak 1 Day Number of people with onset of respiratory symptoms and major events (action taken/findings) 0 1 visitor 5 1 resident 8 1 resident 10 1 resident 11 4 residents 12 5 residents 13 4 residents DHS notified of outbreak 14 1 resident, 4 ACF staff members Laboratory specimens collected. ACF advised to implement infection control measures 15 1 resident, 1 ACF staff member Specimens confirmed positive for influenza A (H3N2) by PCR assay. Antiviral therapy recommended 16 1 DHS staff member 17 2 residents Antiviral therapy implemented 18 1 ACF staff member Summary.* Residents (n = 42): 20 Inf (19 C, 1 P); 10 H; ACF staff (n = 29): 6 Inf (4 C, 2 P); Visitors: 1 Inf (1 C); 1 H; 1 D; DHS staff: 1 Inf (1 C). Outbreak 2 Day Number of people with onset of respiratory symptoms and major events (action taken/findings) 0 2 residents 1 5 residents 1 ACF staff member 2 2 residents 5 ACF staff members 2 visitors 3 3 residents 4 ACF staff members 4 2 residents 1 visitor 5 1 ACF staff member DHS notified of outbreak. Laboratory specimens collected. ACF advised to implement infection control measures 6 1 ACF staff member 8 1 ACF staff member Specimens confirmed positive for influenza A (H3N2) by PCR assay 9 2 residents Summary.* Residents (n = 32): 16 Inf (15 C, 1 P); 8 H; 1 D; ACF staff (n = 31): 13 Inf (3 C, 10 P); 3 H; Visitors: 3 Inf (3 P). ACF = aged-care facility. DHS = Victorian Department of Human Services. PCR = polymerase chain reaction. * Inf = developed influenza A (C = confirmed; P = probable); H = hospitalised; D = died. 2: Infection control measures for influenza A outbreaks in aged-care facilities (ACFs)* Restrict visitors from entering the ACF. Isolate sick residents in their rooms until 5 days after the onset of illness or until symptoms have completely resolved. Exclude sick staff from work for 5 days from the onset of symptoms of a respiratory illness or until symptoms have resolved. Restrict all admissions of new residents during the outbreak; Cancel daily activities programs. Instruct staff to increase hand washing, wear masks while providing care to symptomatic residents and enhance environmental cleaning. * Recommended by the Victorian Department of Human Services to control the outbreaks described here.

Rebecca J Guy MAppSc, MAppEpid · Richard Di Natale MB BS · Sean Tobin MB BS, MPH, FAFPHM · Priscilla M Robinson PhD, MPH, MHlthSc · Graham Tallis MB BS, FAFPHM · Heath A Kelly MB BS, MPH, FAFPHM · Stephen B Lambert MB BS, MAppEpid, FAFPHM · Alan W Hampson BSc, MSc

The ultimate consequence of failing to live sustainably is that we push our own species to extinction “In search of sustainability” was predominantly an Internet conference held over 9 months. Each month was dedicated to a particular theme, and a keynote paper and several related discussion papers formed the basis for an Internet debate on each theme (www.isosconference.org.au). The nine themes were water, human health and wellbeing, land use and natural ecosystems, energy, equity and peace, economic systems, climate, labour force and work, and transportation and urban design. The Internet conference culminated in a one-day face-to-face meeting at the Shine Dome in Canberra on 14 November 2003, which was attended by 190 delegates from around Australia. Twenty-four eminent Australian scientists and researchers presented papers summarising the nine core themes, with an emphasis on defining a path towards sustainability. I attended as a self-funded delegate, motivated by my passion and engagement in a spectrum of environmental issues. In this report, I have chosen to concentrate on the themes of greatest relevance to health and sustainability, and have given preference to contributions from the medical profession. Doctors, because of their credibility in public debate and their knowledge of the devastating health effects of environmental degradation and pollution, have an important role to play in community discussion about sustainability. Several of the speakers were members of the newly established Doctors for the Environment (www.dea.org.au), which has been established to provide an educational role for colleagues and a forum for the profession to add its voice to the sustainability debate. The term “sustainability” was defined very broadly in the opening session as the capacity of human systems to provide for the full range of human concerns over the long term. Human health and wellbeingTony McMichael (Director, National Centre for Epidemiology and Population Health, The Australian National University [ANU], Canberra) proposed that human health be embraced as a key indicator for sustainability, emphasising that current measures of national “wellbeing”, such as gross national product, do not correlate with a population’s health or wellbeing. He stated that gains in longevity and population numbers have come at the cost of depleting the world’s natural capital and degrading the ecosystems on which our survival ultimately depends. He offered several examples of how the impact of human activity on our biosphere is having increasingly detrimental effects on human health: damage to the stratospheric ozone layer, widespread degradation of productive land, the depletion of fresh water supplies, and overfishing and exhaustion of many of the ocean’s fish stocks. Modelling of human-induced global climate change indicates that, at present, 45% of the world’s population are exposed to the Anopheles mosquito, and at risk of contracting malaria. A rise in global temperature of merely 3°C would lead to an expansion of the range of the Anopheles mosquito, increasing the at-risk population world-wide to 60%. Other vector-borne diseases, such as Ross River virus, could be similarly affected. Tord Kjellstrom (National Centre for Epidemiology and Population Health, ANU) stated that “sustainability is the health promotion challenge of the 21st century”, adding that many of the changes needed at an individual level to improve our personal health are synonymous with the changes that will lead to a more sustainable way of living. Examples included taking the opportunity to walk or cycle in preference to burning fossil fuels in personal motor vehicles, and eating fresh local produce in preference to imported processed foods. He concluded that all members of society have a role to play in making “sustainability-based behaviours” the social norm — just as non-smoking has become the norm. Colin Butler (National Centre for Epidemiology and Population Health, ANU) pointed out that many factors may disrupt health, including environmental influences (floods, earthquakes, and climate change) and human activities (war and terrorism). “. . . denial of our increasingly unsustainable lifestyles will simply deepen the crisis we are in.” The goal to live more sustainably needs to become the primary objective of human endeavour. Transportation and urban designChris Johnson (NSW Government Architect) alluded to studies in the UK comparing “battery-raised kids” (those driven to school in a four-wheel-drive and bundled through the gates) with “free-range kids”, who were allowed to walk or cycle to school. The findings showed that free-range kids had better psychological development and school performance. He explained the concept of the “ecological footprint”,1 a scientific approximation of the area of land that each individual requires to meet his or her material needs and assimilate waste. “While this is an increasingly useful tool to assess the impact of our consumption patterns, we need to incorporate the element of liveability when we look at how we might design the cities of the future.” A proposed model of future city design included multiple-storey apartments with rooftop gardens and urban greenbelts. This greater density of living would allow more land for agriculture and biodiversity conservation. Economic systemsRichard Denniss (The Australia Institute, Canberra) argued that “economic growth is not only the target of economic policy and treasury but has become the priority for all areas of government policy”. But gross domestic product (GDP), as a measure of economic growth, does not correlate with a healthy, sustainable society. Paradoxically, loss of human life through trauma or natural disaster contributes a gain in GDP, whereas if members of society were to choose more leisure time and to engage in healthy activity this would be reflected as a downturn in GDP. Denniss urged the adoption of measures such as the genuine progress indicator2 as an alternative to GDP, and proposed that sustainability, encompassing human wellbeing and environmental integrity, should be mandated in all government policy and decision making. Equity and peaceSue Wareham (President of the Medical Association for the Prevention of War [Australia]) emphasised the waste of resources in war and preparations for war. As the sophistication and cost of weaponry increase, there is an increasing potential for even wealthy nations to overstep their capacity to support their own people. Expenditure on basic services, including health and education, are often the hidden casualties of war. The changing nature of weaponry is also having a devastating impact on human health. The contamination of both urban and rural environments in Iraq by the use of depleted uranium munitions will leave a legacy for the health system that will last long after the US-led occupation. The debateThe day concluded with a panel discussion. General agreement was reached that the Australian population, and most populations of the “developed” world, are no longer living within the Earth’s ecological limits. The ultimate consequence of failing to live sustainably is that we push our own species to extinction. While this seems fertile ground for pessimism, the core focus of the debate was how we might transform this situation. Some promoted technological and market-based solutions, working essentially within the existing frameworks established by industry and government. This generated considerable controversy, as others were seeking a more radical departure from our current societal norms, with the view that we already have much of the required knowledge and technology to bring about effective change. Here the emphasis was on generating cultural change through empowering individuals to take personal action, complemented by the development of positive role models. Jenny Goldie (National Director of Sustainable Population Australia) expressed concern that the issue of population size had been neglected throughout the conference. To highlight the population issue, she pointed out that, on the basis of our current consumption patterns, our population would need to be halved if we are to live within the ecological limits of our country. Our current consumption patterns are sustained by exploiting the resources of other countries. Bryan Furnass, a retired physician, gave his perspective on the issues surrounding sustainability: “The problem lies in the three P’s: population, pollution and poverty; the solution lies in three E’s: ecology, education and ethics”. In his conference summary, Ian Lowe (Griffith University, Queensland) suggested that further debate and action towards sustainability would not occur until more people understood the true meaning of sustainability. “If you look at the Earth from space, where’s the economy? The reality is that you see a ball of blue and green surrounded by a thin atmosphere of gases; you see the environment that sustains us. If you look closely you can make out borders of continents, some landmarks which roughly define country boundaries; this is the society that we have established, and then you have the economy which is a creation of our society.” Any human endeavour that leads to a compromise of ecosystem integrity will not be sustainable in the long term. OutcomesThe context of the debate and recommendations from the conference were summarised in a communiqué.3 In addition, the conference organisers are producing a book (expected to be available this year), with contributions from 14 of the conference speakers, which will reflect the breadth, urgency and relevance to national and international human health of the sustainability debate.

Nick J Towle MB BS(Hons), BMedSc

Objective: To assess compliance with current standards of playgrounds where children have sustained a fall-related arm fracture.Design, setting and participants: Between October 2000 and December 2002, a consecutive prospective series of 402 children aged under 13 years who fell from playground equipment and sustained an arm fracture was identified by emergency department staff in five Victorian hospitals. Trained field testers measured playground equipment height, surface type and depth, and surface impact attenuation factors to determine compliance with safety standards.Main outcome measures: Playground compliance with current Australian safety standards.Results: Ninety-eight percent of playgrounds had a recommended type of surface material. The mean surface depth was 11.1 cm (SD, 5.0 cm) and the mean equipment height was 2.04 m (SD, 0.43 m). Although over 85% of playgrounds complied with recommended maximum equipment height and surface impact attenuation characteristics, only 4.7% complied with recommended surface depth.Conclusion: Playgrounds where children have sustained an arm fracture generally comply with all important safety recommendations except surface depth. Playground fall-related arm fracture requires specific countermeasures for prevention, distinct from head injury prevention guidelines.

Shauna Sherker PhD, MSc, BSc · Joan Ozanne-Smith MD, FAFPHM, MPH

Objective: To investigate the source and risk factors associated with Australia’s largest outbreak of Legionnaires’ disease.Design and setting: Epidemiological and environmental investigation of cases of Legionnaires’ disease associated with visits to the Melbourne Aquarium; two case–control studies to confirm the outbreak source and to investigate risk factors for infection, respectively.Participants: Patients with confirmed Legionnaires’ disease who visited the Melbourne Aquarium between 11 and 27 April 2000 were compared (i) with control participants from the community, and (ii) with control participants selected from other visitors to the Aquarium during this period.Main outcome measures: Risk factors for acquiring Legionnaires’ disease.Results: There were 125 confirmed cases of Legionnaires’ disease caused by Legionella pneumophila serogroup 1 associated with the Aquarium; 76% of patients were hospitalised, and four (3.2%) died. The Aquarium cooling towers were contaminated with this organism. Visiting the Aquarium was significantly associated with disease (odds ratio [OR], 207; 95% CI, 73–630). The case–control study indicated that current smoking was a dose-dependent risk (multivariable OR for currently smoking > 70 cigarettes/week, 13.5; 95% CI, 5–36), but chronic illness and duration of exposure at the site were not significant risks.Conclusions: This study showed an association between poorly disinfected cooling towers at the Aquarium and Legionnaires’ disease in visitors, and confirmed current smoking as a critical risk factor. The rapid response, publicity, and widespread urinary antigen testing may have resulted in detection of milder cases and contributed to the relatively low apparent morbidity and mortality rates. The urinary antigen test allows rapid identification of cases and may be changing the severity of illness recognised as Legionnaires’ disease and altering who is considered at risk.

Jane E Greig PhD, MAppEpid · John A Carnie FAFPHM, MPH · Graham F Tallis FAFPHM, MPH · Bernard Zwolak MAppSc, BEd · William G Hart MB BS(Hons), FAFPHM · Charles S Guest PhD, FAFPHM · Norbert J Ryan PhD, BAgrSc · Jennie A Leydon BAppSc · Agnes G Tan BTech(Food)Hons, MHlthAdmin · Ian R Gordon PhD, AStat

Non-compliance with treatment of pulmonary tuberculosis (TB) by an individual can put the community at risk of transmission of TB. Public health (detention) orders can be issued to detain non-compliant individuals, but this is a last resort and rarely used. Two recent cases in New South Wales illustrate the process of issuing a public health order in NSW, and some of the issues that may arise. The NSW law can also be applied to patients with severe acute respiratory syndrome (SARS) or HIV/AIDS. The other states and territories have similar laws, which often apply to a broader range of diseases and have fewer limits on issuing and extending orders.

Sanjaya N Senanayake FRACP, MB BS(Hons), BSc(Med) · Mark J Ferson MD, FRACP, FAFPHM

Nicola Petrosillo,* Vincenzo Puro,† Giuseppe Ippolito‡ * Clinical Director, † Epidemiologist, ‡ Scientific Director, National Institute for Infectious Diseases “L. Spallanzani”, Rome, 00149, Italy. petrosilloATinmi.it To the Editor: In their article describing the Australian experience of border screening for severe acute respiratory syndrome (SARS), Samaan and coworkers add new insights about the low efficacy of this measure in identifying SARS cases at entry into a country.1 To our knowledge, this is the first report on this issue from a low-risk area for SARS.2 Indeed, as summarised by Samaan et al, other available data derive from countries where people with SARS, entering at the early stage of the epidemic, generated a sustained local transmission of SARS-associated coronavirus (SARS-CoV) disease. Among the reasons for a low sensitivity of entry screening, Samaan suggests that subjects may evade screening by making false declarations or by taking anti-pyretic drugs, or by simply being in the incubation period with no symptoms or only mild symptoms. To contribute to this debate, we report the experience of our Institute, which was designated as a referring centre for SARS by the Italian Ministry of Health. In Italy, where only four imported probable cases of SARS were identified and no local transmission occurred,3 entry screening was implemented at the two international airports of Milan and Rome. In particular, travellers and crews arriving from World Health Organization SARS-designated areas, directly or after transiting in other EU countries, were provided with health alert cards and screened for body temperature.4 Suspected SARS cases identified at Rome airport were to be referred to our institute. However, of the 72 subjects attending our admission unit for clinical evaluation for possible SARS, none was referred by the airport authorities. Among these patients was one of the four people with SARS arriving in Italy: an airline flight crew member coming from a SARS-designated area who passed both exit and entry screening, despite complaining of mild fever before his departure. He was admitted 6 days after arrival, at which time the clinical picture had evolved into full-blown SARS. He was discharged after 2 weeks. Among the measures recommended by WHO to reduce SARS-CoV spread, the identification of symptomatic subjects at border departure screening was the only measure with some evidence of efficacy, although this only reduced on-flight transmission.5 Conversely, evidence from several sources, including Samaan et al, showed that screening travellers (visual inspection and screening for fever) as they disembark identifies very few SARS cases and is of questionable value.1 We agree with the conclusions of Samaan et al that, in the light of a possible resurgence of SARS or similar diseases (avian flu), entry screening should, at least, be more focused, and needs further evaluation, including cost-effectiveness analysis.

Nicola Petrosillo · Vincenzo Puro · Giuseppe Ippolito