Environmental health

There are many contaminated soil sites in Australia. Contamination may be from human activities (eg, smelters, industrial waste dumps, old gasworks) or from naturally occurring sources (eg, surface mineralisation). Concentrations of contaminants may vary markedly across a site. Their distribution may be localised or quite extensive. Common contaminants include lead, arsenic, cadmium, petrol and diesel products, and polycyclic aromatic hydrocarbons. People living on or near a contaminated site will often be concerned about potential effects on their health. Assessing their exposure potential and/or measuring levels of biological markers often allays concerns, but occasionally confirms them (eg, elevated blood lead levels and subtle cognitive effects have been found in some people living near the Port Pirie lead smelter).

Andrew J Langley FAFPHM FAFOM

Urban air pollution levels are associated with increased mortality and cardiorespiratory morbidity. These health effects occur even at exposure levels below those stipulated in current air-quality guidelines, and it is unclear whether a safe threshold exists. Air pollution in Australia and New Zealand comes primarily from motor vehicle emissions, electricity generation from fossil fuels, heavy industry, and home heating using wood and coal. In individual patients a direct link between symptoms and air pollution exposure may be difficult to establish and may not change their clinical management. However, avoiding exposure during periods of peak pollution may be beneficial. Although there is some evidence that urban air pollution in Australia and New Zealand has been decreasing (through reduced car use, improved emission-control technology and use of more energy-efficient devices in the household and in industry), pollution levels are still unsatisfactory. Further reductions may prevent hundreds of cardiorespiratory hospital admissions and deaths each year.

Tord E Kjellstrom MedDr, MEng · Anne Neller BSc, PhD · Rod W Simpson BSc, PhD

The risk of contamination of drinking water supplies with microbial pathogens is minimised by modern approaches to water management, but continues to be the major public health concern. Chemical contaminants usually pose little health risk except at very high levels, but debate continues over the potential adverse health effects of low-level, chronic exposure to compounds such as disinfection byproducts. Recreational water contact can be associated with adverse health outcomes either from microbial infections or exposure to cyanobacterial toxins. Environmental issues such as increasing salinity and global warming are likely to affect the sustainability of our current drinking water supplies and increase the threat of waterborne disease outbreaks. New technologies, use of alternative water sources, such as rainwater tanks, water reuse and restrictions will undoubtedly be part of the solution to our diminishing water resources, but have the potential to introduce new health threats.

Karin Leder FRACP, MPH, DTHM · Martha I Sinclair PhD · John J McNeil FRACP, PhD, FAFPHM

About four million cases of foodborne infectious disease occur annually in Australia; new foodborne pathogens, such as enterohaemorrhagic Escherichia coli, are emerging. Climate change, combined with changes in how we produce and distribute food and how we behave as consumers, have the potential to affect foodborne disease in the coming century. Foodborne disease outbreaks are now more far-reaching (and sometimes global) due to modern mass food production and widespread food distribution. There are strong seasonal patterns for Salmonella and Campylobacter infection in Australia. Global warming may increase the incidence of infections, such as salmonellosis, and diseases caused by toxins, such as ciguatera.

Gillian V Hall MB BS, PhD · Rennie M D'Souza MB BS, PhD · Martyn D Kirk MAppEpid

How a peace-loving suburban Sydney GP, practising primary prevention her way, ended up in solitary confinement I've always believed that it's part of my job description as a doctor for me to be aware of environmental issues and to address them as best as I can. So, I've been a long-time supporter of Greenpeace (www.greenpeace.org) and a member of the Medical Association for Prevention of War (in NSW, called Health Practitioners for Global Responsibility; www.mapw.org.au, mapwATmapw.org.au). And, since 1997, this desk-bound GP has worked as a volunteer "medic/deckhand" on Greenpeace ships, like the Rainbow Warrior, for a couple of months each year. As medic, I ensure that the ship's hospital, which doubles as my sleeping cabin, is ready for emergencies, illness or injury. It's well stocked, with resuscitation equipment, surgical supplies and drugs; we are prepared for anything, from draining a pneumothorax to flying out someone with a spinal injury. For example, I've attended to crew after they were "rained on" with heavy metal tools as they climbed up an oil tanker and treated hypothermia after cold water immersion. I also train crew in first aid, including resuscitation (and working out team approaches in emergencies) and practise primary care and preventive medicine, from mosquitoproofing the ship to discussing outbreaks of worms. When not working as a medic, I am under the charge of the bosun, who assigns me to deckhand jobs — for example, painting the mainmast, restacking the hold or standing watch (which involves working a night shift), with opportunities to improve navigation and radio skills. When the ship is engaged in protest actions, I can either stay aboard as part of the back-up crew or volunteer to be involved as an activist. I've been directly involved in several campaigns. My first was in Central America after Hurricane Mitch swept through in October 1998, where I worked alongside locals, hauling bulk bags of rice and beans, tents and boxes of clothing and medicines into wharfside sheds for later distribution. My most recent expedition, to Sweden, provided a very different experience. ProtestOn 4 June 2002, the Rainbow Warrior and her crew embarked on a protest involving the cargo vessel ms Fagervik, which had dumped a large amount of oil into the Baltic Sea in February 2001. Although evidence suggested that the Fagervik's spill had been deliberate, the local Swedish court had decided to prosecute the ship's owners for an accidental spill (with a small fine) rather than for a deliberate spill (a criminal offence). Greenpeace wanted to protest about the facts that deliberate oil spills are frequent (about 1000–2000 a year in the Baltic) and virtually go unpenalised. We believe that ship owners and industry should bear the full financial liability for the effects of oil discharges, whether or not intent can be proven. Our specific goal was to board the Fagervik en route to the port of Norrköping (about 160 km south of Stockholm). The action took place in the usual non-violent manner that Greenpeace is committed to. We spent the first day of the protest in a rubber Zodiac boat doing action manoeuvres — painting slogans, hanging banners, and getting "climbers" (those who climb up ships' hulls) on board the Fagervik. ArrestIn the early evening on that first day of the protest, I joined a few other protestors on board the Fagervik. As part of the protest, I chained myself to the boat, as did Kristina, a 27-year-old German. The Swedish police boarded the ship that same evening, and at 10 pm Kristina and I were arrested. We were charged with aggravated trespass and taken to the town lockup to be held in solitary confinement. It was an unprecedented reaction to a Greenpeace protest. We had been told, in the routine legal briefing before the campaign, that such a charge, with a two-year prison sentence, was possible but unlikely. More likely was a charge of minor trespass, with release within four days. Under Swedish law, there is no bail; one can be held in custody indefinitely until trial — which, I was told, could be many months off. In solitaryThat night, I was put into a concrete basement cell, 1.5 m by 3 m, that boasted a floor mat to sleep on and a drain hole, which others had clearly used as a toilet. I, too, later resorted to using the hole for the same purpose, as it could take up to an hour after pressing a buzzer before a guard would respond to take me to the actual toilet. The cell walls, floor and mat were encrusted with recent faeces and blood. Later, I found out that my dingy cell was more generally used as the "drunk cell", for those who were drug or alcohol affected when arrested. My watch and warm boat suit and gumboots were confiscated and I was issued cotton pants, a shirt and plastic scuffs to wear. I felt not only isolated but also powerless; contact with Kristina and my personal lawyer was denied me; later we presumed that this was because of a fear of terrorism; that there was a risk of "collusion" between my lawyer and myself (I was allocated a State lawyer). I was also denied direct contact with my family and it was days before I was finally able to make contact with the Australian consulate. The seamen's mission priest and the prison nurse were other eventual, permitted visitors. In the first few hours, I observed my fear and confusion growing. Then, I remembered Victor Frankl's words in his book Man's search for meaning: 1 Everything can be taken from [us] but one thing: the last of the human freedoms — to choose one's own attitude in any given set of circumstances, to choose one's way. I resolved to apply myself to keeping mentally clear and stable. I began by getting a rough idea of the time from my meal deliveries. Then, knowing the link between exercise and wellbeing, I began a workout program that encompassed every exercise I had ever learnt and devised ways of timing half-hour walking periods without a watch. I'd practised yoga and meditation for many years, and drew on that practice to maintain an attitude of acceptance and calm. It became an incredible comfort to me when, each day, the inner reality of the meditation space became stronger as my small, shabby and uncertain external world shrank in importance. Initially, what there was to read was in Swedish. Greenpeace members attempted to send books, music, and clothes, but not much was allowed through. So, I began drawing. One kind guard gave me pencils and paper, and would sharpen them on his shift, saying that he trusted me not to use them as a weapon. By the time I was released, one whole wall of my cell was covered with paper and my own huge mural of Sydney Harbour. The guards would stop by to see my drawings, and indeed they became friendlier during my imprisonment, sometimes offering me a second cup of tea in the day. A guard confided "I like what you do. Tonight I give 500 kronas ($100) to Greenpeace". Many asked whether I really was a doctor and one sought my advice concerning his dying father. Meanwhile, the small fiord township of Norrköping was anticipating a large and complex trial and Greenpeace continued the Fagervik protest for several more days, with a flotilla of small boats and climbers on board (as well as continuing arrests). Greenpeace also mounted a networked international campaign calling for our release. The media took hold of the story, with incredibly supportive coverage of our stance. ReleaseI was working at my wall, well prepared for a long stay, when a guard came into my cell to tell me that I was to be released forthwith. It was 14 June, ten days after our arrest. My reactions ranged from relief to confusion, knowing that a trial and possible further imprisonment lay ahead. The police superintendent came to my cell, shook my hand, and apologised for keeping us in cells intended for overnight use only. The guard on duty farewelled me with a hug, sorry to see us go. I thanked him for the pencils. Kristina and I emerged from the building to be met with banners, flowers and friendly faces I did not know from the Stockholm Greenpeace office. I still had no shoes and one large Swede gave me his sandals. Again, I found myself watching my reactions: ordinary things, like seeing the sky and breathing the air seemed wonderful. I'd been used to solitary silence and was now being interviewed by the mass media. On release, I learnt that during our imprisonment a large export company had announced it would not use the Fagervik or any "dirty" ships (ie, sea-polluters) for transport — I felt a deep sense of effort rewarded. On trialTwo weeks later, four Greenpeace activists, including myself, were found guilty of aggravated trespass and given a two-year suspended sentence. This means that, if we work in any future protest actions in Sweden, we risk getting arrested and having to serve out our sentence. We can understand some of the reasoning behind this sentence — a year ago, Sweden was shaken by violent anti-globalisation demonstrations in Gothenburg. However, we plan an appeal, as it's important to make a distinction between violent protest and the right to non-violent, thoughtful protest about community issues. In the courtroom, I was asked if I regretted my actions. Through a translator, I replied along these lines: I do not regret my actions. What I regret is the harsh reaction by this legal system to a peaceful protest. As a medical doctor in Australia, I see people dying of cancer and babies born with abnormalities. It isn't enough for me to just keep treating sick people — I also feel compelled to speak up about the issues behind some of these illnesses. I understand that pollution in the Baltic Sea is already so high that pregnant women are advised not to eat the fish from it. I believe it is important to encourage governments to enforce restrictions on industrial release of what is unsafe into the water, air and soil. PrivilegedSo, was going to prison worth it? It was a privilege to be able to speak and act for what I believe matters. Environmental issues are not remote from primary care, they are increasingly recognised as an integral part of it.

Elizabeth D Rickman MB BS

The recent pioneering Public Report Card 2002 — Aboriginal and Torres Strait Islander health, entitled No more excuses,1 outlines where we are today and how the health of our Indigenous population compares with that of other similar countries — New Zealand, Canada and the United States. Produced by the Australian Medical Association, it is a "warts-and-all" assessment which is designed to show what is working and where we need to do better. Where do we stand on health?There have certainly been some gains. The health of Indigenous infants has improved dramatically, although from a low baseline, and most of the gains occurred 20–30 years ago.2 The current infant mortality rate for the Aboriginal and Torres Strait Islander population is almost three times that of the general Australian population, twice that of the Maori, and 50% higher than the mortality rate of US Indigenous infants.3 This is some improvement on previous rates, but we can and should do better. Death rates overall for Indigenous people in Australia are still three times as high as for the rest of the population: diabetes death rates are eight times as high, respiratory deaths four times as high and circulatory conditions almost three times as high.4 These are unacceptable statistics for treatable and preventable conditions. On the other hand, there are number of recent good news stories. Programs in the Northern Territory and elsewhere have shown that birthweight, the critical factor in the survival of newborn infants, can be improved.5,6 More dramatically, death rates from pneumonia have dropped by around 40% since 1996 (derived from Australian Bureau of Statistics data). This is important, because this reduction is likely to be due, in part, to recent government initiatives for promoting pneumococcal vaccination. This is a real indication of the kind of rapid and substantial gains that can be achieved through application of knowledge we already have. (Well done, even if long overdue.) Progress in providing access to health services for Aboriginal and Torres Strait Islander communities is much too slow. There is a gross shortage of doctors working in Indigenous health, with an estimated 60% increase required (ie, at least 500 doctors). The number of nurses also needs to increase by 25%, and there are sizeable deficits in all the other health professions.7 There has been some improvement in basic services and facilities to some areas, but too many Aboriginal and Torres Strait Islander communities still lack adequate water, electricity and sewerage services.8,9 In other fields influencing health, there has been some modest improvement in educational benchmarks, but still only a third of Aboriginal and Torres Strait Islander children reach Year 12 at school.10 Most tellingly, however, are the data for the most reliable overall measure of health — median age at death, currently 51 years for the Aboriginal and Torres Strait Islander population. There has been no improvement at all in this measure in the last 10 years.3 In this same period, the median age at death for the total Australian population increased by three years, so that the gap in median age between Indigenous people and the rest of the population has now increased to a staggering 26 years. Median age at death is much higher for the Indigenous populations of New Zealand (59 years), Canada (65 years) and the United States (63 years) and, in contrast to the situation in Australia, has been progressively increasing for the last 25 years,11 and probably for much longer. What about health spending?Spending on Aboriginal and Torres Strait Islander health is increasing, but, incredibly, the Commonwealth Government, through programs under its direct control, still spends less per capita on Indigenous people than it does on the rest of the Australian population — 74c on Indigenous Australians for every $1 spent on the rest of the population! The real increase in spending on Indigenous health between 1995–96 and 1998–99 was 15%.12 This is worthwhile, but nowhere near enough to cater for the higher levels of illness among Indigenous people. There has been a major new initiative, the Primary Health Care Access Program, with three key features: needs-based funding, funds pooling and community control. However, the funding for the program is totally inadequate, and at this stage only selected communities can participate in a program which is needed for Indigenous people throughout Australia.13 The consequences of the funding shortfall are major deficiencies in the crucial prevention and early treatment services required to break the cycle of ill-health. Why do we do so much worse than other countries?What is it about Australia that stops us from achieving the gains seen in the health of the Indigenous populations in other Western democracies, or, for that matter, in developing countries around the world? There is, after all, nothing absolutely unique either about the disease pattern or the history and circumstances of the Australian Indigenous population. Heart disease, respiratory conditions, injuries and diabetes are also the major conditions for the Indigenous populations of other countries. Dispossession, forcible relocation, removing children from their families, and heavy-handed paternalism are certainly not unique to Australia. Nor is Australia incapable of doing well with health and health services. Depending on which measurement you take, Australia is arguably the second- or third-healthiest country in the world, with a proud record in confronting difficult and complex issues such as AIDS and cancers in women.14 Why is the government not doing more?It is symptomatic of our lack of progress that this report card, and its call for action, comes not from the government, but from health professionals. Surely one would hope that some response, some soul searching, some rethinking would be evoked by the fact that over the last 10 years, despite some good news, the overall mortality of the Australian Indigenous population, alone among Western nations, has not improved, is much worse than for the Indigenous populations of New Zealand and North America, and that the gap between the mortality rate of the Indigenous population and that of the rest of the Australian population is becoming wider. But no, there is simply a deafening silence; a case of industrial deafness. Shortfalls in medical services for rural areas have produced major government programs and initiatives, and a massive injection of funds. Where is the response to the huge shortage of doctors and nurses to work in Indigenous health, and the major gaps in the workforce of all the other health professions? For any other section of the population there would be a massive outcry and appropriate remedial action. In fact, for Aboriginal and Torres Strait Islander health, the Commonwealth Government seems to be tied up with a curious logic that requires "good news" from spending less on people with worse health before it will fully rectify the health service deficiencies needed to address the worse health! Australia is locked into a cycle of endless consultation, policy and strategy formulation and measurement. Report after report is produced showing that Indigenous health is poor, improvement patchy at best, and that, overall, the gap between Indigenous and non-Indigenous health is widening. These reports reach the highest levels of Australian public and political life and are simply noted, or evoke defensive bureaucratic responses. We must act on the reports, not just note them. Flat-lining for 10 years is not good enough! Many worthwhile activities are under way, but would any informed observer really claim that current or planned prevention and treatment services, staff provision and training plans, and environmental improvements, will do the job, or are anywhere near sufficient to bring about the Indigenous health gains seen in other countries most like Australia? What do we need to do?We don't need new solutions, new strategies, some magic bullet. We need to implement strategies, like the National Aboriginal Health Strategy,15 that have been around for more than a decade. The Report Card reinforces previous calls for a national program to build up the necessary community-controlled health services for prevention and treatment; for the Primary Health Care Access Program to be given the funds required to provide those services; for a National Training Plan to train the staff, particularly Indigenous staff, required to deliver those services; and for a National Infrastructure Plan to rectify the continuing deficiencies in water supply, sanitation, education and other basic services. Australia spends over $50 billion per annum on health for its total population.16 It isn't that the modest funds required for adequate health services for Aboriginal and Torres Strait Islander people are out of reach, or that the services required are beyond our technical capacity. It is ultimately a commitment to implement the recommendations of the endless reports, and this is what the AMA, in support of Aboriginal and Torres Strait Islander organisations, is urging on the nation. Straws in the wind?Despite the general lack of progress, there are straws in the wind. The appointment of a new Health Minister and a new head of the Commonwealth Department of Health provides a fresh opportunity for dealing with the issues highlighted in the Report Card. Death rates of the NZ Maori and the Indigenous peoples of Canada dropped by 30% in the 1970s.17 Over a 40-year period, the health of the Indigenous populations of the United States improved twice as rapidly as that of the non-Indigenous population.14 Australia can do the same, and that should be our aim. Summary of the AMA Report Card on Aboriginal and Torres Strait Islander health Status Comment Infant mortality rate Indigenous rates are 2 times the total population rate Rapid fall in the 1970s. Rates in Indigenous Australians almost twice as high as those of the NZ Maori and US Indigenous populations Low birthweight Indigenous babies are twice as likely to have low birthweight. Little overall improvement since 1991, but effective programs developed and implemented in the Northern Territory and South Australia Expectation of life The gap between Indigenous and non-Indigenous people is 20 years In North America and New Zealand, the life expectancy gap (Indigenous v non-Indigenous) is 5–7 years Median age of death For Indigenous people this is 25 years less than for non-Indigenous people There has been no improvement in the median age of death in the Indigenous population in Australia in the past 10 years Standardised mortality ratios Indigenous rates are three times those of the total population High rates for diabetes, respiratory, circulatory and other conditions in the Indigenous population Mortality from pneumonia A dramatic decline in Indigenous rates since 1996 Pneumoccocal and influenza vaccines may be contributing to the decline in mortality from pneumonia Health workforce Estimated at least 59% increase in doctors required, and a 25% increase in nurses Required increase related to difficulties in accessing preventive and early treatment services Infrastructure 21 communities lack water, 80 lack electricity and 91 sewerage Some improvement, but significant gaps Education Year 12 retention rates are 36% for Indigenous people v 73% for the total population Some improvement, but significant gaps Health funding 15% real increase in government funding between 1995–96 and 1998–99 Level of health spending is 22% higher for Indigenous people but a needs index of 200% is required Aboriginal Community Controlled Health Services (ACCHS) OATSIH funding of community-controlled services increased by 50% between 1995–96 and 1999–2000 ACCHS with a network of culturally appropriate healthcare services provides a model for Indigenous health services OATSIH = Office for Aboriginal and Torres Strait Islander Health.

Ian T Ring MB BS, FAFPHM · Ngaire Brown B Med, MPHTM

Disobedience, in the eyes of anyone who had read history, is man’s original virtue. It is through disobedience that progress has been made — Oscar Wilde, 1881 The invitation to contribute this piece to the Journal was disconcerting. I told the Editor I felt previous contributors to the Power of One series were all distinguished retirees. What was he trying to tell me? I have just turned 51, but it seems some believe I have been around forever and should write a retrospective piece. Sinking smokingRecently, I was leaked a staff training CD-ROM from British American Tobacco (Australia). Five senior executives sat in front of the camera blubbing about the inexorable fall in smoking rates and how, as the plug had been pulled, this could only get worse. As the remaining water drained from the pool, they tried to inspire their staff by talking up hopes of snatching profit from brands that smokers were inspired to believe were at the luxury end of the market. Luxurious carcinogens! It was desperate stuff, but heartening all the same. In the early 1960s, nearly 60% of men and 30% of women in Australia smoked.1 Today, daily smoking by adults has fallen to under 20% for the first time,2 and shows no signs of having bottomed out. In NSW, lung cancer in men has been falling for 18 years and female lung cancer has stopped rising.3 National death rates from coronary heart disease fell by 59% in men and 55% in women between 1980–2000, in large part because of changes in risk factors like smoking.4 Along with vaccine uptake, the fall in the road toll and arresting the HIV/AIDS epidemic, the fall in the smoking rate is one of the major public health achievements of the past 40 years. Innocents sometimes introduce me as "the person" who is responsible for the revolution in the way smoking is now regarded. This nonsense derives from their youth, mixed with thoughts of David and Goliath — as if a single individual could ever be said to be responsible for turning around something as complex as community and political perceptions of smoking. The metaphor of being pecked to death by ducks provides a more apposite description of the way things work in public health. Strategic pecks that irritate and distract gradually build to a point where those under attack — in this case, the tobacco industry — develop a debilitating siege mentality. While the public appetite for dragon-slayer mythology demands there should be individuals who stand over public health carcasses, many, often unsung, people have oxygenated the huge changes achieved in smoking in Australia. MOP UP and BUGA UPA BUGA UP refacing, circa 1983. Today, smokers huddle in doorways and excuse themselves from meetings. To smoke with equanimity is increasingly to wear a badge of immaturity, low education or resigned addiction. Thirty years ago, it was very different. The tobacco industry had infected smokers with the thought that they had a monopoly on all that was interesting, convivial and sensual. Epidemiological revelations rather ruined all that; but it was advocacy that ensured the translation and transition of epidemiologists' conclusions into policy and law reform. In the late 1970s, I was bored witless in my first job as a community health educator, employed by the NSW Health Commission. While I gave interminable Rotary Club talks to half-sozzled businessmen about the "drug problem", tobacco advertising adorned every conceivable public space. Drug pushers were very publicly jailed while tobacco industry executives were quietly knighted. So, in 1978, with a few colleagues, I formed MOP UP — Movement Opposed to the Promotion of Unhealthy Products. We put out a precocious press release and in the next week were covered by the Sydney Morning Herald as "the latest pebble in the shoe of sin industries".5 We engineered the removal of Paul Hogan from the Winfield advertising campaign;6 "MOP UP's slingshot cuts down the advertising ogre" read one headline. MOP UP re-energised the debate about tobacco advertising that Nigel Gray (then head of the Anti-Cancer Council of Victoria) and Cotter Harvey (founder of the Australian Council on Smoking and Health) had started in the 1960s. At our first meeting — held in the lecture theatre of the Sydney morgue in Camperdown — someone stood up and declared, impatiently, that our political letter-writing plans were pathetic and that, if we had guts, we would take more direct action. BUGA UP, the graffiti movement, was born and over the next eight years revolutionised ordinary people's understanding of the politics of tobacco control.7 My modest involvement was to take ongoing responsibility for the billboard on a shopfront directly opposite the entrance to News Ltd, but my admiration for the dozens of courageous people who risked much over a decade of civil disobedience is boundless. We held a 20-year reunion in October this year. (For a powerpoint collection of BUGA UP's 'greatest hits' see http://tc.bmjjournals.com/cgi/content/full/11/3/DC1). Truth in advertising: the German brand West shows a smoking Olympic athlete "lighting the fire" of a stick-figure woman in front of Australia's Uluru, about the time of the 2000 Sydney Olympics. When I first started in tobacco control, people at parties would occasionally give me wide berth as a probable teetotal morals crusader who would soon move to turn the music down and pluck sweets from children's mouths. MOP UP, and especially BUGA UP, changed all that. Understanding that the tobacco industry is a pariah of the corporate world rapidly became a litmus test for a whole set of values about the abhorrence of putting profit above all else. Today, one never hears a tobacco industry executive in the media. As my colleague Stan Glantz, professor of medicine at the University of California, San Francisco, has said: "They are like cockroaches; they spread disease and don't like to be seen in the light." No respectable politician would now ever risk public association with these executives, and this change in business community status has facilitated the incremental adoption of a legislative program that puts Australia in the forefront of nations trying to reduce tobacco's health toll. Getting the message outThose heady days and my first degree in media sociology gave me a taste for the nature of news values. They blooded me for a career where I have tried to translate epidemiologists' conclusions into discourses that gel with community concerns, and then needed to truncate them into soundbite-length summations if they were to have any hope of making the news. I have always had enormous respect for the power of the news media to influence the way that communities think about issues. My honours thesis on imagery in advertising for psychotropic drugs in medical journals was tabled into the Senate Hansard by Peter Baume in 1979.8 That lit a fire within me: there were ways in which academic work could climb out of its (mostly) cosseted sanctuary and thus get to influence political debates. A luxurious Sunday for me is an undistracted day of writing. Since 1976, I have published over 370 original articles, editorials, letters and commentaries in peer-reviewed journals and another 105 in throwaways. I have written 10 books and large reports. A few of these have become citation classics in my field,9-11 but if I was to nominate my most influential writing without hesitation I would name some of my 93 newspaper opinion pieces, my 130 letters to newspapers or some of my extended radio and TV interviews during critical periods of advocacy for change, like the tumultuous period of advocacy required after the Port Arthur gun massacre in 1996. Years of watching my citation rate splutter upward and 11 years of editing an international journal (Tobacco Control) have taught me that scholarship, for all its importance, exists in intellectual backwaters and rarely influences practice, public or political opinion. Colleagues boast of a paper being cited a few hundred times or of speaking to 5000 people at an international conference. In my opinion, a gloves-off opinion piece in a morning newspaper, followed by a round of interviews on breakfast radio, on the day that a vital public health political decision is to be made will be read, and often discussed, by incomparably more people than a journal's readership. Outside agentAdvocacy, by its nature, involves contested debates — there are always losers when change occurs; so often, they are determined to resist change, and angry when it happens. Public health advocacy often requires pushing governments to act and being critical of inaction. This can brand advocates as troublemakers, with all that can go along with that. I have known David Hill, now the director of the Anti-Cancer Council of Victoria, since 1978 and count him as a close friend. A few years ago, when I was feeling a little disconsolate at being plainly excluded from some key national committees appointed by a minister for health whom I had occasionally criticised, David counselled me to consider that every cause needs different people to work "inside and outside the political tent". He said that those on the inside greatly appreciated that someone with my judgement and determination was outside helping keep policy agendas alive that would otherwise be at risk of neglect, being largely off-limits to those working on government committees. Magnificent mentorsMayer mailI count three mentors in my life. Henry Mayer (1919–1991), Professor of Political Theory at the University of Sydney, invited me to lunch after reading an analysis I wrote of the use of sexually seductive imagery in a doctor-directed advertisement for a bronchodilator.12 Henry was a Renaissance man who read everything from impenetrable European psychoanalytic theory to debates about radio bandwidths. From that day on, seldom a week passed in the next decade when a bulging packet of eclectic pages torn from his astonishing reading habits did not arrive in the mail. "Read this", he'd have scribbled. To this day, I am compelled to open my mail and email before anything else, so exciting were the contents of the material he often sent me. I found out later that Henry was in the same habit with dozens of other people he favoured. My imagination owes him an enormous debt. Godfather GrayNigel Gray, then head of the Anti Cancer Council of Victoria, invited me to go with him to Papua New Guinea in 1983 to help convince the government to ban tobacco advertising. It did, although the law remains poorly enforced. Nigel quickly burst any preconceptions I had about senior, venerable figures in medicine being aloof, arrogant and irrelevant. Besides being great fun, Nigel has an appetite for energetic people who, like him, were prepared to stay for the long haul, always searching for opportunities to reignite concern about tobacco industry actions or complacency in government. He taught me that public health's successes tend to creep along almost imperceptibly and about the importance of setting 10–20-year windows on achievement. He remains the godfather of tobacco control advocacy for many of us.13 "Fearless" LeederStephen Leeder, then head of Community Medicine at Westmead Hospital, asked me to work with him in 1986 and has been a major influence ever since. While he has written some of the most articulate public health policy analyses, and cuts the mustard with most powerbrokers, it is his incandescent humanity that sets him apart for me as one of Australia's most inspirational figures in public health. Affectionately known to many of us as "Fearless" Leeder, Steve's writing and speeches drip with his values. Working with Steve for 16 years has exposed me not just to his intellect, but to his unerring encouragement of others. Whenever I have had moments of doubt about writing what I think and upsetting someone powerful, he has seldom hesitated to say simply, "You must say this . . . if you won't, who will?". He's been a wonderful role model. Citizen ChapmanWinner of the Lung Slayer Award. This portrait, of a 34-year-old man with emphysema, was a rejected entry in the 1984 John Player Portrait Award, National Portrait Gallery, London. An alternative exhibition was held on the footpath outside the gallery (that's me holding the painting). Most days I pinch myself in disbelief that I get paid to do what I would gladly do for nothing as a citizen. My 20 years (1982–2002) as a director and chair of the Australian Consumers' Association (Choice magazine) count as an experience I value enormously. I have swapped tactics with some of the most tenacious exponents of rat-cunning advocacy that you could ever hope to meet. Today, I have seven researchers working with me on a critical history of the tobacco industry as revealed through their internal documents (see http://tobacco.health.usyd.edu.au/). Each day, I see their growing incredulity at what they are discovering and the way this translates into passion about carrying on this work, using scholarship as an instrument of shame that drives policy change. The other day we found an item that read "Australia is a laboratory for the global anti-smoking network. Both anti-smoking policies and the individuals who promote them are exported from Australia and stimulate anti-smoking activities worldwide."14 It's been a huge privilege to be a part of that.

Simon Chapman PhD

To the Editor: Over the past 20 years, the prevalence of obesity in the Australian population has more than doubled — from 8.1% in 1981 to 20.5% in 2000.1,2 The rapid and widespread nature of the obesity epidemic suggests that environmental change is a major contributing factor. The patterns and types of foods consumed by Australians have changed markedly within a single generation. One major area of change is the availability and consumption of "fast" foods.3 A key feature of fast-food marketing is the use of "upsizing", a strategy designed to provide the consumer with a "value-for-money" addition to their meal. Upsizing is commonly employed within the context of "meal deals": complete meal options comprising the major food item (burger or chicken product) and, for a small extra cost, larger serving sizes of items such as hot chips and soft drink. Recent data from a US survey have shown that upsizing provides disproportionate increases in energy content relative to purchase cost.4 However, no published data have demonstrated the impact of point-of-sale fast-food upsizing on total energy, fat and sugar availability for Australian fast-food meal-deal options. On 28 July 2002, we purchased major meal deals and the advertised upsizing portions from the four major fast-food chains present in most large Australian cities: McDonald's, KFC, Red Rooster and Hungry Jack's. In order to assess six portions of each meal deal, we purchased two from each of three outlets. The weight and volume of chips and soft drink (non-diet variety) were measured, and nutrients were analysed using the AusNut and AusFoods Australian food databases.5 A summary of our findings is presented in the Box. On average, a 12% increase in purchase cost increased energy availability by 23%, with a 25% increase in fat (10.3 g) and a 38% increase in sugars (18.8 g). The upsizing meal option providing the greatest energy gain was the "fillet burger combo" from KFC (50% increase in energy for a 16% increase in cost). Large meal deals provided on average 5733 kJ (35.4% energy from fat and 21.4% energy from sugar). Based on data from the 1995 National Nutrition Survey, these single meal deals constitute 52% and 77% of the average daily energy intake of male and female Australians, respectively.6 Upsizing is a marketing strategy aimed at increasing the purchase cost of the items by providing the consumer with an added incentive or greater value. Using this strategy, upsizing meal deals double the energy gain relative to the additional cost. Importantly, upsizing also increases fat and sugar intake. With the growing disease burden of overweight and obesity on the Australian healthcare system, the public needs to be aware of the passive increase in energy consumption that can occur in pursuit of "value-for-money" eating options. Excess consumption of sugar and fat from fast-food meal choices adds mainly "empty calories" to the diet, with little nutritional gain and with a real risk of expanding the nation's waistline. Percentage increase in cost, energy content, fat and sugars for various upsizing meal options from four major fast-food outlets Percentage increase Cost Energy content Fat Sugars McDonald's Big Mac McValue meal (medium)* 10.1% 17.8% 16.2% 34.1% Big Mac McValue meal (large)* 20.2% 39.5% 33.1% 80.7% KFC Fillet burger combo (large)† 16.1% 50.3% 56.4% 52.7% Red Rooster Chicken roll combo (large)† 16.6% 27.5% 22.0% 39.7% Hungry Jack's Whopper value meal (large)† 9.2% 15.7% 14.4% 30.2% * % Increase relative to "small" size. † % Increase relative to "regular" size.

David Cameron-Smith · Shane A Bilsborough · Timothy C Crowe

In October 2000, a 10-year-old Aboriginal boy from the Darwin region of the Northern Territory was referred to hospital with a 24-hour history of abdominal pain, initially generalised, but then localising to the right iliac fossa. The pain was accompanied by occasional vomiting, but no fever or diarrhoea was noted. At laparotomy, a gangrenous, unruptured appendix was removed. Postoperatively, the patient made a good recovery. Neither he nor any family members had travelled outside the Northern Territory. Histological sections of the surgical specimen showed changes typical of acute suppurative appendicitis. Closer examination, however, revealed numerous round-to-oval structures resembling trophozoites (see Box). When the possibility of invasive amoebiasis was raised, staining of the section with Entamoeba histolytica-specific sera confirmed the diagnosis. E. histolytica serology was negative. DiscussionE. histolytica is a protozoan parasite of humans that causes infectious colitis and amoebic liver abscess. It has recently been recognised that invasive disease is caused exclusively by the species E. histolytica, while the morphologically identical species E. dispar exists in the colonic lumen as a harmless saprophyte.1 Patients with invasive amoebiasis living in Australia and other developed countries generally acquire the infection outside their country in a region where the pathogenic species is known to be endemic. While cases of amoebiasis in Australians who have not travelled overseas have been reported,2-6 all except one pre-date the recognition of pathogenic and non-pathogenic species, and in none was the primary source identified. Isolated appendicitis due to E. histolytica is a rare condition. Even in regions where the organism is endemic, it causes less than 1% of cases of appendicitis.7 The diagnostic method of choice for amoebic colitis is testing for parasite antigen in stools.1 In this case, for the first time, the species-specific antibody normally used in the stool antigen test was adapted for immunohistochemistry and confirmed E. histolytica infection. Possible alternative methods for confirming the diagnosis include the polymerase chain reaction (PCR) or detection of E. histolytica-specific antibodies or parasite antigen in patient serum.1 However, PCR is not readily available outside research laboratories. The sensitivity of the E. histolytica antibody test in intestinal disease is 52%, a likely explanation for the negative serological test. It is curious that no outbreaks of the readily identified and much more common manifestations of this infection, namely amoebic colitis and amoebic liver abscess, have been recently reported in northern Australia. The potential public health significance of a case of proven autochthonous infection in an Australian population is reinforced by its high transmissibility in settings where hygiene may be suboptimal.8 Furthermore, there is a well documented possibility of prolonged latency between infection and the development of invasive disease.1 Both these factors support the merit of selective screening and appropriate treatment of at-risk contacts if invasive disease is detected. The use of new diagnostic techniques, such as the adapted staining method we used, will enable a more accurate determination of the endemicity of E. histolytica in Australia. Entamoeba histolytica in an inflamed appendix A: Periodic acid–Schiff stain, showing trophozoites (arrowed) within an inflammatory infiltrate. B: Immunoperoxidase stain of trophozoites (arrowed) using E. histolytica-specific sera. Note the surrounding necrotic tissue.

James S McCarthy FRACP MD · David Peacock MB BS · Kevin P Trown FRCPA · Patrick Bade FRACS · William A Petri Jr MD · Bart J Currie FRACP

Objective: To describe the natural history of rheumatic manifestations of Ross River virus (RRV) disease.Design: Prospective longitudinal clinical review.Setting: North Queensland local government areas of Cairns, Douglas, Mareeba and Atherton during January to May 1998.Participants: General practice patients diagnosed with RRV disease on the basis of symptoms and a positive RRV IgM result.Main outcome measures: Rheumatic symptoms and signs assessed as soon as possible after disease onset and on two subsequent occasions (up to 6.5 months after onset).Results: 57 patients were recruited, 47 of whom were reviewed three times (at means of 1.1, 2.4 and 3.6 months after disease onset). Results are reported for these 47: 46 (98%) complained of joint pain at first review, with the ankles, wrists, fingers, knees and metacarpophalangeal joints (II–IV) most commonly involved. Prevalence of joint pain decreased progressively on second and third reviews, both overall (92% and 68% of patients, respectively), and in the five joints most commonly affected. The prevalence of other common rheumatic symptoms and signs, and use of non-steroidal anti-inflammatory drugs, also progressively declined over the three reviews.Conclusions: Earlier studies may have overestimated the prevalence and duration of symptoms in RRV disease. Progressive resolution over 3–6 months appears usual.

David Harley PhD, FAFPHM · David Bossingham FRCP, FRACP · David M Purdie MMedSc, PhD · Nirmala Pandeya BSc, MMedSc · Adrian C Sleigh MD, MPH, FRCP

Objective: To describe the natural history, treatment and cost of Ross River virus-induced epidemic polyarthritis (RRV disease).Design: Questionnaire-based longitudinal prospective study.Participants and setting: Patients in the greater Brisbane area, Queensland, diagnosed with RRV disease by their general practitioners based on clinical symptoms and paired serological tests between November 1997 and April 1999.Main outcome measures: Scores on two validated quality-of-life questionnaires (Clinical Health Assessment Questionnaire and Medical Outcomes Study Short Form 36) were obtained soon after diagnosis and one, two, three, six and 12 months thereafter. Scores were compared between patients diagnosed with RRV disease alone and those with RRV disease plus other conditions.Results: 67 patients were enrolled. Most patients with RRV disease alone had severe acute symptoms, but followed a consistent path to recovery within three to six months. Other conditions, often chronic rheumatic diseases or depression, were identified in half the cohort; their quality-of-life scores suggested stable chronic illness between six and 12 months after diagnosis. Non-steroidal anti-inflammatory drugs (NSAIDs) were taken by 58% of patients (average use, 7.6 weeks; range, 2–22 weeks). Time off work averaged 1.9 days, and direct cost to the community was estimated as $A1018 per patient.Conclusions: Symptom duration and frequency of long-term symptoms may have been overestimated by previous studies of RRV disease. Disease persisting six to 12 months after RRV diagnosis was largely attributable to other conditions, highlighting the need to seek other diagnoses in RRV patients with persistent symptoms.

Andrea D Mylonas BA, RN · Allison M Brown RN, Grad Cert CDM · Tracy L Carthew RN, BN · David M Purdie MMedSc, PhD · Nirmala Pandeya GradDipAppSc, MMedSc · Louisa G Collins BEc, MPH · Andreas Suhrbier MA, PhD · Barry McGrath MB BS, PhD · Elizabeth J Reymond FRACGP, PhD · Philip C Vecchio FRACP, MBA · Ian D Gardner PhD, FACTM · Ferdinandus J de Looze MB BS, MSc

In 1990, while the Royal Commission into Aboriginal Deaths in Custody was in progress, a group of Aboriginal women requested a meeting with the Federal Minister for Aboriginal Affairs so they could talk with him about issues of deep concern. They were granted 10 minutes. Two minutes into the meeting, as they told the Minister of the escalating incidence of violence within our communities, the Minister interrupted: "I know the problem. You tell me some solutions."1 Most Indigenous Australians regard research and researchers with cynicism and suspicion. We have good reason. We have been researched to death and beyond. Research does have an important role in helping find solutions. It can uncover what is happening and why. If designed and implemented appropriately, it can navigate a way forward and show what is, or is not, working. An accurate description, analysis and understanding of "problems" determines the actions of activists, workers in the field, policy-makers and service providers. Research therefore has a vital role to help inform both Indigenous peoples in their pursuit of appropriate services and non-Indigenous policy makers as we work together. In this issue of the Journal, Williams et al (page 300), reporting on assault-related admissions to hospital in Central Australia, conclude: ". . . assault-related admissions to hospital in the proportions we describe suggest a significant public health problem that requires attention."2 Their article is important, if only to strengthen the voices of Aboriginal women, who have been saying for some time that violence, in its many forms, is escalating at an alarming rate within our communities.3 But more is needed. Williams et al present their results from a reductionist research focus on morbidity and mortality. These parameters represent only the end-result of a vicious cycle of violence — a cycle that has had profound and lasting impacts on Indigenous families and communities across generations.4 No reference is made to the context, which embraces where, why and how such violence is occurring. A reference is made to "many resources . . . developed to assist healthcare workers, communities and individuals with alcohol and violence", but these are not discussed. Research into the health status of Indigenous peoples must begin to focus beyond statistical data. For research to have value and to be of benefit, we must try to find out if the strategies referred to are working or not, and why. Some researchers have observed that "there is abundant evidence that psychosocial factors have a profound impact on health", but that "little research to date has targeted the possible biopsychosocial pathways by which social, environmental and contextual conditions of living affect health".5 Indeed, the Australian Institute of Health and Welfare, while recognising the multiplicity of factors that might account for poor health status, relies predominantly on biomedical indicators of health.9 This fails to embrace the less easily measured aspects of community living and wellbeing, now deemed to be of prime importance by Indigenous peoples and public health researchers alike.7 The 1986 Ottawa Charter of Health Promotion outlines the fundamental conditions and resources for health: peace, shelter, education, food, income, a stable ecosystem, sustainable resources, social justice, and equity, which requires, among other things, equity in housing, education, income, and social power.8 Its principles resonate strongly with punyu. The word punyu, from the language of the Ngaringman of the Northern Territory, explains that concepts and functions of health or wellbeing must be considered from an interdisciplinary and multidisciplinary approach. Punyu encompasses person and country, and is associated with being strong, happy, knowledgeable, socially responsible (to "take a care"), beautiful, clean, and safe — both in the sense of being within the law/lore and in the sense of being cared for.9 Being well would therefore be an "achieved quality, developed through relationships of mutual care".10 We do not have peace in Indigenous communities, and all the other prerequisites listed here for health and wellbeing are also left wanting. The Ottawa Charter and the subsequent Sundsvall Statement bring into sharp focus the connectedness between human beings, their physical and social environments and their health and wellbeing. They emphasise that "Health is created and lived by people within the settings of their everyday life; where they learn, work, play and love. Health is created by caring for oneself and others, by being able to make decisions and have control over one's life circumstances and by ensuring that the society one lives in creates conditions that allow the attainment of health by all its members."11 This view echoes the same beliefs that underpin the quest for equality in health, which ensures all people have a right to be part of the process that impacts on their wellbeing at both personal and professional levels within the health service, education and research industries. As we reflect on this major public health problem, we must also consider our potential for doing things differently. There is an appealing reciprocity about the Indigenous punyu and the Western new public health movement, with its strong ecological framework. There exists an opportunity for strong partnerships between Indigenous and non-Indigenous healthcare professional educators and practitioners in shaping or reshaping the future education of healthcare professionals and meaningful health research, even research that focuses on violence. The Minister was right. We do need to focus on solutions. Some Indigenous Australians have argued for process evaluation research, looking at the application and outcomes of interventions and services within our communities. The search for solutions will have to involve greater discussion between Indigenous and non-Indigenous researchers in consideration of the more ecologically grounded interpretation of health promoted by Indigenous peoples, the Ottawa Charter and the Sundsvall Statement. We must develop ways of thinking about and engaging with problems, such as assault-related injuries, as we work together to find better tools for changing the wellbeing of Indigenous communities.

V Judy Atkinson BA, PhD · Jenny Graham DipOT, MSc(Ed), AFCHSE · Gloria Pettit BA, MA · Liz Lewis BA

To the Editor: I read with interest the article on cervical screening by Dickinson.1 Cervical screening has been the most successful public health measure introduced for the prevention of cancer, and the Pap test has been highly effective in reducing cervical cancer mortality and morbidity. In New South Wales, between 1972 and 1999, the age-standardised incidence and mortality of cervical cancer fell by 49% and 66.6%, respectively.2 The overseas experience is similar, with the best screening programs reporting a 70% reduction in mortality rates, with slight annual mortality increases since 1986.3 That women continue to die from this potentially preventable disease emphasises the limitations of the current screening method and highlights the need for new directions. The conventional Pap test is "yesterday's tool for today's world", let alone tomorrow's! The Pap test is prone to errors at all levels, but, most importantly, at specimen collection and cytological interpretation. Consequently, relatively high numbers of false negative results are associated with the test. Further, the Pap test is only partially successful in predicting the biological behaviour of the cytological abnormality. As Dickinson states, minor abnormalities that come and go are unimportant, and can cause unnecessary alarm. These minor and transient abnormalities often lead to colposcopy, biopsy, surgical treatment and subsequent cytological and clinical or colposcopic follow-up, at a considerable cost to individual women, the screening program and taxpayers.4 Recent developments in cervical cytology and molecular biology have opened up new horizons.5 Liquid-based cytology, human papillomavirus (HPV) DNA testing and new molecular markers will help us to accurately select the patients who are likely to have biologically aggressive disease with a high probability of progression.4,5 With refinements, these new technologies will not only dramatically reduce the frequency of Pap test screening, but they may postpone the age for starting screening from 18 years to perhaps 25 or even 30 years. These new technologies come at a price. Liquid-based cytology costs about $30 and HPV DNA testing is about $90, and no Medicare rebates are currently available for these tests. The additional cost of these new technologies should be considered in the context of the cost of diagnosis, treatment and subsequent cytological and clinical follow-up of biologically insignificant disease. The money saved from improved patient selection for treatment and reduced frequency and late commencement of screening would allow more resources to be allocated to enrolling women (who are currently underscreened) and to funding these new technologies.

Ibrahim M Zardawi

To the Editor: Life expectancy in developed countries increased by an average of about 20 years during the 20th century. An editorial in the Journal by Rodger referred to mortality in populations having screening mammography.1 Data quoted indicated that there had been only slight changes in breast-cancer mortality in Australia up to 1996. Data for 1999 are available in the report of the Australian Bureau of Statistics Causes of death, published in December 2000.2 The standardised all-causes death rate per 100 000 for all persons in 1989 was 758.9 and in 1999 was 584.2, a reduction of 23.0%. For women, the standardised death rate attributable to breast cancer in 1989 was 27.2 and in 1999 was 22.1, a reduction of 18.75%. Recent decreases in breast cancer mortality of similar magnitude have also been observed in the United Kingdom and the United States.3 However, screening mammography could only be responsible for a small portion of these changes, because population screening has been in place for little more than a decade and the benefits of earlier detection and treatment would take more than five years to become evident. The causes of these dramatic reductions in death rates are not yet understood. Regarding the effect of population screening mammography on mortality rates, this is limited to breast-cancer-specific mortality and cannot be expected to translate into a reduction in overall mortality. In a recent overview of the situation in Sweden,4 breast-cancer-specific mortality in the screened group was 22% lower than in the non-screened group. However, the age-adjusted relative risk for total mortality was 1.00 (95% CI, 0.98–1.02). In other words, the mammographically screened population died less frequently from breast cancer, but nevertheless died at the same rate as the non-screened population (from other causes such as heart disease and other cancers). If we consider that, in the age group 40–79 years, breast cancer accounts for about 3% of total mortality, a reduction in breast cancer mortality of 25% would be 25% of 3%, or 0.75%. This change is so small that it would probably never be possible to show an effect of breast-cancer screening on overall population mortality. It is therefore realistic to regard the benefits of screening mammography as limited to early detection and treatment (possibly with improved quality of survival) and a reduction in breast-cancer-specific mortality.

In reply: I agree with Gough and welcome the more recent data showing up to an 18.75% reduction in breast cancer mortality in Australia in the 10 years from 1989. Obviously, this cannot be attributed solely to the now 10-year-old National Mammographic Screening Program, but it may result from a combination of the screening program, ad-hoc screening before the program, and the more rigorous use of adjuvant therapies based on the results of clinical trials. That breast screening is unlikely to have an impact on overall population mortality gives the lie to the conclusions of Olsen and Gøtzsche's overview,1 which are based only on overall mortality. Nevertheless, Gough and I agree that screening mammography is likely to deliver other benefits through detection of earlier-stage disease and a reduction in deaths from breast cancer.

Malaria remains a global crisis that kills at least one to two million people per year, mainly children in sub-Saharan Africa.1 Forty per cent of the world's population is at risk of malaria, and each year more than 300 million people have episodes of acute malaria. In recent times, there has been a breakdown in malaria control programs. This has been caused by failure of health systems in the poorest countries, as well as the emergence of mosquitoes resistant to insecticides and malaria parasites resistant to cheap, widely available drugs. In addition, population movements, large-scale development projects, civil wars and conflicts, as well as environmental changes, have all acted in concert to increase the number of individuals at risk of malaria. In Papua New Guinea, for example, malaria is the commonest cause of outpatient presentation and accounts for an estimated 27% of all attendances at health facilities.2 In some Papua New Guinea provinces, malaria is the reason for more than 40% of health centre attendances, and equals pneumonia as a primary cause of death.2 In recognition of the need for a renewed attack on malaria, a global strategy for malaria control was presented to a World Health Organization Conference of Health Ministers in 1992.3 The strategy, now incorporated into the Roll Back Malaria Campaign, promoted a new philosophy emphasising malaria control (in contrast to eradication), and acknowledging the need for different approaches to disease control in different populations. For example, the approach to malaria control in children and pregnant women in Africa is different to that in adult refugee populations. The strategy emphasised the importance of political commitment, such as that given by the heads of State and governments of African countries in Nigeria in 2000 (the Abuja Declaration).4 All participants resolved to commit to an intensive effort to reduce the burden of malaria by strengthening health systems, implementing action plans, improving local capacity, promoting early recognition and treatment of clinical malaria, and reinforcing efficacious preventive measures such as the use of impregnated bednets and chemoprophylaxis. An important component of the strategy is the development of new antimalarial drugs and vaccines. Vaccines have been shown to be one of medicine's most cost-effective interventions. A malaria vaccine that protects for one to five years with 50% efficacy could substantially reduce all-cause child mortality in endemic areas. The cost of such an intervention compares very well with that of using insecticide-treated bednets, and is likely to have major economic as well as social benefits for the populations currently threatened by malaria. An "experiment of nature" suggests that developing a vaccine should be possible. Although many children die of malaria, the majority survive the life-threatening risk of the first few years of exposure and develop clinical immunity. Provided they continue to be exposed to malaria, this immunity protects them from severe disease for the rest of their lives, except during pregnancy. Unfortunately, the immune response that correlates with protection in these lifelong residents of endemic areas has not been identified, so development of a vaccine that mimics this immunity will be difficult. Moreover, malarial parasites demonstrate extreme antigenic diversity. Recent developments, including better methods for antigen production, improved adjuvants and novel delivery systems, provide optimism that sustained and appropriate long-lived immunity can be achieved. Vaccines could be directed against the sporozoite stage of the malaria parasite to prevent infection, or against the stages in human blood — the asexual stage to prevent clinical disease, or the sexual stage to prevent transmission. The malaria vaccine which has been studied in most detail is designed to induce immunity to the sporozoite and the infected liver cell (ie, to stop sporozoites invading liver cells and to kill sporozoite-infected liver cells). In early studies it was shown to induce protective immunity against experimental challenge.5 Under conditions of natural exposure (in semi-immune adult men in The Gambia),6 the vaccine was shown to be safe and well tolerated, with an estimated efficacy (decrease in malaria infection) of 70% in the first nine weeks of follow-up. However, over the 15 weeks of observation, the efficacy fell to 34%. Further trials will determine whether improved efficacy can be achieved in young children. Australian research efforts have led to a multicomponent recombinant protein vaccine targeting the asexual blood stages. This vaccine was tested recently by the Papua New Guinea Institute of Medical Research and its collaborators. The vaccine caused a 62% reduction in parasite density in children, without any harmful side effects.7 Further development will be necessary to produce a vaccine sufficiently efficacious for routine use. In the past there has been a serious lack of funding for research into malaria, partly because companies engaging in this type of research did not expect it to be profitable. A major change has occurred of late, with increased funding from the Wellcome Trust in the United Kingdom, and from the United States through the National Institutes of Health. A grant from the Bill and Melinda Gates Foundation has funded the Malaria Vaccine Initiative of the Program for Appropriate Technology in Health (PATH) (http://www.malariavaccine.org). This worldwide initiative has the specific goal of enhancing the transition of the many promising candidate vaccines from the laboratory to "proof of principle" research in phase I clinical trials. It has funded Australian projects developing vaccines from asexual stage (merozoite) antigens by researchers at Monash University, La Trobe University and the Queensland Institute for Medical Research, partnered by Biotech Australia (New South Wales), the Cooperative Research Centre for Vaccine Technology (Queensland) and Progen Industries Limited (Queensland).8 There are still many challenges in developing a malaria vaccine, such as the need to cope with diverse antigenic types and the importance of stimulating a lifelong response that is boosted by natural infection. Vaccine-induced sterilising immunity that is not boosted by exposure to malaria could put an individual at increased risk when the vaccine-induced immunity wanes. Most importantly, we need vaccines that can be incorporated into national immunisation programs as part of a coordinated, holistic approach to malaria control. Research to find new methods for vector control and new drugs must also continue, as we know from past antimalarial campaigns that a single technology will not be sufficient to control this devastating disease.

Graham V Brown PhD, FRACP · John C Reeder PhD

To the Editor: As noted in the letter by Chapman and Jamrozik,1 there was substantial prescribing of bupropion sustained release (Zyban SR; GlaxoSmithKline) following its Pharmaceutical Benefits Scheme (PBS) listing from 1 February 2001. The drug has been the subject of extensive publicity following reports of adverse drug reactions and deaths of patients while taking bupropion. Although bupropion has been shown to be effective in two key clinical trials,2,3 there are no studies of effectiveness when prescribed in the context of Australian general practice. We conducted a study of short-term effectiveness involving 11 general practice registrars working in eight practices in south-west and southern Sydney. Each registrar identified from practice prescribing records 10–15 patients prescribed bupropion after 1 February 2001. These patients were followed up via a telephone questionnaire 10 weeks after the date of prescription. The questionnaire elicited information on the use of bupropion, patient-reported abstinence rates, adverse effects and use of support services. Biochemical validation of smoking status was not conducted. Interviews with 151 patients were conducted between April and August 2001 (see Box). Patients completing seven weeks or more of therapy were significantly more likely to report both continuous abstinence (P = 0.01) and point-prevalence abstinence (P = 0.002). Eighty-three patients reported adverse effects, the five most common being insomnia (14%), headaches (11%), nausea (8%), dry mouth (5%) and irritability (4%). No convulsions were reported. Patients who made use of one or more support services for cessation counselling were no more likely to report point-prevalence abstinence at follow-up than those who did not (P = 0.8). Our study was not based on a random sample of GPs or patients, and we did not collect data on the total number of patients treated with bupropion in these practices over the study period. Bearing in mind these limitations, the study has a number of notable findings. Despite the wording of the PBS authority "for use within a comprehensive treatment program'', fewer than half the patients reported using any support service. There was also a low rate of completion of the recommended course of treatment (less than 20% of patients). While the short-term abstinence rates among the patients followed up were encouraging, and not dissimilar to rates found in clinical trials,2,3 there is clearly a need to look at strategies to encourage patients to adhere to the prescribed course of treatment and to make use of cessation support services. We suggest patients be invited back for at least two follow-up GP visits following prescribing of bupropion, as well as being made aware of other support services. Ten-week follow-up survey of patients prescribed bupropion sustained release (Zyban SR) for smoking cessation (n = 151) Patients taking all or part of course of drug therapy 124 (82%) Mean duration of therapy (weeks) 4.6 (range, 1–12) Patients completing at least seven weeks of therapy 24 (19% of those who took all or part of course) Patients reporting continuous abstinence at 10 weeks 47 (31%) Patients reporting point-prevalence abstinence at 10 weeks 57 (38%) Patients reporting adverse effects 83 (68% of those who took all or part of course) Patients accessing one or more support services (general practitioner, Quitline, ZAP*) 69 (46%) *ZAP = Zyban Action Plan (trademark of GlaxoSmithKline)

Nicholas A Zwar · Alia Nasser · Elizabeth J Comino · Robyn L Richmond

In 1997, South Australian women around the age of menopause had one of the highest reported rates of hormone replacement therapy (HRT) use in the world.1 Among women aged 55–64 years, 60% had used HRT and nearly 40% were current users, with a mean length of HRT use of 70 months. HRT is effective at relieving menopausal symptoms, and many women can stop taking HRT within a few years without recurrence of these symptoms. For the women who do experience return of menopausal symptoms after ceasing HRT, there has been the comfort of observational studies that showed that long-term HRT use, although increasing the risk of breast cancer and thromboembolic disease, reduced osteoporosis, bowel cancer, cardiovascular events, Alzheimer's dementia, and possibly stroke.2 Critics of long-term HRT use have argued that selection of relatively healthy women to receive HRT may have influenced its reported long-term effects in unrandomised observational studies.3 Two large randomised trials of postmenopausal long-term HRT use were commenced in the 1990s to determine the benefits and risks. The Women's Health Initiative (WHI) in the United States (see website <http://www.whi.org>) focuses on defining the value of different strategies (eg, low-fat diet, calcium and vitamin D supplementation) that could potentially reduce the incidence of heart disease, breast and colorectal cancer and low-impact fractures in postmenopausal women aged 50–79 years. The Women's International Study of long Duration Oestrogen after the Menopause (WISDOM) (http://www.generalpractice.adelaideuni.org/research_index.htm [No longer available]) is a UK-initiated, placebo-controlled study of women aged 50–69 years taking oestrogen, or oestrogen and progestogen, for 10 years. Endpoints of the study include fracture, cardiac events, cancer, dementia, thromboembolism, quality of life, and death. Some Australian women have been recruited to the WISDOM study. Late in the evening (Australian time) of 9 July 2002, the American Medical Assocation posted a report of a WHI trial and an accompanying editorial on its JAMA website.4,5 The report revealed that this randomised, placebo-controlled, double-blind trial to evaluate combined oestrogen and progestogen therapy in postmenopausal women had been stopped early because there was compelling evidence that health risks exceeded health benefits. Graham Colditz (Professor of Medicine at Harvard School of Public Health and one of the authors of the JAMA editorial), who was visiting Australia at the time, and the Cancer Council, New South Wales, were ready to issue press releases (embargoed until 11.30 pm that evening) highlighting the 26% increased risk of breast cancer in women taking HRT. One of these releases was headed "Women advised to stop combined hormone replacement therapy". By the next morning (10 July), the Australian media were awash with headlines and reports that fuelled considerable alarm among women taking HRT. On the same day, the Australian Therapeutic Goods Administration (TGA) requested that the Australian Drug Evaluation Committee (ADEC) establish an Expert Committee to examine the JAMA article and provide advice on the significance of the study outcomes in the Australian context, the necessary and appropriate action required of the TGA, and the information that should be provided to Australian health professionals and consumers. The rapidly convened ADEC Committee reviewed the JAMA article and editorial and gave the TGA its report, which was released on the TGA website in the late afternoon of 11 July. The report noted that the WHI trial was designed to investigate the efficacy and safety of long-term combined HRT in preventing diseases such as coronary heart disease and hip fracture in postmenopausal women. It was not designed to study the effects of HRT being used to treat menopausal symptoms or established osteoporosis. The mean age of women in the study was 63 years, with two-thirds being over 60. This, and the apparently high frequency of cardiac risk factors in the population (one-third being overweight and one-third obese, 50% being previous or current cigarette smokers, one-third having received treatment for high blood pressure, and over 10% having raised cholesterol requiring medication), may have led to a higher risk of cardiovascular events. However, this must be set against a likely underestimate of the excess risk as a result of treatment dropout and crossover. There was no difference in overall mortality between the HRT and control groups for the duration of the study (mean, 5.2 years). The absolute increase in disease risk for an individual woman shown in the study was small: among 10 000 women in the age group studied and with their characteristics taking combination HRT for a year, there would be seven more cases of coronary heart disease (37 v 30), eight more cases of invasive breast cancer (38 v 30), eight more cases of stroke (29 v 21), and eight more cases of pulmonary embolism (15 v 7), but six fewer bowel cancers (10 v 16) and five fewer hip fractures (10 v 15), than among women not using HRT. Over the five years of the trial, there would be one extra case of an adverse event per 100 women taking the combined HRT continuously. The Expert Committee noted the increase in harm reported was smaller in the first two to three years after starting HRT than it was after three or more years of combined HRT use. Conclusions of the Expert Committee of the Australian Drug Evaluation Committee Combination hormone replacement therapy (HRT) in any form should not be used for long-term disease prevention in postmenopausal women, because the benefits are not sufficient to justify the risks. This conclusion is not necessarily restricted to the particular products used in the trial, but could potentially apply to all oestrogen/progestin combination hormone products. Women can be assured that short-term use of combination HRT and other products to manage symptoms of menopause remains an appropriate treatment option, but women should discuss their particular medical circumstances with their doctors, as individual factors may affect the risks and benefits for them. This is even more so for younger women with a premature menopause, in whom the benefits of HRT would be expected to be greater, and the risks are probably smaller. The continued use of combined HRT for women with established osteoporosis is also an acceptable option for many, but women should discuss the benefits and risks with the treating doctor. In another arm of the Women's Health Initiative study, which has not been discontinued, the use of oestrogen alone for the prevention of disease in postmenopausal women who have had a hysterectomy continues under investigation. It is unsafe for women who have a uterus to use oestrogen without progestin, as use of oestrogen alone increases the risk of uterine cancer. The conclusions of the Expert Committee are presented in the Box. The Committee recommended that the TGA ensure updating of product and consumer information for all products used in combination HRT, undertake a full review of the use of combination HRT in long-term treatment and prevention of osteoporosis, and review all ongoing trials using combination HRT for chronic diseases. The WHI trial report and the abrupt cessation of the combined oestrogen plus progestogen trial have raised concerns among health practitioners, prescribers and consumers of combined HRT products. The previously anticipated health benefits from prolonged combined HRT use — reduced heart disease and strokes — were not borne out in the WHI study. However, the absolute risks associated with HRT are small. Women who are currently taking combined HRT, and their doctors, should not panic, but consider these new findings carefully in the light of their reasons for starting and continuing HRT before deciding whether to continue or stop. In women with osteoporosis, the benefit of a reduced fracture rate with long-term combined HRT must now be balanced against the increased risks of breast cancer, stroke, heart disease and thromboembolism. The relative efficacy and safety of HRT must be considered against that of other interventions, including ensuring adequate calcium intake and vitamin D status, exercise, or taking bisphosphonates or selective oestrogen-receptor modulators.

Martin H N Tattersall MD FRACP

The NCCI is supporting many projects for improvement Many countries place great importance on their strategy for cancer control. The precedent was set by former US President Nixon's "war on cancer", declared in 1971, with the goal of reducing cancer incidence by 50% by the year 2000.1 This optimistic aim occasioned an unprecedented expansion of the US National Cancer Institute, its budget reaching $3.5 billion in 2001.2 More recently, the UK National Health Service embarked on a comprehensive reform of cancer services.3 The high profile of cancer in Western countries relates to its associated high morbidity, the high level of public awareness of the disease and the rapidity of research advances. In 1997, Dr Michael Wooldridge, the then Federal Minister for Health and Family Services, contracted the Australian Cancer Society (now the Cancer Council Australia) to establish the National Cancer Control Initiative (NCCI). The formation of the NCCI was based on a conviction that a better return for expenditure on cancer could be obtained, and that the time had come to introduce new evidence-based cancer-control measures.4 Although an array of cancer-control activities was already in place, it was envisaged that the NCCI could make these processes less capricious by applying a national focus, establishing agreed priorities and forming strategic partnerships across government and non-government sectors.5 The NCCI sees cancer control as comprising "all actions that reduce the burden of cancer in the community [including] every aspect of care, from prevention and early diagnosis to curative treatment and palliative care, all underpinned by the best scientific evidence available".6 The NCCI is concerned with assessing both existing programs and potential new developments for their clinical effectiveness, cost–benefit and equity. Its brief extends to managing strategic projects concerned with translating new findings into public health and clinical practice. The NCCI's activities have mainly revolved around cancer care, early diagnosis, and information needs. To provide good-quality clinical care, we need to know what good care is, what care is currently being provided, what gaps exist, and what opportunities there are for improvement. Defining good-quality care requires evidence-based clinical guidelines. The NCCI has been involved in various projects in this area, including production of guidelines on colorectal cancer for specialists, general practitioners and consumers; production of consumer guidelines on prostate cancer; development of guidelines for psychosocial care of patients with cancer; and development of an evidence-based model of optimum utilisation of radiotherapy. The assessment of current care requires management surveys, ideally involving all relevant specialties and representative groups of patients. One of the NCCI's initiatives has been the funding, through a Commonwealth grant, of a national survey of over 2000 patients with colorectal cancer. Improving clinical care requires a range of information-dissemination and learning strategies, with incentives to apply best care. In financial and practical ways, the NCCI is supporting many projects for improvement, including a consultative project, sponsored by the NCCI in collaboration with the Cancer Council Australia and the Clinical Oncological Society of Australia (COSA), to assess the limitations of cancer care provision; development of a national consumers' cancer organisation to increase the scope and effectiveness of consumer involvement; a review, in conjunction with COSA and state and federal governments, of the infrastructure needs for cooperative group clinical trials; initiatives to achieve earlier diagnosis, such as (i) federally funded pilot studies of colorectal cancer screening;7 (ii) assessment of new screening methods for cervical cancer, ovarian cancer, lung cancer and melanoma; and (iii) a project to improve GPs' expertise in managing prostate cancer and using prostate-specific antigen screening. collaboration with State and Territory cancer registries to improve the documentation of cancer and its outcomes, particularly with regard to staging. (The NCCI has developed a core clinical cancer data set for hospitals,8 which includes information on stage of disease and primary treatment, and is designed to be compatible with data collected by population-based cancer registries.); development of ways to assess the frequency of non-melanoma skin cancer, Australia's commonest cancer, using survey methods similar to those used previously,9 but also considering any new methods that become available. In the future, the NCCI will continue to take a leadership role by consensus through an inclusive, consultative approach in dealing with nationally identified priorities. The organisation's core purpose is to be an expert reference body providing timely advice, identifying appropriate initiatives and making specific recommendations to the federal government and other groups regarding the prevention, detection, treatment and palliation of cancer for all Australians.

J Mark Elwood MD DSc FFPHM · Paul D Ireland PhD

To the Editor: Bupropion hydrochloride was listed on the Pharmaceutical Benefits Scheme (PBS) on 1 February 2001 for use as short-term adjunctive therapy for high nicotine dependence, with the goal of maintaining abstinence. Supply is limited to one application per year, with no repeats, and a maximum quantity of 120 tablets at a dispensed cost of $238.95. From the beginning of February to the end of December 2001, 351 772 bupropion prescriptions had been processed by the Health Insurance Commission (HIC) at a cost of $83.14 million.1 This is equivalent to about 2% of total PBS-related drug expenditure in Australia.2 Given this high cost, it is reasonable to consider the extent to which this investment represents value for money. An important first step is to assess the penetration of bupropion into the population of regular smokers in Australia. One indicator of this is the proportion of regular smokers who have filled a bupropion prescription (Box). Estimates suggest that 22.8% of the population aged 20 years and over (25.2% males and 22.8% females) are current regular smokers.3 Seventy-three per cent (14 099 273) of the Australian population were aged 20 years or over in June 2001.4 Combining population and age-specific smoking prevalence estimates results in an estimated 3 198 738 current regular smokers aged 20 years and over. Given that the PBS guidelines allow for only one prescription of bupropion per smoker per year, an estimated 11% (351 772 prescriptions divided by 3 198 738 smokers) of current regular smokers filled a prescription for bupropion in 2001. Excluding smokers aged less than 20 years will have minimal effect on this estimate, as the incidence of high nicotine dependence in this group is likely to be low. Applying this method to each State and Territory reveals marked variation between them in the apparent proportions of smokers filling a prescription for bupropion. For example, an estimated 16.5% of all smokers in Tasmania had such a prescription filled, compared with 8% in Victoria. Although data from the HIC may be incomplete,5 the same method is applied to each jurisdiction in compiling them. Key unanswered questions relate to the extent to which (i) smokers complete a full course of bupropion, (ii) the field effectiveness of bupropion in aiding smoking cessation is comparable with abstinence rates achieved in clinical trials, and (iii) bupropion is used in conjunction with a comprehensive treatment program. We are currently conducting research to examine such questions. Characteristics of bupropion use in Australian States and Territories, February to December 2001, inclusive ACT WA Vic Tas SA Qld NT NSW Total Population (≥ 20 years) 225 797 1 372 378 3 550 348 338 108 1 110 897 2 602 539 131 542 4 767 664 14 099 273 Current regular smokers (≥ 20 years) 53 448 316 608 804 455 74 507 245 553 593 268 33 254 1 077 132 3 198 225 Bupropion prescriptions processed 4 470 46 186 64 482 12 279 32 455 81 619 3 803 106 478 351 772 Total cost of prescriptions processed $1 043 863 $10 854 828 $15 253 431 $2 920 481 $7 713 913 $19 237 576 $881 709 $25 238 851 $83 144 652 Proportion of current regular smokers who used bupropion 8.4% 14.6% 8.0% 16.5% 13.2% 13.8% 11.4% 9.9% 11.0%

Christopher M Doran · Anthony P Shakeshaft · Jennifer A Gates · Julia E Fawcett · Richard P Mattick

Each year many people are killed or injured by lightning due to misinformation and inappropriate behaviour during thunderstorms.1 Analysis of the circumstances surrounding lightning strikes shows that, while there has been a large decrease in the number of lightning casualties in farming and outdoor work, there has been a smaller relative increase in sports-related casualties.2,3 Moreover, with large crowds gathering to participate in or watch an outdoor event, the potential exists for mass casualties to occur from a lightning strike at any one venue. Hence, there is a need to develop specific approaches for lightning safety at sports events. In Australia, fatality rates for lightning strikes have fallen from 0.21 per 100 000 population in 1910–19194 to about 0.01 per 100 000 population in the 1990s. From 1990 to 1999, 23 fatalities were directly attributable to lightning (Australian Bureau of Statistics, personal communication). Furthermore, from 1993 to 1998, lightning was responsible for 95 hospital admissions (Dr R Cripps, Research Centre for Injury Studies, Flinders University, 2001, personal communication). From these figures, we can estimate that the mortality rate from lightning strikes in Australia is currently about 10%. This is below the generally accepted mortality rate of 30%,5 although other authors have reported mortality rates as low as 5%.6 In 1998, the Lightning Safety Group, a group of lightning experts in the United States, developed guidelines for lightning safety,7 which have since been applied to a variety of sports and recreational pursuits.8-11 However, there have been no clear recommendations for lightning safety at events with large numbers of spectators. Our aim is to present specific, practical recommendations to reduce the risk of lightning casualties in outdoor sporting and recreational activities in Australia. General guidelinesThe general guidelines presented here are based on the recommendations made by the Lightning Safety Group and those adopted by the US National Athletic Trainers' Association (Box 1).6,7 Proactive planThe proactive plan should commence on the day before activity, where weather forecasts provide important warning of possible thunderstorm activity.8 Increased awareness of lightning risk should continue on the day of activity until play has finished and the crowd has dispersed. The most basic level of warning involves observation of the weather in the local area. The first flash of lightning or clap of thunder, no matter how far away, should heighten lightning-awareness. The level of risk depends to a large degree on one's location relative to the storm system, which can be determined by the "flash-to-bang" rule (see below). Further useful information can be obtained by liaison with the Bureau of Meteorology <http://www.bom.gov.au>. In recent years, major advances have been made in technology for identifying and locating lightning. In Australia, there is a network of sensors that enable cloud-to-ground flashes to be mapped to within a few hundred metres. Together with other details about local weather conditions, the Lightning Location System can provide real-time displays of lightning strikes and determine the speed and direction of movement of the thunderstorm. This information can be used to estimate the likely future path of the thunderstorms and their probable arrival times at various venues. Chain of commandDuring the formulation of specific lightning safety guidelines, a specific person should be given responsibility for monitoring the weather for signs of a developing thunderstorm. The nominated "weather watcher" should have the authority to postpone the event and have competitors, officials and spectators moved to safe areas. Appropriate people to nominate as weather watchers include the event supervisor, trainers or other medical personnel, or the ground manager. When lightning threatens, the weather watcher is responsible for recognising the danger and activating the lightning protection plan. This should include a signal to the referees and umpires, as well as a method of informing those at risk (ie, players, officials and spectators) of the action required. Safe structures and locationsNo place is absolutely safe from the lightning threat; however, some places are safer than others (Box 1).1,12 It is important to have already identified safe structures and the most appropriate way of moving people into these facilities. The best choice is a large, fully enclosed building. Criteria for suspension and resumption of activitiesThe "30/30" rule is recommended for lightning safety and serves as a guide for the suspension and subsequent resumption of activity.7,13 The first part of this rule (a flash-to-bang count of 30 s) is a guide to the suspension of activity. The flash-to-bang count is one of the most practical techniques for estimating the distance to lightning activity. It is based on the fact that light travels faster than sound. Given that sound travels at a speed of about one kilometre every three seconds, the time that elapses between the flash of lightning and clap of thunder can be divided by three to give a measure of how far away the storm is in kilometres.8,14 The overall message is to seek shelter when the lightning activity is too close, but how do we define what is meant by too close? Currently, most experts agree that the accepted "safe" distance is no less than 10 km.1,7-10,15 This means that as the flash-to-bang count approaches 30 seconds, all people at risk should be seeking or already inside safe shelters. The second part of the 30/30 rule provides the criteria for resumption of play. Here it is recommended that people wait 30 minutes after the last sight of lightning or sound of thunder. This figure is based on the observation that a typical storm moves at about 40 km/h. Thus, waiting 30 minutes allows the thunderstorm to be about 20 km away, minimising the probability of a nearby strike. It is important to emphasise that blue skies and lack of rainfall are not adequate reasons to breach the 30-minute return-to-play rule.1,7,9 Dissemination of InformationIt is important that all participants, officials and spectators are warned of the potential dangers of lightning and how to minimise their risk of lightning-related injury. Practical ways in which this can be achieved include: reading lightning safety messages over the public address systems; and placing notices and safety instructions in event programs and in high-traffic areas at each venue (eg, entrance, change rooms, clubhouse). The information should contain clear and specific instructions about: criteria for suspension and resumption of athletic and recreational activities; and locations of the safety shelters and the best way to access them, as well as suitable alternative shelters. It is important to have a back-up plan in the case of power or equipment failure. Crowd strategiesThe first critical issue in crowd safety is that of safe shelters for large numbers of people. Ideally, crowds should be evacuated to safe areas before the storm is within 10 km of the venue (30-second flash-to-bang count). Given the practical constraints of moving large crowds, it is imperative that a formal assessment is made of existing structures (eg, grandstands, lightning gantries), as simple, cost-effective modifications can dramatically improve the protection offered to the crowd by these structures. Guidelines are provided by the Australian Standard on Lightning Protection.16 Spectators present in structures that are certified as lightning-safe can be advised to remain seated at times of increased lightning risk. Conversely, spectators present in unsafe areas or in structures that have had no formal assessment must be evacuated to safe shelters (Box 1). The importance and size of the event are also critical in decisions regarding safety of spectators. When larger groups are involved, more time is required to properly secure the area. Thus, as time requirements change, the distance at which lightning is considered a threat must be increased. In their report to the Organising Committee for the Sydney Olympic Games, Andrews and Mackerras (personal communication) recommended three phases of lightning safety (Box 2). Their recommendations, which were based on use of the Bureau of Meterology's Lightning Location System, should be implemented for major events where large crowds are expected. ConclusionThe important components of any lightning safety policy include a proactive approach; vigilant monitoring of the local weather; a specific chain of command; a method of delivering the message to those at risk; definition of safe structures; and definition of the criteria for both suspension and resumption of activity. Large events require careful consideration of crowd numbers, length of time required to ensure protection for all present, and appropriate shelters. The more far-reaching the event and the more people involved, the more economical it may be to use formal lightning location systems in early-warning surveillance. 1: General lightning safety recommendations Develop a proactive approach that includes monitoring the local weather from the day before activity until play has finished and the crowd has dispersed. Establish a specific chain of command. This includes choosing a designated weather-watcher and specifying the method of warning the people at risk. Define and list safe structures and locations. Define the criteria for both suspension and resumption of activity. Safe structures Large/substantial building (with electric and telephone wiring and plumbing to provide a safe pathway for the current to the ground). Fully enclosed metal vehicle (acts as a Faraday cage and guides the lightning current around the passengers). Buses are an excellent shelter and can be strategically placed around a venue to protect larger groups of people. Unsafe locations and situations Open field. Close vicinity to the tallest structure in an area (eg, tree, communication tower, light pole). Small structures such as rain/picnic shelters, tents, interchange bench. Indoor and outdoor swimming pools. Use of indoor phones. Umbrellas, golf clubs, bats, or any other object that increases an individual's height. The "30/30" rule A flash-to-bang count of 30 seconds indicates that lightning is 10 km away. This is associated with significant risk that the next strike could be at the observer's location. Thus, activity should be suspended and people moved to designated safe shelters. Wait 30 minutes after the last lightning or thunder before recommencing play. 2: Three phases of lightning safety for the Sydney 2000 Olympic Games Yellow: State of increased lightning awareness Intended to give 60 minutes advanced warning of a storm front reaching 10 km from a venue. (The direction and speed of travel of the storm front are taken into consideration, so that the anticipated time taken for the storm to reach 10 km from the venue is 60 minutes.) Orange: Activation of the lightning protection plan Intended to give 30 minutes advanced warning of a storm front reaching 10 km from a venue. Depending on the venue's requirements, all competitors should be moved to protected areas. Patrons should be advised to remain in position if they are already in a safe area, or move to a protected area as shown on a map. Individuals in transit should be advised to complete their transit as soon as possible. People in cars and buses should be advised not to commence transit and to remain in their vehicles. Red: State of increased lightning risk Declared when lightning activity is within 10 km of a venue. By this stage, all movements and evacuations should be complete, with the venue now secure from lightning. (Adapted from Andrews and Mackerras, 2001, personal communication.)

Michael Makdissi MB BS, BSc(Hons) · Peter Brukner MB BS, FACSP

Rapid treatment of people believed to be infected, and chemoprophylaxis of all close contacts, are the essentials of both immediate and broader public health management of this disease Although not common, invasive infection with Neisseria meningitidis can be devastating to affected patients and families, and, despite modern treatment, has a case-fatality risk of about 9%.1 In a small proportion of affected patients the disease runs a fulminant course, with death supervening in less than 12 hours. As a result, the disease is a cause of public alarm and receives intense media coverage. In its initial stages the disease may not be recognised, yet an adequate response requires decisive and rapid action from both clinicians and communicable disease control services. To help practitioners meet these demands, in 1996 the National Health and Medical Research Council published guidelines for controlling meningococcal disease.2 These guidelines have recently been superseded by guidelines produced by the Communicable Diseases Network.3,4 While vaccines are available against some serogroups of meningococci (polysaccharide vaccines effective against serogroups A, C, W-135 and Y, and conjugate vaccine against serogroup C), they are not currently recommended for routine use in Australia. As a consequence, and as there is no vaccine against serogroup B, the mainstay of the public health control of invasive meningococcal disease rests on timely and effective treatment of cases and public health interventions to prevent secondary cases (those which follow and are associated with primary cases). Meningococci may be associated with a wide range of clinical syndromes, from asymptomatic nasopharyngeal carriage, through pneumonia, septic arthritis and conjunctivitis to meningitis and septicaemia. Meningococcal septicaemia, with or without meningitis, can be particularly life-threatening and has considerably higher mortality than meningococcal meningitis. Invasive meningococcal disease and meningococcal conjunctivitis may be followed by secondary cases, and both require public health interventions.5 The most characteristic feature of meningococcal septicaemia is a haemorrhagic (ie, petechial or purpuric) rash that does not blanch under pressure. Deaths from meningococcal septicaemia may be prevented by early antibiotic treatment. Patients with suspected meningococcal septicaemia who are given parenteral benzylpenicillin by general practitioners are 2.5 times less likely to die than those not given penicillin.6 The greatest benefit of parenteral penicillin is seen in those who are most ill — those with a haemorrhagic rash. For optimal benefit, benzylpenicillin should be given intravenously. However, if this is not possible, it is quite appropriate to administer benzylpenicillin intramuscularly. All general practitioners should have benzylpenicillin in their surgeries and emergency bags, and should be ready to administer it immediately to a patient with an acute systemic febrile illness and either a petechial or purpuric rash. Box 1 shows dosage guidelines based on United Kingdom recommendations,7 presented in this form here for simplicity in emergency situations. There are other, equally valid guidelines available.8 The use of empirical benzylpenicillin does not necessarily obscure a microbiological diagnosis. While giving penicillin before blood and cerebrospinal fluid specimens are taken does reduce the proportion of positive cultures, it is still possible to isolate meningococci from nasopharyngeal swabs or detect meningococcal DNA by polymerase chain reaction.9 Characterisation of meningococci from these sources may be useful in the public health management of affected patients. Patients presenting to a hospital emergency department with suspected invasive meningococcal disease need to be seen urgently. If a presumptive diagnosis of invasive meningococcal disease is made, they should receive their first dose of antibiotics as soon as possible and no later than 30 minutes after arrival. In some patients other bacterial meningitides may not have been excluded, and empirical therapy with cefotaxime or ceftriaxone plus penicillin or amoxycillin should be used.6 These drugs are intended to cover listeriosis, and pneumococcal and meningococcal meningitis. Antibiotic regimens should then be modified as diagnostic and sensitivity information becomes available. If a general practitioner encounters a patient with a non-specific febrile illness which is not sufficiently distinctive or severe to require referral to hospital, the patient should be kept under frequent review. If a rash develops, or the patient's condition deteriorates in any way, the patient should contact his or her general practitioner urgently or go immediately to a hospital emergency department. Once a presumptive diagnosis is made, the relevant public health unit should be notified immediately so that contacts can be identified and the public health response determined. A public health response is required after diagnosis of either a probable or confirmed case of invasive meningococcal disease, or of conjunctivitis caused by infection with groupable meningococci. Meningococci coincidentally isolated from oropharyngeal, genital or anal swabs are of no public health consequence, and do not require a public health response. Nasopharyngeal carriage of meningococci is common — about 10% of the population carry meningococci at any given time,10 not all of which are virulent strains. In North American and European populations the average duration of meningococcal carriage is about nine months; it is an immunising process, with protective antibodies developing soon after acquisition. Factors associated with an increased risk of carriage include smoking and living in crowded circumstances. Contrary to popular belief, a patient with meningococcal disease is not an efficient transmitter of the meningococcus that is causing the illness. Rather, it is the carrier who transmitted the organism to the patient in the first instance who is much more likely to transmit the meningococcus again, causing further cases.11 The public health response targets people who have been in contact with a patient with meningococcal disease in the seven days before onset of disease. The response comprises providing information to contacts (taking into consideration their cultural and literacy needs), and chemoprophylaxis for each person in the network of close contacts. The rationale for chemoprophylaxis is to eliminate meningococci from any carrier within the network of contacts close to the index case and thereby reduce the risk to other susceptible individuals. This rationale must be explained, and the possible adverse reactions and interactions with other medications need to be discussed. Ideally, chemoprophylaxis should be given as soon as possible (within 24 hours) after the diagnosis of the index case. 1: Doses of parenteral benzylpenicillin for treating suspected cases of meningococcal disease Age group Dose of parenteral penicillin Children aged < 1 year 300 mg Children aged 1–9 years 600 mg Adults or children aged 10 years or over 1200 mg 2: Public health responses in defined settings in which a case of invasive meningococcal disease has occurred Setting Information* and chemoprophylaxis Information* only Household† of an affected person All Not applicable Child-care facilities Children and staff in the same room for 4 or more hours at one time in the 7 days before the onset of illness All other children and staff at the facility Education facilities Very close contacts (essentially those who have been "household-like" contacts) All other students in the same classroom (schools) or tutorial groups (universities) Those who have shared saliva with an affected person (eg, mouth kissing, sharing drink bottles and "bongs") All Even though they may not have shared saliva with a case, other members of any sporting team with an affected member should be given information Those exposed to an affected person after the onset of symptoms Very close household-like contacts; health carers who have either intubated the patient without a face mask or performed mouth-to-mouth resuscitation All others concerned that they may have had contact with the affected person after the onset of symptoms * The disease, including the common signs and symptoms, must be described and the mode of transmission explained. Appropriate action if symptoms suggesting meningococcal infection occur should be described. † "Households" include people in the same dormitory, military barracks or hostel bunkroom in the seven days before the onset of symptoms. This also includes those in seats adjacent to the affected person during long distance travel (8 hours or more). Sexual contacts should be managed as household contacts.

Robert G Hall

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

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

"of insects . . . only the ants were troublesome . . . one green as a leaf and living upon trees where he built his nest . . . by bending the leaves together and glueing them . . . their stings were by some esteemd not much less painfull than those of a bee . . ." Joseph Banks, August 17701 Indigenous Australians co-existed with native ants for thousands of years, using them as food (honey ants) and in medicinal decoctions (green tree ants).2 It was the green tree ant (Oecophylla spp.) that first attacked the white invaders from the Endeavour, and a number of native ant species, in particular the jumper or hopper ant (Myrmecia pilosula), still cause significant morbidity. But a foreign ant has now assumed the role of invader. In this issue of the Journal, Solley et al3 (page 521) describe the first Australian patient with anaphylaxis caused by the venom of the Red Imported Fire Ant (RIFA), Solenopsis invicta, and outline the appropriate diagnostic and management strategies, including successful desensitisation. Where did the RIFAs come from? Why are they a threat to our economy as well as our health? Can they be eradicated? February 22, 2001, was a dark day for Australia with the identification of S. invicta at two sites across Brisbane. This ant has the potential to be one of Australia's biggest ecological disasters, with the ability to have an impact on the economy, the environment and society. The ant itself appears innocuous. It is a small (2–6 mm), reddish-brown ant that is hard to distinguish from many other common ants. Its behaviour sets it apart as one of the world's great invaders. The ants will literally boil out of the nest ready to attack in huge numbers. The sting is painful, which accounts for the name "fire ant". Multiple stings are the rule rather than the exception and can be excruciating. The nest is dome-shaped and the colonies consist of up to half a million ants. S. invicta originated in South America, spread to Alabama in the 1930s and now infests 12 US States. Fire ants are thought to have entered Australia via shipping containers. There are two RIFA epicentres, one on the east of Brisbane around the port area, the other in Brisbane's western suburbs and part of Ipswich. The eastern infestation has been identified by DNA testing and chemical analysis of its venom as being from the United States or northern South America. The western infestation may have originated from Argentina (Dr Robert K Vander Meer, Research Chemist, United States Department of Agriculture/University of Florida, Center for Medical, Agricultural, and Veterinary Entomology, unpublished data, personal communication). Despite this multiple encroachment, the pest seems confined to Brisbane. Ecological modelling shows that the ants are capable of surviving in most parts of Australia, while spread modelling suggests that, if uncontrolled, the ants could spread up to 2 million square kilometres (ie, about a quarter of the area of Australia) over the next 30 years.4 A study of the environmental impact of fire ants5 shows that areas infested with the ant have fewer native ant species, lower total biodiversity and an absence of scincoid lizards. The ants can decimate ground-nesting birds, turtles and frogs, and can damage farm, irrigation and electrical equipment.6 The Australian Bureau of Agriculture and Resource Economics7 estimates that the cost of fire ants over 30 years, if uncontrolled, would be $8.9 billion. Australia's response to this invader is a $123 million, five-year National Fire Ant Eradication Program funded by the Commonwealth and the State governments. What about the medical aspects? It is appropriate to compare the RIFA with our most dangerous native ant, the jumper ant: Jumper ants are distributed throughout Australia; RIFAs have only been identified in the Brisbane area. Both jumper ants and RIFAs grasp the skin with the mandibles and sting repeatedly using a retractile stinger on the end of the abdomen. Stings from jumper ants usually cause a local weal-and-flare, while RIFA stings, because of the high alkaloid content of their venom, invariably result in sterile pustules. These pustules should not be broken. Venom proteins from both ants can result in immediate sensitivity. Two proteins have been cloned and sequenced from jumper ants (Myr p 1–2) and four from RIFAs (Sol i 1–4). There is no cross-reactivity between the main proteins of the two ants. Both jumper ants and RIFAs can cause large local allergic reactions that may need to be treated with oral corticosteroids. Up to 3% of Australians describe systemic allergic reactions to jumper ant stings,8 with most allergic sting reactions reported from Tasmania, Victoria and South Australia. In comparison, 30%–60% of people living in areas infested by RIFAs in the United States are stung, with 0.6%–16% of those stung developing anaphylaxis.6 Patients with anaphylaxis should be referred to an allergist/immunologist, and must carry self-injectable adrenalin. The best device, although expensive and still not subsidised by the Pharmaceutical Benefits Scheme, is the EpiPen Autoinjector (CSL, Melbourne). There is no commercial extract for desensitising patients with anaphylaxis to jumper ant venom. A clinical trial of a jumper ant extract has just been completed in Tasmania (Dr Simon G A Brown, Director, Department of Emergency Medicine, Royal Hobart Hospital, personal communication), but commercial production will not occur without financial help from government or private sector sources. At least three commercial desensitising extracts for RIFA venom are available from the United States. Deaths from anaphylaxis to jumper ant stings9 and RIFA stings6 have been documented. Perhaps, with luck and hard work and lots of money, we might eradicate RIFAs from Australia, but no State in the United States has been successful in such a program once the ant has invaded. In some parts of the southeastern United States, stings by fire ants are the commonest cause of anaphylaxis. Let's hope that that is not the case in Australia in 2030. The cost to our health and ecology would be enormous. Interested readers may wish to refer to two excellent web sites: <http://www.dpi.qld.gov.au/fireants/> (Queensland) and <http://fireant.tamu.edu/> (Texas).

Keith I McCubbin · John M Weiner

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

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