Environmental health

Commercially available nucleic acid amplification assays (eg, polymerase or ligase chain reaction) are now the "gold standard" tests for genital chlamydial infection and also have a role in screening for gonococcal infection. Single-dose oral antibiotics are available for treatment of Chlamydia trachomatis, Neisseria gonorrhoeae and Trichomonas vaginalis infections. Strains of N. gonorrhoeae in urban Australia are often penicillin resistant, while strains from South East Asia and those in homosexually active men may show high-level resistance to quinolones. Imiquimod, a novel immune-response modifier, is now available for effective, safe, self-administered treatment of genital warts. The Pap smear remains the cornerstone of screening for precursor lesions of cervical cancer, but human papillomavirus genotyping may have a role in clinical decision-making for women with equivocal or early precancerous lesions. Treatment of primary genital herpes changes the clinical course, and long-term suppressive therapy is effective for those with multiple recurrences.

Francis J Bowden FRACP, MD · Sepehr N Tabrizi PhD · Suzanne M Garland MD, FRCPA · Christopher K Fairley FRACP, PhD

The use of biological agents as weapons of war is not new. In the 14th-century siege of Kaffa, on the Black Sea, the attacking Tartars catapulted bodies of plague victims at the defending Genoese, who contracted the disease and abandoned the city. Over the past century, many countries have developed the capacity to use biological agents to produce casualties in humans and domestic animals and to damage crops and environmental systems. Some biowarfare programs are known to have continued despite the adoption by 144 countries of the 1972 Biological Weapons Convention, which prohibited development or acquisition of such weapons. Early recognition of unusual clinical illness by physicians is an integral part of the public health response to a biological attack. We review the features of four biological agents of greatest concern. In this article, we discuss smallpox, a disease not seen in the world for the past two decades, and botulism. A subsequent article will discuss anthrax and plague. SmallpoxEpidemiologyIn a world declared free of smallpox in May 1980,1 this disease has characteristics that make it particularly suitable for biological warfare. It can be spread person-to-person. With the cessation of vaccination programs over 20 years ago, immunity has waned among those who have been vaccinated, while those born since 1980 are unvaccinated. The virus spreads by the respiratory route (primarily by droplet nuclei or aerosols expelled from the nasopharynx of infected people) or by direct contact (being released from ulcers on the oral mucosa from the time lesions appear on the skin and two to three days after onset of fever). It has also been transmitted by soiled clothing and blankets used by patients. Smallpox spreads rapidly between close family contacts2 and within hospitals when no special precautions are taken.3 Smallpox as a weaponOther features of smallpox that contribute to its suitability as a weapon are the stability of the virus in aerosol form and the likely small infective dose.4 Smallpox virus was added to the biowarfare program of the Soviet Union in 1980. Successful methods of stockpiling large amounts of this virus and delivering it from aircraft or ballistic missiles have been developed.5 With the discontinuation of the Soviet civilian biowarfare program in 1992, hundreds of experienced scientists became available to sell their services and take smallpox virus to other countries.5 The Indian strain of smallpox virus, used in the Soviet biowarfare program, causes a mortality of about 30% in unvaccinated people. Clinical features and diagnosisThe incubation period of 10–14 days ends with sudden onset of fever, headache and backache, usually severe enough to confine the patient to bed. Fever usually continues as the rash develops, with pain associated with pustule growth. Scabs develop and gradually separate, leaving pitted scars. The rash is the most important feature allowing early recognition of smallpox (Box 1). Most cases have been "ordinary type" smallpox, which has pustular lesions, but variant forms ("flat" and "haemorrhagic type" smallpox) occurred rarely and were almost always fatal. Modified smallpox occurred in people with waning immunity after vaccination and those who were vaccinated very early in the incubation period, and comprised a few skin lesions, which evolved more rapidly than those in unvaccinated people. Clinical diagnosis can be confirmed by electron microscopy of vesicular or pustular fluid or scabs, which should be collected and processed under maximum containment conditions. Management and preventionThe only proven effective treatment for smallpox is vaccination before or within three days of exposure, which may abort or modify the severity of an attack. Other treatment is supportive only, plus antibiotic therapy if secondary bacterial infection develops. Strict quarantine with respiratory isolation for 17 days is required of all cases and direct contacts of index cases. Vaccination with vaccinia virus is effective in preventing smallpox for at least five years and may prevent or modify infection for a much longer period, but this varies greatly from person to person. However, very few doses of vaccine are available worldwide at present. Furthermore, smallpox vaccination is associated with more severe adverse effects than any other type of vaccination: for example, encephalitis occurs at a rate of one per 300 000 primary vaccine doses and a quarter of cases are fatal, with some survivors having permanent neurological deficits.4 Therefore, both the World Health Organization and the United States Centers for Disease Control and Prevention have recommended that it should be used only to contain suspected cases and not for mass vaccination.6 BotulismEpidemiologyBotulism is extremely rare in Australia, with no reported foodborne cases since 1991.7 The causative organism, Clostridium botulinum, is an anaerobic, spore-forming, gram-positive rod found in soil (Box 2). It produces a potent neurotoxin that causes paralysis of skeletal and smooth muscle by interfering with acetylcholine release at the neuromuscular junction. Botulism as a weaponBotulinum toxin was first developed as a biological weapon over 60 years ago; it can be aerosolised, or used to contaminate food,8 and the estimated lethal oral dose is 70 µg. The Aum Shinrikyo cult released aerosolised toxin in Japan in the 1990s, but fortunately no cases of botulism resulted. The Soviet Union and Iraq have produced large amounts of botulinum toxin, and Iraq loaded toxin into missiles and bombs.8 Clinical featuresTwo forms of botulism could arise from deliberate release of botulinum toxin — foodborne and inhalational botulism. In contrast, gastrointestinal (infant) and wound botulism arise from infection with C. botulinum, rather than ingestion or inhalation of toxin, and are unlikely to occur in a biological attack. Foodborne botulism, the most common natural form of the disease, results from ingestion of preformed toxin that is produced when food contaminated with C. botulinum has been stored under anaerobic conditions. Cases are mostly associated with improperly home-bottled or preserved foods, but could potentially result from intentional addition of toxin to food. Botulism after inhalation of aerosolised toxin is an unnatural, man-made form of the disease, and would be the intended result of toxin delivery by missiles, bombs or aerosolisation devices. Only one instance of inhalational botulism has been reported, involving accidental exposure of three veterinary personnel to toxin re-aerosolised from animal fur.8 The incubation period for gastrointestinal botulism and probably also inhalational botulism (based on animal studies) is usually 12 to 72 hours. All forms of botulism have identical clinical features, with the exception that foodborne botulism may be preceded by gastrointestinal symptoms (nausea, vomiting, diarrhoea, abdominal cramps).8 The pattern of illness is characteristic: onset with cranial nerve palsies of bulbar distribution, followed by descending motor weakness (from head and chest muscles to upper, then lower, limbs) in a patient with a normal conscious state and no fever.9 Absence of sensory changes is another important negative feature. Reflexes are preserved early, but may be lost with time. Dilated pupils, blurred vision, dry mouth and constipation indicate parasympathetic involvement. Severity of the weakness and its rate of progression vary, depending on the amount of toxin ingested. With modern medical therapy, mortality of foodborne botulism is less than 10%. DiagnosisDiagnosis is initially clinical. The principal differential diagnoses are the Miller–Fisher variant of Guillain–Barré syndrome (a demyelinating condition causing cranial nerve palsies and absent deep tendon reflexes) and disorders of the neuromuscular junction, such as myasthenia gravis. These and other conditions can be differentiated from botulism on the basis of clinical signs (eg, impaired consciousness in brainstem stroke or infection), analysis of the cerebrospinal fluid (infection and Guillain–Barré syndrome), neuroimaging (stroke) and electromyography (myasthenia gravis). Laboratory testing for botulism is complicated and time consuming and is available only through selected public health laboratories. To detect toxin, mice are inoculated with serum, faeces or vomitus; the organism, if present, can also be cultured from these specimens. Results are not available soon enough to assist initial diagnosis or management. Management and preventionPrompt administration of botulinum antitoxin, available in the US but not Australia, lessens disease severity. As the toxin is an equine preparation, serum-sickness-like reactions may occur in some recipients, but anaphylaxis is rare. Otherwise, treatment is supportive. Close respiratory monitoring is essential, and patients should be admitted to an intensive care or high-dependency unit. In one foodborne outbreak, 20% of patients required mechanical ventilation. An investigational toxoid vaccine has been given to laboratory and military personnel in the United States but is not available for more widespread use. 1: Smallpox lesions in an unvaccinated child Evolution of smallpox lesions from papules (top left; three days after onset of fever) to vesicles and pustules (bottom right; nine days after onset of fever). For the first two to three days, the rash of smallpox resembles that of chickenpox, but the two can be differentiated by the following: Smallpox lesions appear after two to three days of prominent prodromal symptoms (fever, headache and backache) and develop slowly (over nine to 10 days). Chickenpox lesions develop rapidly after a one- to two-day prodrome (fever and malaise). All smallpox lesions develop at the same pace and, on any part of the body, appear identical. Chickenpox lesions are much more superficial and develop in crops over a two- to four-day period, with scabs, vesicles and pustules seen simultaneously on adjacent areas of skin. Smallpox lesions are most concentrated on the face, arms and legs, and may occur on the palms or soles. Chickenpox lesions are most dense over the trunk and almost never found on the palms or soles. 2: Clostridium botulinum Gram-positive rods with characteristic subterminal spores (Gram stain; original magnification x 1000). (Picture courtesy Microbiological Diagnostic Unit, Public Health Laboratory, University of Melbourne, VIC.)

Michael Whitby FRACP, FRCPA · Alan C Street FRACP · Tilman A Ruff FRACP · Frank Fenner MD, FRS

Screening by high-quality programs successfully detects cancers at an earlier stage In 2002, the 10th anniversary of Australia's national program of mammographic screening for breast cancer, it is perhaps timely to reflect and review. The need for reassessment is highlighted by the recent furore in the breast-screening world1-4 precipitated by a Cochrane review by Olsen and Gøtzsche.1 In this issue of the Journal, the article by Barratt et al5 (page 266) also encourages us to review breast-screening policies — in this case for women 70 years and over who are no longer in the target group for free mammographic screening (50–69 years). Barratt et al5 estimated the benefit of screening women 70–79 years to be about one-third to three-quarters that achieved in women aged 50–69 years. As women age, the benefit of screening — reduced risk of death from breast cancer — is increasingly offset by the other causes of death. Furthermore, while the benefit is delayed, the hazards of screening — tests for false-positive films, discomfort and anxiety — are immediate. Thus, with increasing age, the data show a further decline in benefit, which is exaggerated when adjustment is made for qualit-of-life factors.5 Barrett et al also provide a rough estimate of the cost-effectiveness of screening older women. The wide range of cost estimates (per quality-adjusted life-year saved) underlines their imprecise nature, but suggests that mammographic screening of women aged 70–79 years is as cost-effective as screening the other outlier group — women 40–49 years. However, Barratt et al remind us that the estimation of benefits, harms and costs would be improved with data from randomised trials in the appropriate age group — which unfortunately are still lacking. In 1999, 63.7% of women in the target age group for mammographic screening in Victoria (50–69 years) were screened.6 In view of Barratt and colleagues' estimates of benefits and costs per quality-adjusted life-year saved, it could be argued that money for screening older — or younger — women could be better spent on recruiting more women in the target group to achieve the desired 70% participation. Trials of mammographic screening commenced in the 1960s and seven have been completed and reported. On the basis of these trials, which showed a reduction in mortality from breast cancer in screened women, mammographic screening recommendations have been drawn up (eg, in the United States), and in several countries political decisions were made to institute national programs (eg, in the United Kingdom, Australia and New Zealand). In 2000, Gøtzsche and Olsen, publishing a "Cochrane review" of the seven trials in the Lancet,7 reported that they found no reliable evidence that screening for breast cancer reduced mortality. However, this report did not fulfil the Cochrane Group protocol for such a review. Since then Gøtzsche and Olsen have worked with the Cochrane Breast Cancer Editorial Group, and in October 2001 part of their review was accepted and included in the Cochrane Library.1 Almost simultaneously, the Lancet published Gøtzsche and Olsen's review in full on its website, and a research letter in its printed journal2 with an editorial commentary3 criticising the Cochrane Breast Cancer Editorial Group for interference. The whole episode has drawn a flurry of criticism and countercriticism.4. After all this, what should women believe, especially as the systematic review of Barratt et al5 suggests that screening for women over 70 years may be of some benefit (and as cost-effective as it is for those under 50 years), on the basis that screening is beneficial in women aged 50–69 years? Although clinical-trial methodology has improved in four decades, population-health intervention studies remain notoriously difficult to perform because of problems associated with large cohort numbers, the randomisation process and guaranteeing reliable stratification. It is not surprising that the seven, now old, trials can be criticised. However, not all would suggest ditching them and their conclusions on these grounds. The Cochrane Breast Cancer Editorial Group has not accepted the other conclusion of Olsen and Gøtzsche — that screening leads to more aggressive treatments8 — and has not included that section of their review in the Cochrane Library. Others4 reject Olsen and Gøtzsche's conclusions because they are based on all-cause mortality, which may be inappropriate in population studies. Do we have other surrogate measures to guide us? Cancer registry data from Victoria9 suggest a "slight downward trend since 1994" in breast cancer mortality, but it cannot be assumed that any of this trend is due to screening. However, from 1982 to 1996, there was no change in breast cancer mortality in Australia.10 The impact of breast screening may be seen more readily in the stages at which breast cancer is detected. In 1997, when the national program was six years old and well established, 30% of new breast cancers were detected through screening. Data suggest that screen-detected invasive cancers were smaller, less likely to involve nodes, and, if node positive, more likely to involve fewer nodes (Box).11 Tumour size, nodal involvement and number of nodes involved — the basis of the tumour–node–metastases (TNM) staging system — are all known to be of prognostic significance. Hence, it is likely that the cohort of women with screen-detected invasive cancer will have a better prognosis and live longer, provided lead-time bias does not negate the prognostic effect of lower staging by detecting cancer earlier while not influencing the natural history of the disease. The prognostic significance of non-invasive cancer (ductal carcinoma in situ), its treatment and the appropriateness of various local and systemic treatments for any breast cancer can be debated and argued. However, the histopathological prognostic (TNM) data would suggest that mammographic screening by high-quality programs successfully detects cancers at an earlier stage, giving a better prognosis and probably improved survival. Women should be made aware of these facts, along with any doubts raised by reviewers of somewhat out-of-date trials. Impact of breast screening on stage at which cancer is detected11 Tumour size/node involvement Screen detected All cancers < 15 mm 60.3% 42.7% Node positive 22.5% 30.0% 1–3 nodes positive 18.7% 23.4% > 3 nodes positive 8.4% 14.2%

Alan Rodger

How real is the threat, and how prepared are we? The world changed on September 11, 2001, and again on October 4, when the first case of inhalational anthrax in the United States raised worldwide fears of bioterrorism. Although the threat of bioterrorism in Australia has been assessed as low,1 defence and civil authorities had upgraded preparations before the 2000 Olympics.2 Those plans, coordinated by Emergency Management Australia, provided a basis for responses by state emergency services, health services and postal services to the numerous false alarms, "white powder" incidents and hoaxes that followed the US events. No anthrax spores or human anthrax cases associated with these incidents have been detected in Australia, but understandably they have caused considerable public anxiety. In retrospect, it now appears that the anthrax-containing letters in the US were probably of domestic origin, with no targets outside that country.3 After the US incidents, health departments were swamped with calls from the public asking what had been done to protect them. They wanted to know how to protect themselves, and whether they needed antibiotics, vaccines for anthrax or smallpox, or gas masks. Health authorities emphasised communication to reassure those who were worried, as well as to provide authoritative information and planning advice about anthrax and other conceivable threats. Should a biological incident ever occur in Australia, communication would be even more important, not only in managing the emergency, but also in minimising community alarm, which could cause more damage than the biological agent itself. In any incident, healthcare agencies would play a key role in recognising resulting illnesses and managing the health consequences. The anthrax threat has highlighted the importance of multidisciplinary approaches to biological emergencies. Security intelligence must be wedded to health intelligence, and the lessons learned from past disaster management appropriately applied. As an editorial in the Lancet recently said, "Appropriate reaction to such deliberate attacks, but also to any other emerging epidemic, by a well-organised and well-functioning public health system requires preparedness at all times on all levels".4 Australia's federal system requires close collaboration between the Commonwealth, States and Territories. Emergency service responses are coordinated by Emergency Management Australia. Public health agencies work with emergency services in the States and collaborate through the Communicable Diseases Network Australia and the Public Health Laboratory Network to coordinate national reporting, surveillance, laboratory diagnosis and public health responses for communicable disease outbreaks. Biosecurity planning in Australia has built on these existing disease and disaster surveillance systems.2 Recently, these networks have collaborated to revise training schedules and case definitions to support the earliest possible recognition of any event resulting from deliberate release of a biological agent. Health authorities, through the Communicable Diseases and Public Health Laboratory networks and the network of Chief Health Officers of the States, have also strengthened their linkages with Emergency Management Australia, the federal department of Defence and other government agencies. Anthrax: The review of Australia's policies has adapted advice from the US Centers for Disease Control and Prevention (CDC), World Health Organization (WHO) and United Kingdom Public Health Laboratory Service for local needs. Guidelines for anthrax treatment and post-exposure prophylaxis have been developed by public health physicians, microbiologists and infectious disease specialists, and endorsed by Australia's Chief Health Officers and directors of public health services. It has been agreed that primary care providers should not prescribe chemoprophylaxis in the event of suspected anthrax. Instead, they should immediately contact their local public health unit for advice about referral for diagnosis and further management (contact details for State and Territory health authorities are available on Fact sheet — anthrax <http://www.health.gov.au/pubhlth/strateg/communic/factsheets/anthrax_fact.htm>). To minimise inappropriate antibiotic use, general practitioners should not provide individuals with a contingency supply of antibiotics for prophylaxis. State and Territory health authorities are ensuring that there are adequate supplies of appropriate antibiotics in case of an emergency, and the Commonwealth Government is working with pharmaceutical companies to ensure continuity of supply. Anthrax vaccine is not currently registered for use in Australia and is not recommended as a first-line response to an anthrax incident. Smallpox: The US government's intention to procure 250–300 million doses of smallpox vaccine for mass vaccination appears to have been modified after expert advice. Existing vaccine is effective but has significant adverse effects. The calf-lymph-derived live smallpox vaccine used in the WHO smallpox eradication program is associated with a post-vaccinal encephalitis rate of 3–4 per million primary vaccine doses.5 Forty per cent of encephalitis cases are fatal, and some survivors have permanent neurological deficits. Progressive vaccinia occurs among those who are immunocompromised. WHO guidance is that, given the substantial risk of adverse events after vaccination, mass vaccination of populations is not recommended when there is little or no real risk of exposure. Despite the stated intention of the US to develop a new vaccine supply against a possible bioterrorism incident, no country is planning to give smallpox vaccine routinely to its citizens. Smallpox is not transmissible until the onset of rash, when the individual becomes ill and is likely to be confined to bed. This provides the rationale for measures to contain any outbreak: after the first cases are identified and isolated, contacts are vaccinated; vaccination prevents or ameliorates disease, even when it is undertaken after exposure to the virus.5 Thus, both WHO and CDC recommend an approach which involves early case detection and post-exposure vaccination with a view to "ring fencing" any outbreak.5-7 Australia has no smallpox vaccine available at present. As a precautionary measure, the Commonwealth Government has arranged with international agencies to secure access to vaccine in the unlikely event of a smallpox incident; arrangements have also been made to secure supplies of vaccine to be held in Australia. If smallpox were introduced into Australia, we would then be in a position to implement a strategy of surveillance, quarantine and vaccination. WHO has pledged support to any country in which an incident occurs, as this would constitute an international emergency. WHO will help countries pool resources to contain any outbreak as rapidly as possible. Conclusions: Although the risk to Australia is regarded as low, we need to be prepared for a bioterrorism incident. Australia's strong public health infrastructure forms the basis for an effective response to any such incident. While much of the initial planning has focused on anthrax and smallpox, progress has been made on public health and clinical protocols for other potential bioterrorism agents. No public health or security system can guarantee complete safety from bioterrorism attack, but Australia's public health expertise will ensure that harm to the community is minimised. For the assistance of doctors, a comprehensive guide for dealing with patient inquiries is available on the website of the Commonwealth Department of Health and Ageing (<http://www.health.gov.au/pubhlth/strateg/bio/index.htm>). This also contains a list of contacts for public health authorities around Australia. Relevant information can also be accessed through the WHO and CDC sites (<http://www.who.int/emc/deliberate_epi.html> and <http://www.cdc.gov>, respectively).

Richard A Smallwood · Angela Merianos · John D Mathews

Objective: To assess the (i) benefits, (ii) harms and (iii) costs of continuing mammographic screening for women 70 years and over.Data sources and synthesis: (i) We conducted a MEDLINE search (1966 – July 2000) for decision-analytic models estimating life-expectancy gains from screening in older women. The five studies meeting the inclusion criteria were critically appraised using standard criteria. We estimated relative benefit from each model's estimate of effectiveness of screening in older women relative to that in women aged 50–69 years using the same model. (ii) With data from BreastScreen Queensland, we constructed balance sheets of the consequences of screening for women in 10-year age groups (40–49 to 80–89 years), and (iii) we used a validated model to estimate the marginal cost-effectiveness of extending screening to women 70 years and over. Results: For women aged 70–79 years, the relative benefit was estimated as 40%–72%, and 18%–62% with adjustment for the impact of screening on quality of life. For women over 80 years the relative benefit was about a third, and with quality-of-life adjustment only 14%, that in women aged 50–69 years. (ii) Of 10 000 Australian women participating in ongoing screening, about 400 are recalled for further testing, and, depending on age, about 70–112 undergo biopsy and about 19–80 cancers are detected. (iii) Cost-effectiveness estimates for extending the upper age limit for mammographic screening from 69 to 79 years range from $8119 to $27 751 per quality-adjusted life-year saved, which compares favourably with extending screening to women aged 40–49 years (estimated at between $24 000 and $65 000 per life-year saved).Conclusions: Women 70 years and over, in consultation with their healthcare providers, may want to decide for themselves whether to continue mammographic screening. Decision-support materials are needed for women in this age group.

Alexandra L Barratt MB BS, PhD · Les M Irwig MB BCh, PhD · Glenn P Salkeld B Business, PhD · Paul P Glasziou MB BS, PhD · Nehmat Houssami MB BS, MPH

In a recent issue of the Journal, Blake and colleagues described a cluster of three cases of measles from western Sydney.1 The index patient acquired measles overseas, while the other two patients acquired the infection during a hospital visit and probably in the waiting room of a general practice, respectively. Measles is highly contagious and can spread with relative ease in healthcare settings, especially if there is a failure to diagnose the infection, to isolate the infectious patient or to notify the case so that other infection control measures can be implemented. Other recent Australian outbreaks of measles have also been associated with virus importation from overseas and subsequent nosocomial transmission.2-4 Measles was imported in nine separate incidents investigated in Western Australia between March 1999 and October 2000, and subsequently transmitted among hospital patients, visitors and healthcare workers on two separate occasions. Victoria has experienced two outbreaks in the past three years,3,4 and a third is evolving (Dr Sean Tobin, Medical Officer, Communicable Diseases Section, Department of Human Services, Victoria, personal communication). In two of the three outbreaks, the index patient had returned from overseas during the incubation period, and genotyping provided strong evidence that the viruses were imported. All three outbreaks involved predominantly young adults. Healthcare staff aged in their 20s or early 30s accounted for six of the 75 cases in the 1999 Victorian outbreak (a doctor, three nurses, a social worker and a medical student3), and for two of the 51 cases in the first of the 2001 Victorian outbreaks (a medical student [the index case] and a nurse who remained unvaccinated despite being identified as susceptible in the previous outbreak5). In the latter outbreak, an unvaccinated 11-year-old child also became infected after attending an emergency department at the same time as an infectious patient. In the current outbreak, one case was in a 36-year-old hospital orderly, and another in a 30-year-old pharmacy assistant, both almost certainly infected while at work (Dr Sean Tobin, personal communication). The hospital orderly, born in 1965, might have been expected to be immune to measles, having grown up when measles virus was circulating in the community and measles epidemics occurred every two years.6 However, people born between about 1968 (when measles vaccine was first licensed in Australia) and 1981 (when a measles–mumps combination vaccine was introduced to the Australian childhood schedule) grew up when exposure to wild measles virus was decreasing. Because of initial poor vaccine coverage, there was inadequate compensation for the subsequent decline in natural immunity in the population, leaving a proportion of this age group, now aged 20–33 years, at risk of measles infection.7 These cases of measles transmission in healthcare settings in Victoria, Western Australia and New South Wales illustrate failure to implement the published guidelines for measles control.8 These involve four key components: isolate the patient, confirm the diagnosis, identify other cases and identify and protect all susceptible persons. However, the failures may be caused by a general lack of awareness of the guidelines rather than an unwillingness to follow their recommendations. In particular, the guidelines are not useful if measles has not been diagnosed. Measles is now relatively uncommon and more likely to affect young adults than children.2 A high index of suspicion is needed, and measles should always be considered in the differential diagnosis of fever and rash in an unwell adult, especially if the person was born between 1968 and 1981. Had the four key components of outbreak control been implemented in some or all of the reported measles outbreaks, some or all of the infections in these outbreaks may have been prevented. As recommended in the guidelines for measles control,8 vaccination of some or all of the young adults involved in these outbreaks may also have prevented further cases. Australia has recently spent more than $30 million on a highly successful mass-vaccination campaign that has effectively protected school-aged children against measles.9 It seems extraordinary that measles transmission can still occur in hospitals or general practice surgeries. Case reports are very unlikely to reveal the extent of the problem. It might be said that transmission of measles — or any other vaccine-preventable disease — in a healthcare setting is a sentinel sign of system failure. Offering susceptible healthcare workers measles–mumps–rubella vaccine has been made a quality standard for all healthcare workers in the United States,10 and a similar approach may be warranted in Australia. Healthcare providers in hospitals and the wider community should record which staff members are susceptible to vaccine-preventable diseases that may be occupationally transmitted, and should provide facilities for vaccination of all those who wish to protect themselves and their patients. As recommended in the Australian guidelines for measles control, young adults intending to travel to measles-endemic countries should be advised to check and update their measles vaccination status. At a time when measles transmission has probably been interrupted in several Australian States,2,11 it is important to suspect the diagnosis of measles in young adults with rash and fever, especially those with a history of international travel, and to take pro-active infection control measures to prevent measles transmission in healthcare settings.

Heath A Kelly · Michaela A Riddell · Ross M Andrews

Public health is crucial for the promotion and protection of health. Links between preventive action and improved health status (eg, in the case of smoking-related cancers, the decline in sudden infant death syndrome and rates of cardiovascular disease) present strong arguments for increased investment in public health infrastructure. The Public Health Education and Research Program1 has ensured a well-trained public health workforce to support national, state and local initiatives. Partnerships. The importance of partnerships in public health has been recognised and institutionalised. Australia's success in containing the HIV/AIDS epidemic resulted from partnerships between government, the gay community and healthcare workers. The National Public Health Partnership, involving State and Commonwealth governments and non-government organisations, coordinates the national public health effort. Its work is exemplified in the development of model public health legislation, particularly on passive smoking, and definitions of public health core functions. A further example is the EnHealth Council, which includes non-government organisations, industry and governments, and promotes coordinated approaches to environmental health. At State/Territory and local levels, partnerships between government and non-government sectors, communities and public health professionals have been formed to tackle Indigenous health issues, alcohol and drug issues, and for public health planning. Health-status inequities. Worsening inequities in health status are a major concern, especially in regard to Indigenous Australians. Socioeconomic differences in health status are being researched. Factors including employment, education, geographical location, access to health services, transport, levels of social capital and living conditions are recognised as crucial in ameliorating socioeconomic health differences, in contrast to earlier beliefs that behavioural changes would improve health status. Primary care. The Commonwealth has invested heavily in general practice. The Divisions of General Practice and initiatives from the federal Department of Health and Aged Care have encouraged greater involvement of GPs in population health. Increasing vaccination and cervical cancer screening rates are notable successes. The involvement of other primary healthcare workers (community nurses, physiotherapists, dietitians, speech pathologists, pharmacists, social workers and psychologists) needs more encouragement. Some of these groups are more suited, through their training and orientation, to facilitate community participation and develop health-promotion strategies involving sectors such as transport, local government and housing. Drug use. Harm-reduction principles are recognised as progressive and effective.2 In Australia, however, harm minimisation is compromised by the focus on controlling illicit drugs, while insufficient attention is paid to tobacco and alcohol, which account for greater disease burdens. Governments need to commit to long term drug policies, accepting that successful implementation may not achieve short term political recognition. Mental health. Mental illness is recognised by the World Health Organization in its 2001 report as one of the most urgent global health problems. Rates of disease are increasing, but treatment options are limited and preventive strategies inadequate. Australia has responded through a National Mental Health Strategy that sees mental health as a population-wide problem, with individual and community solutions.3 Programs funded under this strategy (and others) are tackling depression and seeking to reduce the rates of suicide among men aged under 35 or over 65 years. The next five years. Economic globalisation presents threats to public health. Chief among these is the growth in the power of multinational companies and the power of international treaties to override national legislation designed to protect health. Deregulation of industry practices threatens food safety. Food scares in Europe (eg, mad cow disease) and Australia (eg, haemolytic–uraemic syndrome in Adelaide)4 indicate problems with relaxing the regulation of food production and retailing. Inequities in health status, especially relating to Indigenous health, will remain a central issue. Other critical issues include the effects of globalisation and environmental deterioration, translation of public health research into policy and practice, food safety, and genetics. There is increasing recognition of the impact of environmental deterioration on health:5 global warming and pollution have both direct and indirect effects on health. Maintaining our environment will remain an important concern for public health.

Fran E Baum PhD · Helen Keleher PhD

Editoral Environment, sustainability and health: the learning curve steepens Recent international strife is showing that a divided, unequal and insecure world is inimical to peace, wellbeing and health. We should be seeking a sustainably ordered world, and not a political New World Order. MJA 2001; 175: 569-570 The dramatic events of September 11, 2001, have compelled a refocusing of minds on wider state-of-the-world issues. Indeed, this refocusing may yet emerge as the silver lining to the cloud of tragedy, trepidation and tension that followed that shocking terrorist episode. Many people, on deeper reflection, are now confronting the question "Why?" — of what underlying malaise is such violence and resentment a symptom? The interdependence, reciprocity and increasing connectedness of the world's nations are now more evident than ever before. We are "globalising". This, in turn, entails an increased flow of information that reveals economic disparities, inequalities of trading regimens, persistence of poverty in many poor populations, and the magnitude and ubiquity of serious environmental deterioration.1 The economic, social and political systems that prevail today have thus heightened the risk of non-sustainability — both by overloading the earth's environmental "carrying capacity" (of humans) and by straining the fabric of social and political cohesion.2 . . . even in the modern, affluent, urbanising world, humankind is dependent on intact life-support systems and is subject to the constraints of environmental carrying capacity. Here, though, there is another tension. Despite the incipient evidence of global-scale environmental damage such as climate change and biodiversity losses,2 and the marked widening of the rich-poor gap over recent decades,1 humankind has undoubtedly done well on various environmental indicators.3 We have manifestly become more efficient at generating material wealth — at creating technology-enriched and comfortable lives — and we have achieved a doubling of average life expectancy over the past century.4 In most countries, fertility rates and infant mortality rates have continued to fall. True, various countries of the ex-Soviet Bloc and of HIV-afflicted Sub-Saharan Africa have experienced recent losses in life expectancy. But, overall, the prospects for the world's health seem good. However, this is where we in the health sector need to get serious about highlighting the significance, and the fundamental determinants, of population health. The world's policy-makers and international agencies are preparing for a major international conference on Sustainable Development, to be held in Johannesburg next September. This will be "Ten Years After Rio" (the United Nations Conference on Environment and Development, held in Rio de Janeiro). Yet, we still have not managed to formulate a clear view of population health as a central criterion of "sustainable development".5 That view would recognise that the prospects for population health are, at least in the long run, largely determined by the conditions and assets of the natural and social environments. Lacking that essentially ecological understanding, we will continue to encounter other limiting, indeed sometimes misguided, views about the significance of population health in the overall schema. The World Health Organization will continue to argue (at least for political reasons) that the population's health is an important input — a resource that enhances economic performance6 (which, in turn, benefits population health7). Others will emphasise that poverty is bad for health, that transnational market forces constrain healthcare for the poor, and that uncontrolled industrialisation poses toxic hazards to local communities. In other settings, however, a more profound argument is now being forged. Through three cycles of scientific assessment, the Intergovernmental Panel on Climate Change (IPCC) has paid steadily more attention to the risks posed to future population health by the continuing change in world climatic conditions.8 Likewise, effects on human health are now a central consideration in the several ongoing international scientific reviews of the human consequences of biodiversity loss, stratospheric ozone depletion, the widespread disruption of ecological systems, and the deregulation of international trade. We have begun to understand that, even in the modern, affluent, urbanising world, humankind is dependent on intact life-support systems and is subject to the constraints of environmental carrying capacity.2 We may achieve some technological alleviation, through developments such as genetic engineering and nanotechnology, but there is no guarantee — and we are rather short of time. The recent international strife has begun to underscore the uncomfortable realisation, for the United States and its Western allies, that a divided, unequal and insecure world is inimical to peace, wellbeing and health. This awareness may, one hopes, prompt serious collective action to avert the various global environmental changes that endanger health and life. Such policy changes will require a broad visionary effort. After all, America's recent rejection of the Kyoto Protocol for reducing greenhouse gas emissions is merely the most notorious of several acts of international policy delinquency. Various myopic governments have preferred immediate national economic growth over the longer-term need for prudent, shared international action in a more equitable world. The US exemplifies this self-serving short-termism, and, in recent years, Australia has sometimes followed suit. However, we are learning that the mere maintenance of economic growth is not what "sustainability" is about.9,10 Our economies should be means to social ends, not material ends in themselves. Further — and this is most important — the human-made economy is embedded within, and is ultimately beholden to, nature's "economy", the biosphere.2 The terrorist attack on New York has shown us that there can be no safe havens in a world riven by environmental stresses, social and political instability, and improvised weapons of mass terror and destruction. The rapid increase in numbers of environmental and political refugees, the outbreaks of slaughter in overpopulated regions (such as Rwanda in 1994), the early, tentative evidence of the impact on health of climate change11-14 — these and other signs tell us that we should now be seeking a sustainably ordered world, not a political New World Order. Our task in this evolving discourse, as health professionals, is to make clear that population health is a central criterion in the sustainability transition.5 Population health should be neither an instrumental policy sweetener nor a sideshow. The long-term good health of human populations is dependent on, and an essential measure of, our stewardship of the natural and social environments.2 Anthony J McMichael Professor National Centre for Epidemiology and Population Health Australian National University, Canberra Butler CD. Inequality, global change and the sustainability of civilisation. Glob Change Human Health 1: 156-172. McMichael AJ. Human frontiers, environments and disease: past patterns, uncertain futures. Cambridge: Cambridge University Press, 2001. Lomborg J. The sceptical environmentalist. Cambridge: Cambridge University Press, 2001. Feachem RG. Globalisation is good for your health, mostly. BMJ 2001; 323: 504-506. McMichael AJ, Smith KR, Corvalan CF. The sustainability transition: a new challenge. Bull World Health Organ 2000; 78: 1067. Bloom DE, Canning D, Sevilla J. Health, human capital and economic growth. Working Group I, Paper 8. WHO Commission on Macroeconomics and Health. Geneva: World Health Organization, 2001 (see www.comhealth.org/docs/wg1_paper8.pdf). Dollar D. Is globalization good for your health? Bull World Health Organ 2001; 79: 827-833. Intergovernmental Panel on Climate Change. Climate change 2000. Impacts and adaptations. Cambridge: Cambridge University Press, 2001. Kates RW, Clark WC, Corell R, et al. Environment development: sustainability science. Science 2001; 292: 641-642. Costanza R, Daly H, Folke C, et al. Managing our environmental portfolio. BioScience 2000; 50: 149-155. Lindgren E, Gustafson R. Tick-borne encephalitis in Sweden and climate change. Lancet 2001; 358: 16-18. Kovats RS, Campbell-Lendrum D, McMichael AJ, et al. Early effects of climate change: do they include changes in vector-borne disease? Philos Trans R Soc Lond B Biol Sci 2001; 356: 1-12. Tulu AN. Determinants of malaria transmission in the highlands of Ethiopia: the impacts of global warming on morbidity and mortality ascribed to malaria [PhD thesis]. London: University of London, 1996. Epstein PR, Diaz HF, Elias SA, et al. Biological and physical signs of climate change: focus on mosquito-borne diseases. Bull Am Meteorol Soc 1997; 78: 409-417. Make a comment

Anthony J McMichael

Asylum seekers and healthcare Screening for conditions of public health importance in people arriving in Australia by boat without authority Kathleen King and Peter Vodicka MJA 2001; 175: 600-602 Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Psychiatry Abstract Objective: To determine the prevalence of tuberculosis, hepatitis B carriage and markers of hepatitis C and HIV infection in people detained in immigration reception and processing centres in Australia. Design and setting: Eighteen-month survey of medical conditions of public health importance in people detained at the immigration reception and processing centres at Curtin and Port Hedland in Western Australia and Woomera in South Australia. Participants: 7000 detainees (5742 adults and 1258 children and teenagers aged < 18 years) between 1 January 2000 and 30 June 2001. Main outcome measures: People treated for active tuberculosis; issuing of health undertakings to report to a chest clinic for follow-up of inactive tuberculosis; and confirmation of hepatitis B carrier status or hepatitis C or HIV infection. Results: Eleven people required treatment for tuberculosis (in nine the diagnosis was confirmed bacteriologically), representing a prevalence of 157 cases per 100 000 population. This rate is much higher than the incidence in Australia in 1998 of 4.93 cases per 100 000 population, but comparable with rates in the source countries. Health undertakings were issued to 973 people (13.9%). Of these, 682 (70.1%) were for inactive tuberculosis (26 in association with hepatitis B carriage [16] or hepatitis C infection [10]); and 156, 58 and two health undertakings were for hepatitis B carriage, and hepatitis C and HIV infection, respectively. Conclusions: The health-screening program at immigration reception and processing centres detects significant numbers of conditions of public health importance, enabling treatment and surveillance to the benefit of the people detained and the Australian community. People arriving in Australia by boat without authority are admitted to an immigration reception and processing centre (also known as a "detention centre"), and undergo a protocol-based health assessment. The protocol for entry health assessments at these Department of Immigration and Multicultural Affairs (DIMA) detention centres was devised by a committee with representatives of the Commonwealth Department of Health and Aged Care, DIMA and State and Territory health authorities. The health assessments are concerned with conditions of public health importance only, and identify the minimal health requirements and vaccinations necessary to protect the health of the people detained and the Australian public. The day-to-day healthcare and continuing medical treatment of the people detained are the responsibility of Australasian Correctional Management (ACM), the company that operates and manages DIMA's detention centres. All people detained are given medical examinations to satisfy the requirements for visa application. This examination is used for granting visas in those who are assessed as engaging Australia's obligations for protection under the United Nations Convention relating to refugees. By the time that this assessment is complete and the people are released from detention, they will have completed the full, formal medical examination for the granting of a temporary protection visa.1 An onshore protection visa can be granted even when a medical condition is present. We describe the conditions of public health importance noted in the health assessment process for the possible granting of visas (Box 1; the tinted entries indicate the health examinations included in our study). Methods Our report includes all people receiving medical screening in the immigration reception and processing centres at Curtin and Port Hedland in Western Australia and Woomera in South Australia between 1 January 2000 and 30 June 2001. Chest x-ray examinations were performed at Derby Base Hospital, at Port Hedland Hospital and at Woomera Base Hospital, and x-ray films were read either by chest-clinic physicians or by private radiologists, or both. Medical examinations for granting of visas were performed by medical advisers or approved medical practitioners of Health Services Australia (a government business enterprise contracted to DIMA to provide health assessments). People suspected on clinical or radiological grounds of having tuberculosis underwent full evaluation by sputum-smear and sputum-culture tests. Personnel of State chest clinics were kept informed of all cases of suspected tuberculosis and were involved in the management of all people treated for the disease. Specimens, including Mycobacterium tuberculosis isolates, were sent for testing to laboratories in the respective capital cities (Adelaide and Perth). Sensitivity testing was to World Health Organization reference standards and included tests to rifampicin, isoniazid, ethambutol and streptomycin, with an indirect test for pyrazinamide. Serological testing for hepatitis B surface antigen (HBsAg) and hepatitis C and HIV infection was by standard methods. People with non-communicable diseases, such as cardiomegaly or diabetes, identified by chest x-ray or during the medical examinations were referred to doctors employed by ACM for appropriate investigation and treatment. Likewise, people with evidence of sexually transmitted diseases were also referred to ACM doctors for treatment. All subjects gave their consent to examination and data collection for health assessment purposes. Results In the 18-month period, 7000 people were examined in the three immigration reception and processing centres for the possible granting of a protection visa. There were 5742 adults and 1258 children and teenagers (< 18 years of age) (5916 males and 1084 females). The reported citizenship breakdown was 48% Iraqi, 42% Afghani and 4% Iranian, with the remainder being Sri Lankan, Pakistani, Syrian, Turkish and Palestinian. Seven men and one woman were diagnosed with culture-positive, fully sensitive, pulmonary tuberculosis and treated for infection. Except for one man aged 68 years, all those with active tuberculosis were between 17 and 35 years of age, with five being under 23 years. A 21-year-old man with an abnormal chest x-ray film was found to have peritoneal tuberculosis. Two other men, both 34 years of age, had radiological and clinical indications of active pulmonary disease and consequently were treated for tuberculosis. Both had very abnormal chest x-ray films; one also had an enlarged cervical lymph node and the other had a strongly positive Mantoux reaction (27 mm). Thus, the prevalence of active tuberculosis in this population was 157 cases per 100 000. HIV infection was diagnosed in two people. In two others the test results were indeterminate. In one of those with indeterminate results, a subsequently performed polymerase chain reaction test gave negative results and he is thought not to have HIV infection. In total, 973 people were issued with health undertakings should a visa be granted, with 682 being undertakings to report to a chest clinic for further follow-up of inactive tuberculosis (Box 2). Other communicable conditions diagnosed and treated that do not require a health undertaking include malaria (average, one case per 200 arrivals), chickenpox and other childhood infectious diseases, scabies, headlice, and one case of cutaneous leishmaniasis. Detainees also consult the doctors employed by ACM for treatment of routine infections, most commonly skin conditions (eczema, impetigo and fungal infections), respiratory tract infections, and urinary symptoms. Discussion The medical screening program at the immigration reception and processing centres has resulted in the detection of a considerable burden of disease of public health importance. In Australia, cases of tuberculosis are generally diagnosed soon after the disease becomes active, so that the incidence and prevalence are similar. It is not strictly correct to compare prevalence with incidence. Nevertheless, to provide some comparison, the rate of active tuberculosis of 157 cases per 100 000 population found in our study is significantly higher than the reported incidence of tuberculosis in Australia in 1998 of 4.93 cases per 100 000 population.2 The case-notification rates of tuberculosis in the principal source countries of our study subjects — Afghanistan, Iraq and Iran — in 1999 were 15 cases per 100 000 population, 142 cases per 100 000 population and 18 cases per 100 000 population, respectively.3 The first and last rates are likely not to represent true incidences in those countries. For example, in 1991, Afghanistan reported a rate of 148.9 cases per 100 000 population. Thus, the prevalence of tuberculosis in the detention population is a reflection of its prevalence in the source countries. Both for treating the people detained and protecting the Australian community, it is important to screen for active tuberculosis among people in detention centres. As would be expected, the prevalence of currently inactive tuberculosis is also high in this population. One of the strategies used for the control and surveillance of tuberculosis is the issuing of health undertakings to visa applicants with tuberculosis or abnormal chest x-ray films. The applicant signs an agreement to report to a State or Territory government chest clinic for follow-up within a specified period should a visa be granted. Health undertakings to present to a chest clinic for follow-up and surveillance of inactive tuberculosis were required in 9.7% (682/7000) of people, while, of the total group, 13.9% required health undertakings for tuberculosis or other conditions. This proportion is similar to that of overseas visa applicants (14%) who were considered by the Health Assessment Service in 2000-2001 to require health undertakings (unpublished data). In 1995, visa holders' initial compliance rate with health undertakings was 58% overall.4 Changes to the undertakings system foreshadowed in that report have resulted in higher initial compliance rates of around 70% (unpublished data). The tracing system in case of default, also introduced in 1995, has increased final compliance rates to around 75%. State and Territory chest clinics have indicated that compliance rates by people holding temporary protection visas with health undertakings are similar to those of the general population of visa holders with health undertakings. Procedural changes have recently been introduced to require holders of temporary protection visas to notify DIMA of their current addresses and this should further increase compliance with health undertakings. Hepatitis B carriage occurred in 2.5% (172/7000) of the population examined. This rate is at the lower end of the expected rate, as most of the people detained come from countries where the prevalence of HBsAg carriage ranges from 2% to 7%.5 The prevalence of HBsAg carriage in Australia is less than 2%.5 Hepatitis C infection occurred in 1.0% (68/7000) of the population examined. It is also likely that this is a lower rate of infection than might be expected, but there are no data for prevalences of antibody to hepatitis C in Iraq, Iran and Afghanistan.6 In Australia, the prevalence of hepatitis C infection is less than 1%.6 It is important that people with HBsAg carriage and hepatitis C infection are followed up in the Australian health system and counselled appropriately. HIV infection was confirmed in two people, giving a prevalence of 0.03%. This rate compares with estimated prevalences of 0.15% for Australia and of less than 0.01% for Iraq, Iran and Afghanistan.7 Overall, the health-screening program at the immigration reception and processing centres detects significant numbers of conditions of public health importance, enabling treatment and surveillance to the benefit of the people detained and the Australian community. References Department of Immigration and Multicultural Affairs. Guidelines for medical and radiological examination of applicants for onshore protection visas. Canberra: DIMA, 2000. National TB Advisory Committee for the Communicable Diseases Network Australia and New Zealand. Tuberculosis notifications in Australia, 1998. Commun Dis Intell 2001; 25: 1-8. World Health Organization. Global tuberculosis control. WHO report 2001. Geneva: WHO, 2001. King K, Dorner RI, Hackett BJ, Berry G. Are health undertakings effective in the follow-up of migrants for tuberculosis? Med J Aust 1995; 163: 407-411. National Center for Infectious Diseases, Centers for Disease Control. Geographic distribution of chronic HBV infection [modified June 1, 2001]. Available at: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/ hep_b/slide_9.htm (accessed July 2001). World Health Organization. Hepatitis C: global prevalence (update). Wkly Epidemiol Rec 2000; 75: 3. UNAIDS/World Health Organization. Epidemiological fact sheets on HIV/AIDS and sexually transmitted infections. 2000 Update (revised). Available at: <http://www.who.int/emc-hiv/fact_sheets/All_countries.html> (accessed October 2001). Authors' details Department of Immigration and Multicultural Affairs, Sydney, NSW. Kathleen King, MB ChB, FRCPath, Director, Special Health Projects. Peter Vodicka, MB BS, DPH, Director, Health Assessment Service. Reprints will not be available from the authors. Correspondence: Dr K King, Department of Immigration and Multicultural Affairs, GPO Box 9984, Sydney, NSW 2001. kathy.kingATimmi.gov.au Make a comment 1: Medical screening services for people coming to Australia by boat without authority Service Type of service/target population When performed Primary purpose* Examiner Initial triage Initial medical examination On arrival/en route To ensure no immediate medical problems ACM nurse and/or doctor Initial medical examination More detailed medical examination including psychological questionnaire and urinalysis Screening for infectious diseases, if indicated clinically Within a few days of arrival at an immigration reception and processing centre To identify medical history and concerns ACM nurse and/or doctor Malarial screening Those coming from or transiting a malaria-endemic country and/or pregnant If presenting with febrile illness or fever in 1st week To identify public health risks ACM Vaccination Children All children Commences within 1 week of arrival Disease prevention ACM Adults If indicated clinically (eg, spouse with hepatitis B infection) When indicated Disease prevention ACM Tuberculosis screening Chest x-ray and medical examination, 12 years or over or symptomatic Mantoux test, Monitoring for pregnant women Within 2 weeks of arrival To identify public health risks ACM Blood screening Test for HIV and hepatitis B and C, ≥ 15 years Within 2 weeks of arrival Required for granting a visa ACM Continuing medical treatment Day-to-day care Referral to specialists Medical tests as required While in detention Continuing care ACM Medical assessment for granting a visa Complete visa medical examination Consider radiological and pathology test results Before granting a visa Required for granting a visa Health Services Australia Release arrangements Where MOC from DIMA's health assessment service has determined that a health undertaking is required Before granting a visa Required for granting a visa ACM + DIMA case officers Tinted entries indicate the health examinations included in our study. ACM = Australasian Correctional Management. DIMA = Department of Immigration and Multicultural Affairs. MOC = Medical Officer of the Commonwealth. *Additional reasons may exist for conducting medical screening and tests. The results of medical and chest x-ray examinations and pathology tests obtained for health management during detention are made available to Health Services Australia for visa requirements. The results of blood tests obtained to satisfy visa requirements are made available to ACM for health management during detention. Back to text 2: Reasons for issuing a health undertaking Reason Number issued Inactive tuberculosis only* Inactive tuberculosis with hepatitis B carriage or hepatitis C infection Pregnancy† Hepatitis B (HBsAg) carriage Hepatitis C infection HIV‡ Other§ 656 26 45 156 58 4‡ 28 * Includes 57 children under 12 years of age referred for prophylaxis with isoniazid. † Pregnant women who did not undergo radiological examination, and showed no clinical evidence of tuberculosis, but will have a chest x-ray examination after confinement. ‡ Includes two cases with indeterminate results. § Includes typhoid (six cases); paratyphoid (two cases); other gastrointestinal diseases (eg, giardiasis); and sexually transmitted diseases (eg, syphilis, gonorrhoea and chlamydial infection) requiring follow-up. Back to text

Kathleen King · Peter Vodicka

Childhood injuries Preventing children drowning in Australia We need to take a scientific approach to drowning prevention W Robert Pitt and Danny T Cass MJA 2001; 175: 603-604

Danny T Cass

Childhood injuries Horse-related injuries in children Andrew J A Holland, Gerard T Roy, Valapha Goh, Frank I Ross, John P Keneally and Daniel T Cass MJA 2001; 175: 609-612 Abstract - Methods - Results - Discussion - Acknowledgements - Competing interests - References - Authors' details - - More articles on Paediatrics Abstract Objectives: To identify the frequency, spectrum and outcome of horse-related injuries in children. Design and setting: Retrospective case series of horse-related injuries in children admitted to the Children's Hospital at Westmead (CHW) from January 1988 to December 1999, the John Hunter Children's Hospital (JHCH) from January 1991 to December 1997 and deaths reported to the New South Wales Paediatric Trauma Death (NPTD) Registry from January 1988 to December 1999. Main outcome measures: Circumstances of injury; helmet use; adult supervision; type and number of injuries identified. Results: 232 children were admitted with horse-related trauma, 97 to the CHW over 12 years and 135 to JHCH over seven years, with one death at each hospital. There were six deaths reported to the NPTD Registry over 12 years. The median age was 11 years (range, 1-17). Girls accounted for 65% of those injured and 75% of children were injured while riding. Falls caused the injury in 76.3% of cases. Head and upper-limb trauma accounted for 216 of the injuries (73%). Five out of six children with severe head injuries died. In the CHW group, helmet use was documented in only 24 riders (38%) and adult supervision in 22 (22.9%). Conclusions: Horse-related trauma accounts for a considerable number of deaths and injuries in children in NSW. The use of a Standards-approved helmet for riding or horse-related activities might have decreased the severity of head injuries. In 1788, six horses — four mares and two stallions — arrived with the First Fleet at Botany Bay, New South Wales. The first paediatric equestrian death was reported in 1830.1 Both the equine and human populations in Australia have grown enormously since then, but there have been few reviews of horse-related trauma in this country.2-4 This is surprising given Australia's considerable rural population and the popularity of horse riding as a sporting and leisure activity. Trauma is the most common cause of both morbidity and mortality in children, and motor vehicle injuries are the most frequent cause of such trauma. Although horse-related injuries in children are not as common, the potential for serious injury or death in a young child is high. An adult horse may weigh over 500 kg, gallop at speeds of up to 65 km/h and kick with a force 1.8 times its weight.5 The physical differences between horses and children predispose towards severe injury and are compounded by the potential for unpredictable behaviour in both species. We reviewed the records of children admitted with horse-related injuries to two paediatric tertiary referral centres — one in Sydney receiving children predominantly from an urban and outer urban environment (the Children's Hospital at Westmead [CHW]), and the other in a more rural environment in the Hunter Valley (the John Hunter Children's Hospital [JHCH]). These two hospitals receive most NSW children admitted with horse-related injuries (except those from southern NSW, who may be admitted to Sydney Children's Hospital). These data were supplemented with cases reported to the New South Wales Paediatric Trauma Death (NPTD) Registry. We wished to establish the extent and spectrum of horse-related trauma in children to determine the most effective approach to injury prevention. Methods We performed a retrospective review of children aged under 18 years admitted to the CHW and JHCH, or reported to the NPTD Registry, with horse-related injuries. Data were collected on age, location of injury, whether the child was riding or not riding at the time of the injury, the mechanism of injury, the injuries and surgical intervention required, complications and final outcome. For children admitted to CHW and reported to the NPTD Registry, data were also collected on documented adult supervision and helmet use. In children who died, the cause of death was identified from the coronial postmortem report. CHW admissions: Data were collected from January 1988 to December 1999. Patients were identified retrospectively from the Paediatric Trauma Database compiled by the trauma research nurse at Westmead and the Royal Alexandra Hospital for Children hospitals (subsequently the CHW). In addition, a retrospective medical record search was made for children discharged with "animal-related injury external cause" code categories. JHCH admissions: Data were collected from January 1991 to December 1997. Patients were identified through a retrospective medical record search for children discharged with "animal-related injury external cause" code categories and a search of the John Hunter Hospital trauma database. NPTD Registry: This records all deaths resulting from trauma in children under 16 years of age in NSW that are reported to the coroner. Data were available from January 1988 to December 1999. The police statement and coroner's report, together with the postmortem findings, were reviewed for children who had died after horse-related trauma. Results Horse-related injuries and deaths identified The Box summarises our data on the 236 children who sustained injuries between January 1988 and December 1999. Girls accounted for 65% of those injured and 75% of children who were injured while riding a horse. Falls, or a fall followed by a further injury, was the mechanism in 76% of cases. There was no trend over time for a change in the frequency or type of injury at either hospital, or helmet use at CHW. CHW: There were 97 children with horse-related injuries, representing 6% of children admitted with all play and sporting injuries and 35% of animal-related trauma over the 12-year period. Thirty-four patients (35%) were transferred from a peripheral hospital. One child, a non-riding two-year-old boy, died in hospital. Of those children injured while riding, 24 (38%) were wearing a helmet, 21 (33%) were not, and for 18 (29%) there was no documentation. The location of the injury event was identified in 41 cases: a farm in 26, private land in seven, a riding school or competition in five, and a public highway in three. In 22, adult supervision was recorded; there was no adult supervision in 31, and this was not documented in 44. None of the children not riding were wearing a helmet at the time of the injury, even when involved in activities requiring close proximity to the horse. In four cases the children's feet were caught in the stirrup when the horse bolted and they were dragged along the ground. JHCH: There were 135 children admitted with horse-related injuries, accounting for 8% of children admitted with play and sporting injuries and 48% of animal-related trauma over the seven-year period. One child, a 13-year-old girl, died in hospital. NPTD Registry: There were six deaths from horse-related injuries (including the two mentioned above), representing 8% of the 78 play-related and sporting-related deaths recorded over the 12 years. There was only one other animal-related death reported to the registry. Five of these children were injured on a farm and one during a competition. An adult was present in three cases. Only two of the four children injured while riding were wearing helmets; one of these helmets was seen to fall off before the child struck the ground. In summary, there were significantly more children injured while riding (81% v 66%; χ2 = 6.741; P = 0.009), and more children injured through falls from a horse as opposed to being kicked or trampled (75% v 52%; χ2 = 17.3; P = 0.001), in the JHCH group compared with the CHW group. Further, there was no difference between the age of the children who survived and those who died, but boys accounted for 50% of fatalities, compared with 34% of admissions. Spectrum of injuries The Box (b) compares the injuries identified. Head and upper-limb trauma accounted for 124 and 92 of the injuries, respectively, representing a combined total of 73%. Significantly more patients had head trauma (58% v 34%; χ2 = 16.66; P = 0.001) and torso trauma (25% v 10%; χ2 = 8.588; P = 0.003) in the CHW group; limb trauma (31% v 54%; χ2 = 12.20; P = 0.001) was more frequent in the JHCH group. Major head injury was the cause of death in five of the six children who died, none of whom were wearing a helmet when their heads struck the ground. Of those children admitted to CHW who survived a head injury, 17 were wearing a helmet, 25 were not and there was no documentation for 10. Although there was no significant difference between the initial severity of head injury between children in these groups, no patient who was wearing a helmet at the time of injury, compared with five children who were not wearing helmets, had a long-term neurological deficit. Treatment and outcome One hundred and fifty patients required 174 procedures under general anaesthesia (mostly either limb fracture reduction and fixation or debridement and suturing of a laceration) and three patients had four procedures under local anaesthesia. There were significant adverse outcomes in 23 survivors (10%), eight of which involved a neurological deficit. Discussion The risk of injury while horse riding has been estimated as between 1 per 320 to 1 per 1000 hours of riding.4,6 The variation in reported population-based risk of horse-related trauma of between 18.7 injuries per 100 000 to 9.5 injuries per 1000 population per year illustrates the difficulties of accurate data collection and variable inclusion of non-riding injuries.7 Interestingly, the overall risk of injury from horse-related activity has been determined to be greater than that of car racing or riding a motorcycle, and the rate of hospitalisation from falls from a horse equivalent to that from playing rugby.8-10Our data indicate that horse-related trauma is a significant problem for children in Australia, particularly those living in rural environments. This probably reflects greater exposure to horses in rural areas, together with greater numbers of riders and riding hours compared with children living in an urban environment.11-14 The true scale of the problem is likely to be even greater than our data suggest, as children with minor injuries may not require admission to a paediatric hospital, and we may not have identified all patients.4 Girls accounted for 65% of horse-related injuries in children in this study and three-quarters of those injured while riding, but only 50% of fatalities. This overall female preponderance, a contrast to the situation for most traumatic injuries, is likely to represent the greater participation of girls in horse-related activities.4,6,13,15-17 The equal sex ratio for fatal horse-related injuries in this review resulted from the number of male preschool non-riders injured while in close proximity to a horse. Sex differences in exploratory behaviour patterns would explain this finding.18 Although the risk of injury in children involved in horse-related activities is high, of perhaps more importance is the severity of such injuries and their potential long-term consequences.2,13,15,16,19 In addition to the six deaths over 12 years in NSW, 230 children had sufficiently severe injuries to require hospital admission. While a kick from a horse may cause a lower-limb fracture or soft-tissue injury in an adult, in a child it may result in a compound skull fracture, thoracic trauma or perforated hollow viscus.2,12 Our findings indicate that the social and economic cost of horse-related trauma in children is considerable: a death every two years in NSW, over 200 children admitted with an average length of stay of three days, and 10% of survivors having complications.4 These negative outcomes must be balanced with the positive health aspects of a sporting activity that involves interaction with a companion animal. The challenge is therefore to improve the safety of horse riding. Our data suggest that some fatalities and injuries might be avoided, or their severity reduced, through a combination of increased adult supervision of preschool age children and the use of appropriate safety measures such as a Standards-approved helmet.6,18,20,21 Although the use of Standards-approved helmets is encouraged by both the Pony Club Association of NSW and the Equestrian Federation of Australia (EFA), it is not a legal requirement as it is for pedal and motor cyclists. Further, their use in place of a top hat or traditional riding helmet may even be disallowed when competing at the higher levels (national, international, Olympic, etc) of dressage competition (E Canapini, National Coaching Manager, EFA, personal communication). Compliance with helmet use in this study, although not fully documented, appeared to be poor and reflects published findings.2-4 While the number of patients in our study for whom there were complete data was small, children wearing helmets when riding appeared less likely to suffer long-term neurological sequelae compared with those who were not. We therefore propose that consideration be given to making the use of a Standards-approved helmet for horse riding mandatory. Although it would not be practical to enforce helmet use in rural areas, compulsory use in all styles of competition, in riding schools, and on public highways might have a follow-on effect on farms and in children who become occupational riders as adults.22 We see no reason why children and adults engaged in horse-related activities should not receive the benefits of helmet use that have been shown in cyclists, and which they currently enjoy by law.23 Acknowledgements Dr P Subramaniam provided assistance with the collection of data from the John Hunter Children's Hospital. Mr A J A Holland was supported by a Surgeon Scientist Scholarship from the Royal Australasian College of Surgeons. Associate Professor J Peat provided assistance with statistical analysis. Competing interests None declared. References Cone TE Jr. Playing with horses. Pediatrics 1971; 47: 784. Pounder DJ. "The grave yawns for the horseman". Equestrian deaths in South Australia. Med J Aust 1984; 141: 632-635. Williams F, Ashby K. Horse-related injuries. Edition No. 23. Melbourne: Monash University Accident Research Centre, 1995. Cripps, RA. Horse-related injury in Australia. Edition No. 24. Adelaide: Australian Injury Prevention Bulletin, Flinders University, 2000. Kriss TC, Kriss VM. Equine-related neurosurgical trauma: a prospective series of 30 patients. J Trauma 1997; 43: 97-99. Bixby-Hammett DM. Pediatric equestrian injuries. Pediatrics 1992; 89: 1173-1176. Hamilton MG, Tranmer BI. Nervous system injuries in horseback-riding accidents. J Trauma 1993; 34: 227-232. Nicholls JP. Safety of horseriding. BMJ 1990; 301: 496. Chapman MAS, Oni J. Motor racing accidents at Brands Hatch, 1988/9. Br J Sports Med 1991; 25: 121-123. Buckley SM, Chalmers DJ, Langley JD. Injuries due to falls from horses. Aust J Public Health 1993; 17: 269-271. Aronson H, Tough SC. Horse-related fatalities in the Province of Alberta. Am J Forensic Med Pathol 1993; 14: 28-30. Hobbs GD, Yealy DM, Rivas J. Equestrian injuries: a five-year review. J Emerg Med 1994; 12: 143-145. Christey GL, Nelson DE, Rivara FP, et al. Horseback riding injuries among children and young adults. J Family Pract 1994; 39: 148-152. Thompson JM, von Hollen B. Causes of horse-related injuries in a rural western community. Can Family Physician 1996; 42: 1103-1109. Barone GW, Rodgers BM. Pediatric equestrian injuries: a 14-year review. J Trauma 1989; 29: 245-247. Nelson DE, Bixby-Hammett D. Equestrian injuries in children and young adults. Am J Dis Child 1992; 146: 611-614. Campbell-Hewson GL, Robinson SM, Egleston CV. Equestrian injuries in the paediatric age group: a two centre study. Eur J Emerg Med 1999; 6: 37-40. Lam LT, Ross FI, Cass DT. Children at play: the death and injury pattern in New South Wales, Australia, July 1990-June 1994. J Paediatr Child Health 1999; 35: 572-577. Ingemarson H, Grevsten S, Thoren L. Lethal horse-riding injuries. J Trauma 1989; 29: 25-30. Finch C. Sports injury prevention. In: Ozanne-Smith J, Williams F, editors. Injury research and prevention: a text. Melbourne: Monash University Accident Research Centre, 1995. Rivara FP. Fatal and non-fatal farm injuries to children and adolescents in the United States, 1990-3. Inj Prev 1997; 3: 190-194. Condie C, Rivara FP, Bergman AB. Strategies of a successful campaign to promote the use of equestrian helmets. Public Health Rep 1993; 108: 121-126. Cameron MH, Vulcan AP, Finch CF, Newstead SV. Mandatory bicycle helmet use following a decade of helmet promotion in Victoria, Australia — an evaluation. Accid Anal Prev 1994; 26: 325-337. (Received 2 Jan, accepted 16 Aug, 2001) Authors' details The Children's Hospital at Westmead, Royal Alexandra Hospital for Children, The University of Sydney, NSW. Andrew J A Holland, FRCS, FRACS, Senior Research Fellow, and Clinical Lecturer, Department of Academic Surgery; Valapha Goh, RN, Trauma Research Nurse; Frank I Ross, BAppSc(Nurs), MPH, Clinical Nurse Consultant; Daniel T Cass, PhD, FRACS, William Dunlop Professor of Paediatric Surgery; John P Keneally, MB BS, FANZCA, Head, and Clinical Senior Lecturer, Department of Anaesthesia. The John Hunter Children's Hospital, Newcastle, NSW. Gerard T Roy, FRCS, FRACS, Paediatric Surgeon. Reprints: Mr Andrew J A Holland, Department of Academic Surgery, The Children's Hospital at Westmead, Royal Alexandra Hospital for Children, Locked Bag 4001, Westmead, NSW 2145. AndrewH3ATchw.edu.au Make a comment Children with horse-related injuries admitted to the Children's Hospital at Westmead (CHW), January 1988 to December 1999, John Hunter Children's Hospital (JHCH), January 1991 to December 1997, and horse-related deaths reported to the New South Wales Paediatric Trauma Death (NPTD) Registry, January 1988 to December 1999 (a) Demographic characteristics and manner of injury CHW survivors (n = 96) JHCH survivors (n = 6) NPTD Registry deceased (n = 134) Age (years) Median 10 11 11.5 Range 1-15 1-17 2-14 Sex Boys 33 (34%) 46 (34%) 3 (50%) Girls 63 (66%) 88 (66%) 3 (50%) Activity Riding 63 (66%) 109 (81%) 4 (67%) Not riding 33 (34%) 25 (19%) 2 (33%) Mechanism Fall 50 (52%) 101 (75%) 2 (33%) Fall plus further injury 13 (14%) 11 (8%) 3 (50%) Kick 28 (29%) 19 (14%) 1 (17%) Bite 0 2 (2%) 0 Trampled 5 (5%) 1 (1%) 0 (b) Details of injuries and number of children affected CHW survivors (n = 96) JHCH survivors (n = 134) NPTD Registry deceased (n = 6) Head injuries Concussion 19 17 0 Skull fracture 18 10 3 Intracranial haemorrhage 8 3 4 Cerebral contusion 7 1 2 Facial fracture 10 4 0 Soft tissue injury 6 10 3 Totals 68 in 56 patients 45 in 42 patients 11 in 5 patients Spinal injuries Cervical spine 1 3 1 Lumbar spine 0 1 0 Totals 1 in 1 patient 4 in 4 patients 1 in 1 patient Torso injuries Liver or spleen 11 1 1 Kidney 5 2 0 Soft tissue 5 3 1 Pulmonary contusion 3 2 0 Haemothorax/pneumothorax 2 5 0 Rib fracture 2 2 0 Pelvic fracture 2 2 0 Myocardial infarction 0 0 1 Hollow viscus perforation 1 0 0 Bladder haematoma 0 1 0 Totals 31 in 24 patients 18 in 14 patients 3 in 3 patients Limb injuries Upper limb fracture 26 58 1 Lower limb fracture 4 14 1 Upper limb soft tissue 2 4 1 Lower limb soft tissue 2 1 0 Totals 34 in 30 patients 77 in 73 patients 3 in 2 patients Back to text

Gerard T Roy · Valapha Goh · Frank I Ross · John P Keneally · Daniel T Cass

The research enterprise The Menzies Centre for Population Health Research A unique and supportive local population was a vital ingredient in the Centre's success Terence Dwyer MJA 2001; 175: 617-620 Early days: the Tasmanian Infant Health Survey and Sudden Infant Death Syndrome - The post-SIDS era: taking stock - New directions - Genomics - The future - References - Authors' details - - More articles on Psychiatry I ACCEPTED THE CHAIR IN COMMUNITY HEALTH at the University of Tasmania in 1985 with the intention of setting up a research centre that focused on epidemiological research into preventable causes of disease. While I did not know how the centre would be funded, I was certain that Tasmania would be a very competitive site for such research. Already, valuable epidemiological studies on iodine deficiency, hydatid disease and asthma had been conducted in the absence of significant research infrastructure.1 The "Island State" provided a perfect source population for unbiased selection of cases and comparison samples or controls. Further, the land area and population size (around 500 000 people) made follow-up of cohorts relatively easy. Thus, Tasmania had important advantages for the two major strategies used to search for environmental and lifestyle causes of disease — case-control and cohort studies. Funding from the Menzies Foundation came about through the input of three people — Basil Hetzel, then Chief of the Commonwealth Scientific and Industrial Research Organisation Division of Human Nutrition in Adelaide, who had a close association with the Menzies Foundation; Professor Ian Lewis, Dean of the Medical School at the University of Tasmania and a member of the Menzies Foundation Board; and Eric Wigglesworth, the Director of the Foundation. To determine the likely success of such a centre, the Foundation Board held a three-day workshop attended by representatives of State and Federal health departments and the World Health Organization, notable Australians in the field of public health, and distinguished British epidemiologist Sir Richard Doll. History of the Menzies Centre 1987 Workshop ("Towards a Centre for Population Health Research") in Hobart, Tasmania. 1988 Official opening in January. Collection of Tasmanian Infant Health Survey (TIHS) data began (prospective study on Sudden Infant Death Syndrome [SIDS]). 1990 Designated as a World Health Organisation Collaborating Centre for the Prevention of Cardiovascular Diseases. 1991 Provides prospective evidence confirming importance of prone sleeping position as a cause of SIDS (Lancet 1991; 337: 1244-1247). 1992 Evidence that SIDS death rate was falling after a national campaign on infant sleeping position. 1993 Research helps explain how prone position interacts with other factors to increase risk (N Engl J Med 1993; 329: 377-382). 1995 First follow-up of TIHS cohort searching for early life influences on childhood diseases. Shows that the major decline in SIDS deaths from 1991 onwards is the result of changes in infant sleeping position (JAMA 1995; 273: 783-789) 1997 Contract signed with AMRAD pharmaceutical company. Provides funding for Genetic Epidemiology Unit. 1997-2000 Follow-up of the Tasmanian Infant Health Survey cohort into childhood provides important evidence about early life determinants of risk for osteoporosis, blood pressure and asthma (J Clin Endocrinol Metab 1998; 83: 4274-4279; J Bone Miner Res 1999; 14: 146-151; BMJ 1999; 319: 1325-1329; Thorax 1999; 54: 664-669). 2000 Named "Tasmanian Icon" by State Premier. Core funding doubles. Key events Major scientific achievements. Subsequently, the Menzies Foundation Board decided to support the establishment of an epidemiology research centre, to be named the Menzies Centre for Population Health Research. The Foundation then met with the Tasmanian Premier and Minister for Health, who matched the Foundation's initial contribution of $100 000 per year. Early days: the Tasmanian Infant Health Survey and Sudden Infant Death Syndrome Before my departure from Sydney University, I had been reviewing the data on disease distribution in Tasmania. Sudden Infant Death Syndrome (SIDS), with an annual rate in Tasmania twice the national average, stood out. The head of neonatology at the Royal Hobart Hospital, Neville Newman, convinced me that this should be the subject of a major research effort. The cause had not been clearly identified, and epidemiological research had been limited. With helpful input from Geoffrey Berry, Professor of Biostatistics at Sydney University, we planned the first prospective cohort study on this condition. Preliminary work began just before the decision of the Menzies Foundation to support the establishment of the Centre. The epidemiology research group within the Medical School at the University of Tasmania consisted of one epidemiologist, the research fellow Trevor Beard, and limited support staff. Even with the extra $200 000 that the establishment of the new Centre brought, it would not have been realistic to work on a broad front. It was decided that we would focus most of our effort on the new SIDS research program. The next step was to build an appropriately skilled team. We advertised for another epidemiologist and a biostatistician, but it proved very difficult to attract qualified applicants. It seemed that Australian academics were either not interested in living in Tasmania, or were not confident their careers would flourish there. This problem was compensated for by a stroke of good luck when a young Tasmanian medical graduate, Anne-Louise Ponsonby, became our first postgraduate student, working on SIDS. She put an incredible amount of intelligently directed energy into the SIDS program, and together, with financial help from the Australian Rotary Health Research Fund, we were able to develop momentum in the project. In 1988, we initiated the first full data collection for the cohort study — a huge endeavour that involved measurements each year in 1500 infants and their mothers on three occasions in the first three months after birth. That we could get this work under way was pleasing, but we needed to find well-qualified biostatisticians. Given the previous lack of success with advertising in Australia, I decided to use our international network. Sir Richard Doll referred Michael Jones, a young Master of Science graduate from Oxford, who was recruited to our ranks, and then Laura Gibbons, from the University of Massachusetts, joined us. This relatively small and young team of investigators coordinated the conduct, data management and analysis of the SIDS program. They also assisted with less well resourced but developing areas in cancer and cardiovascular disease. In late 1990 evidence was accumulating from case-control studies that prone sleeping position might be a major cause of SIDS, but the research was retrospective, creating concerns that recall bias might explain the findings. We had the only prospective data in the world and were able to show that the association was equally strong prospectively, ruling out recall bias.2 A number of countries, including Australia, launched campaigns to encourage parents not to place babies on their stomachs in the cot, with astonishing results — the death rate from SIDS in Australia fell from 507 in 1990 to 139 in 1998, with similar falls in a number of other countries.3 While our work was not the only important contribution to the understanding of this major cause of SIDS, it provided an important piece of evidence needed for solving the puzzle. Later, in 1993, our team explained why prone sleeping position seemed to exert a different effect in winter than summer and a different effect across countries.4 Then, in 1995, we provided evidence that showed clearly that the fall in deaths could only be attributed to the changes in prevalence of prone sleeping position.5 This success will undoubtedly rank as one of the major contributions of the Centre in the years to come. It also established the organisation as one which, in its special location, could have a significant impact on international medical science. It was the much-needed platform that would underpin future recognition and opportunities. The post-SIDS era: taking stock The death rate from SIDS fell so rapidly after the prone sleeping position campaign that, by late 1991, it was clear there would eventually be insufficient cases occurring annually in Tasmania for epidemiological research (when we started the SIDS program, there had been an average of 27 cases a year for an extended period, and by 1998 there were only three). While this outcome was tremendously gratifying, it was clear that the research money to support our staff of now approximately 20 would dry up unless we repositioned our research program. This was confirmed by the National Health and Medical Research Council (NHMRC) Regional Grants Interview Committee's decision not to recommend refunding of our cohort study for 1992. We went from triumph to a period of considerable adversity. One of our first responses was to tell the Tasmanian public that we needed its financial and moral support. They responded generously. With a major public fundraising appeal, helped greatly by our Board and new Chairman John Tomlinson, and a timely decision by the United States National Institutes of Health, we were able to continue the study long enough to thoroughly evaluate the impact of the prone sleeping intervention campaign. In 1992, I took some time to review where we were going as an organisation and to think about where our future research opportunities might lie. I visited people like Richard Doll in Oxford, who had provided very helpful mentoring since 1987. I also had discussions with Ken Rothman (author of Modern epidemiology6), and Dimitris Trichopoulos at Harvard. These visits confirmed that, if we were to continue to conduct work of global significance, we would have to search even more thoroughly for gaps in knowledge that might be filled by an epidemiological approach. I was also convinced that we would need to develop stronger working relationships with basic scientists if we wished to use epidemiology to understand aetiology. These strategies were challenging, but all our team had learned a great deal from the SIDS research experience. While overseas, I also upgraded my skills in organisation and management by attending a management course in Salzburg, led by Peter Drucker, one of the world's most prominent management theorists. New directions The perspectives gained during my overseas visit were incorporated into planning from 1992 onwards. The major new strategy we decided on was to follow the Tasmanian Infant Health Survey (TIHS) cohort, now numbering 11 000 infants and children. The focus would be to search for links between early life exposures and later disease, using our extensive database of infant measurements that provided information on more than 450 variables measured during the first three months of life. One disease we looked at was asthma, an important disease for which preventable causes had not yet been identified and for which there was a shortage of good epidemiological data. This investigation would be coordinated by Anne-Louise Ponsonby, with help from David Couper, a biostatistician who had joined us from Seattle. We also increased our activity in research on the development in childhood of risk factors for cardiovascular disease and diabetes. Fitting into this theme was the new program started by a recent recruit from the Garvan Institute in Sydney, Graeme Jones (we were finally starting to see interest in work opportunities from well-qualified Australians outside Tasmania). He had a strong track record in osteoporosis in the elderly, and he used that background to focus on the impact of early-life factors on bone density in childhood. Fortuitously, interest in the "Barker hypothesis", which concerns the impact of fetal development on later disease, was gaining momentum. We were well placed to make an important contribution in this field, and our capacity was greatly enhanced by the addition of Ruth Morley, from the Institute of Child Health in London. Supplemented by smaller research efforts in cancer and adult cardiovascular disease, by 1994 we were able to see evidence that the research program was growing again. Between 1994 and 2000, the team was able to attract 17 new NHMRC grants from 38 applications submitted. This overall level of success was built on the tremendous preparedness of the Tasmanian public to be involved in the research. Response rates for case-control studies in this period were about 90% for cases and 80% for controls sampled from the electoral rolls, with comparable figures for cohort follow-up. In addition to our growing research effort we took on an important role in ensuring that knowledge was transferred to countries with less developed research capacity. The World Health Organization designated our institution as a Collaborating Centre for the Prevention of Cardiovascular Disease (CVD) a decade ago. That role has expanded steadily to the point where the Centre is assisting in studies on CVD in countries including Vietnam, Fiji and Samoa, where CVD and diabetes are producing an unexpectedly high disease burden. Genomics For the first seven years (1988-1995) the Centre focused solely on the environmental and lifestyle causes of disease. Meanwhile, others had been using the deep family pedigrees available in Tasmania to search for genetic causes of diseases following a Mendelian pattern of inheritance. Novel genes or linkages were discovered for several conditions, including multiple endocrine neoplasia and Huntington's disease. These successes were based on special features of Tasmania that are replicated in few other locations, namely (i) a population descended largely from identifiable founder families; (ii) comprehensive genealogical records; (iii) a modern healthcare system capable of identifying disease outcomes; (iv) a demonstrated capacity to involve the population in studies; and (v) organisational structures to facilitate the research. In 1995, David Mackey, a Tasmanian medical graduate and ophthalmologist at the Victorian Eye and Ear Hospital, approached us. He was undertaking important work in Tasmania on the more complex genetics of glaucoma. He wanted a base in Tasmania, and the Walter and Eliza Hall Institute, in Melbourne, was seeking a Tasmanian institution to manage new research and development syndicate funds to support his research. We accepted the role and our interest in the use of epidemiology to find genes for human diseases increased. Then, in 1996, the Australian pharmaceutical company AMRAD approached us about increasing its involvement in gene discovery in Tasmania through the Menzies Centre. We agreed, on the condition that the funding would be for a genetic unit that would employ people who could provide intellectual input to the work from a Tasmanian base. AMRAD signed a contract in 1997 for a five-year grant of $2.5 million, and, in 1998, we attracted Tasmanian molecular geneticist Michele Sale to coordinate the work. With financial and other help we were able to very quickly get projects under way in multiple sclerosis and osteoarthritis, and have continued to develop activity with Cerylid, a spin-off from AMRAD formed to operate its discovery arm. The genomics development has also led to an increase in postgraduate student training at the Centre, with five PhD students currently enrolled. The future During the past 12 months there have been several important developments for the Centre, driven by our very committed Board, chaired by Jean Trethewey, and strongly supported by the Dean of the Faculty of Health Science at the University of Tasmania, Allan Carmichael. The Tasmanian Government introduced an "Icons Program", which supports the Tasmanian Symphony Orchestra and our State cricket team. To this list Premier Jim Bacon added the Menzies Centre, with a commitment to provide $500 000 a year to help our organisation develop its capabilities. This, together with a large donation in 2000 from the United States-based Atlantic Philanthropies Inc, has placed us in a previously unimagined position to recruit more staff and drive our research program. To enable us to undertake these future developments with vigour, the University of Tasmania Council has established the Menzies Centre as an independent company limited by guarantee, remaining within the university structure. In 2002, the Centre will become the "Menzies Research Institute". Already, the Centre has grown to support a staff of 60. The new institute is likely to start 2002 with a budget of approximately $5 000 000 that will see staff numbers increase to more than 100, working on both environmental and genetic causes of disease. A major NHMRC grant of $2 290 000 over the next five years will enable us to study a cohort of Australians first measured as schoolchildren in 1985. They will be followed up for the emergence of adult disease, and it is anticipated this will provide the first direct evidence available on the impact of childhood lifestyle and biology on diseases such as coronary heart disease. A collaboration with similar cohorts in the US and Finland has already been established. A new director of the Cohort Studies Unit, Alison Venn, who has a strong background in this research strategy, has been recruited from the Centre for the Study of Mothers' and Children's Health at La Trobe University to coordinate developments. A large adult cohort study in Tasmania, with a focus on exposures that occur closer to the time of disease development, will also commence in 2002. Both studies will benefit from the input of a now-strong biostatistics group of three staff headed by one of our own PhD graduates, Leigh Blizzard. The level of genetic research activity will expand greatly. Tasmania presents opportunities as good as any in the world for gene discovery, and we intend to take up these opportunities. An increasing number of epidemiological studies at the Centre are focused on finding novel genes or validating candidate genes identified through animal or cell studies, or bioinformatic "data mining". This growth in activity reflects the recognition by commercial and government sources of the opportunities here, as well as the developing capacity of our genetic unit. Increasingly, our "environmental" epidemiologists and biostatisticians are developing their interests and skills in genetic research. This has not only led to the more rapid development of a critical mass for projects on gene discovery and validation, but has also opened up the possibility for in-depth investigation of gene-environment interaction. Projects with this focus are already under way in multiple sclerosis. There is great scope for us to contribute in an internationally significant way to the understanding of gene-environment interactions using Tasmania's unique population and our skill base. In the coming decade Australia will be relying more and more on its medical research institutes to maintain its competitive advantage in a knowledge-based global economy. We are confident that the new Menzies Research Institute will be making its contribution. References King H, editor. Epidemiology in Tasmania. Canberra: Brolga Press, 1987. Dwyer T, Ponsonby AL, Newman NM, Gibbons LE. Prospective cohort study of prone sleeping position and sudden infant death syndrome. Lancet 1991; 337: 1244-1247. Australian Bureau of Statistics. Deaths, Australia, 1990, 1998. Canberra: ABS, 1998. (Catalogue no. 3302.0/3303.0.) Ponsonby AL, Dwyer T, Gibbons LE, et al. Factors potentiating the risk of SIDS associated with the prone position. N Engl J Medicine 1993; 329: 377-382. Dwyer T, Ponsonby AL, Blizzard CL, et al. The contribution of changes in the prevalence of prone sleeping position to the decline in SIDS in Tasmania. JAMA 1995; 273: 783-789. Rothman K. Modern epidemiology. Boston: Little John and Co., 1986. Authors' details Menzies Centre for Population Health Research Terence Dwyer, MD, FAFPHM, Director. Reprints will not be available from the author. Correspondence: Professor T Dwyer, Menzies Centre for Population Health Research, 17 Liverpool Street, Hobart, 7000 TAS. t.dwyerATutas.edu.au Make a comment

Terence Dwyer

Fitness and fads The epidemiology of dog walking: an unmet need for human and canine health Adrian E Bauman, Schroeder J Russell, Susan E Furber and Annette J Dobson MJA 2001; 175: 632-634 Abstract - Main findings - Further interpretation using DogEpi concepts - Authors' details - - More articles on Psychiatry Abstract Objective: To describe the prevalence of dog walking in New South Wales, and to identify potential health gains if more dogs were walked. Design: Cross-sectional analytical survey. Setting and participants: 894 adults in NSW in 1998 (among the owners of approximately two million domestic dogs in NSW who were potential participants in dog-walking behaviours). Interventions: None yet. Main outcome measures: Dog walking hours per week; other DogEpi concepts to illustrate the public health gains include the DAF (dog attributable fraction), and the BBR (benefits to bites ratio). Results: The response rate to the survey was 74%. 46% of households in NSW had a dog and, overall, dog owners walked 18 minutes per week more than non-dog owners. However, more than half of dog owners did not walk their dogs, and were less likely than non-owners to meet recommended levels of physical activity sufficient for health benefits. If all dog owners walked their dogs, substantial disease prevention and healthcare cost savings of $175 million per year might accrue. Conclusions: There are potential benefits of dog walking for human health; currently, among dog owners, much of this benefit remains to be realised. There are also likely benefits for canine health. Dog walking should be promoted through national strategies recommending "Walkies for all by the year 2010". About half of all homes in Australia have a pet, with dogs being the most prevalent, reported in about 40% of all households; these rates are similar to United States estimates for dog ownership.1,2 Although most dogs are loved and well cared for by their owners, a key question is whether dogs might improve human health. The notion that dogs might promote good health has been explored elsewhere, with studies of the psychological companionship and supportive role of dogs, and the use of "dogs as therapy" for older, institutionalised adults.3,4 Other, small-scale studies have associated dog ownership with lower blood pressure, or even reduced re-infarction rates, among people with coronary heart disease.5,6 One area which has been less studied is the concept of dog walking, which provides physical activity for both dogs and people. Some surveys have proposed that people who own dogs are more active than those who do not,5,7 although this is not always the case.2,8 Nonetheless, this area has received much less attention than other pet-related research. This article focuses on the epidemiology of dog walking, which generally has been ignawed by researchers, and eschewed by epidemiologists. Hence this report cuts to the bone and unleashes an incisive public health argument for increasing dog walking in Australia. The primary research question was whether dog owners were more active than non-dog owners. In addition, the potential benefits of increased dog walking were estimated, using innovative DogEpi concepts. Methods This study was based on two population-based physical activity surveys carried out in New South Wales in March and November 1998.9 Respondents were adults, randomly sampled from the Electronic White Pages. Questions were asked about dog ownership, and the amount of time the respondent had spent walking his or her dog in the previous week. Standard physical activity questions about walking and moderate and vigorous physical activity in the previous week were also asked.10 The study variables were total time engaged in dog walking, any walking and total physical activity. Respondents were considered to have achieved "recommended levels of physical activity" for health benefit (150 minutes of at least moderate activity a week), based on the US Surgeon General's report.11 Analyses were carried out with SPSS,12 and included bivariate comparisons of proportions and means, and adjusted odds ratios using forced-entry logistic regression models to adjust for possible confounders. Results Main findings Of the 1208 adults approached, 894 (74%) responded. They were aged 25-64 years, with a mean age of 44.4 years (95% CI, 43.9-44.9 years). Almost half (45.6%) were male, 75% were married or had a partner, and 28% reported some tertiary education. Overall, 47.1% achieved the US Surgeon General's recommended 150 minutes of total physical activity per week, and 27% achieved this only through walking. About 46% of the sample reported that they had a dog at home. Among dog owners, the mean reported time allocated specifically for dog walking each week was 0.95 hours (95% CI, 0.77-1.13 hours per week), which was less than half of the average of two hours in total from all types of walking reported by dog owners each week (see Box). Among dog owners, 59% reported no dog walking, 26% reported up to 2.5 hours per week, and 15% reported at least 2.5 hours per week. The Box shows the mean time spent in physical activity according to dog ownership status. Those who owned dogs walked only 0.3 hours (about 18 minutes) more per week than non dog-owners. However, those who owned dogs and walked them less than one hour per week walked less, in total, than non dog owners (P = 0.01). Only those who walked their dogs for more than an hour per week walked significantly more or were significantly more active in total than non dog-owners. Further, the median number of walking sessions per week was 3.0 for both dog owners and non-owners (P = 0.98). All dog-walker categories were slightly less likely to reach the 150 minute per week "health-enhancing" threshold, except for those who walked their dogs for 2.5 hours. For overall physical activity, similar proportions of owners and non-owners achieved 150 minutes of total activity per week (46.9% and 47.3%, respectively), and dog owners who did not walk their dogs were significantly less likely to meet the guidelines. Only those who walked their dogs for at least an hour a week were more likely (odds ratio, 1.89) than non-owners to achieve sufficient physical activity for health benefits (Box). Further interpretation using DogEpi concepts This section describes innovative interspecies epidemiological approaches to understanding the data. DogEpi concepts are not meant to hound researchers, nor meant to be a golden (standard) retriever of epidemiological wisdom, but they are descended from the litter of current epidemiological thought, some of which is scatological. Firstly, the notion of dog walking to total walking ratio (DWTWR) and dog walking to total physical activity ratio (DWTPAR). The DWTWR, which is the percentage of all walking that was dog walking, was 22.9%. For 12% of the population, dog walking was half of their total walking. As a percentage of all physical activity, the DWTPAR was 13%, with 9% of the population doing at least half their total activity as dog walking. More important is the DAF (dog attributable fraction), which is an epidemiological estimate of the proportion of disease which might be prevented if all of the dog owners walked their dogs for at least 150 minutes per week. If this occurred, the population prevalence of sufficient physical activity would increase from 47% to 71%. Such an increase in physical activity would be about 5-10 times as great as most population-level interventions designed to promote activity.9 From this level of change in dog walking, and assuming a population-attributable risk of 18% for physical inactivity and coronary heart disease (CHD),13 it can be estimated that the maximal DAFcardiovascular is about 9% of the total burden of CHD. Other estimates of the DAF for diabetes and colon cancer, along with other health benefits of being active, including reduced doctor visits and medication costs, could be estimated in addition to this cardiovascular DAF. Direct healthcare cost savings can be estimated for specific increases in physical activity levels.13 A conservative estimate suggested that A$36 million might be saved annually for coronary heart disease for every 5% increase in the prevalence of adults who are "sufficiently active".13 Thus, if all dog owners walked their dogs more, this would be a 24% increase, resulting in direct healthcare cost savings of around $175 million per year. These savings would accrue rapidly, as cardiovascular risk reduction occurs sooner following the initiation of physical activity than after smoking cessation or dietary change.14 Nonetheless, it is important to calculate the other benefits and also the potential adverse effects and costs of keeping dogs as pets in Australia. The benefits of mental health improvement and stress reduction may be considerable, but are not used here in order to provide a conservative estimate of overall dog benefit. The adverse effects include the risks of zoonoses, but these are low. One public health issue is dog bites, which are estimated to cost $1.5 million in Victoria in direct healthcare costs.15 This is clearly an overestimate for the risks of dog walking, as only a quarter of dog bites occur in open space, roads or paths.16 However, we can use this overestimate to calculate a preliminary population health benefits to bites ratio (BBR) for the increased risk of dog bites and the risk reduction for heart disease to estmate the potential benefits versus risks of dog walking. We find that, even if only half of dog owners increased their dog walking to 150 minutes per week, then the resulting national savings of $87.5 million, divided by national dog bite costs of around $7 million, would give a very favourable cost benefit to bites ratio. Discussion In general, dog owners are not more active than non-owners, unless they practise regular, sustained dog walking. This article identifies the human health benefits of dog walking, and points to the need to encourage those with dogs to walk them more. It is possible that adults in the household other than the survey respondent also contributed to the time dogs are walked, so, from the canine perspective, our data could be an underestimate. Nonetheless, it would be a useful health-promotion strategy for inactive non-dog owners to acquire a dog in order to initiate regular moderate walking. There are reciprocal benefits for canine health -- from the dog's perspective, the amount walked is generally "never enough". This may be one way in which dog and human health might be improved, providing a biologically plausible explanation for the xeno-transmission of mortality gradients shared between pets and their owners, and described recently in the British Medical Journal.17Dog walking is an important potential benefit of dog ownership. As about half of adult Australians are physically inactive, and the public health benefits of being active are comparable to those of smoking cessation,18 dog walking should become widely recommended by human and canine health advocates alike. We should paws then, put our best feet forward, and take "man's best friend" for a walk more often. We advocate a campaign to promote "Walkies for all by the year 2010". Acknowledgements We thank NSW Health for data collection. Competing interests None declared. References Beck AM, Meyers NM. Health enhancement and companion animal ownership. Ann Rev Public Health 1996; 17: 247-257. Headey B. Health benefits and health cost savings due to pets: preliminary estimates from an Australian national survey. Soc Indicat Res 1999; 47: 233-243. Robb S, Stegman CE. Companion animals and elderly people — a challenge for the evaluation of social support. Gerontologist 1983; 23: 277-282. Francis GM, Turner J, Johnson S. Domestic animal visitation as therapy with adult home residents. Int J Nurs Stud 1985; 22: 201-206. Anderson WP, Reid CM, Jennings GL. Pet ownership and risk factors for cardiovascular disease. Med J. Aust 1992; 157: 298-301. Friedmann E, Thomas SA. Pet ownership, social support and one year survival after acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial (CAST). Am J Cardiol 1995; 76: 1213-1217. Serpell J. Beneficial effects of pet ownership on some aspects of human health and behaviour. J Roy Soc Med 1991; 84: 717-720. Simons LA, McCallum J, Simons J. Pet ownership and future health. Med J Aust 1997; 167: 231-232. Bauman AE, Bellew B, Owen N, Vita P. Impact of an Australian mass media campaign targeting physical activity in 1998. Am J Prevent Med 2001; 21: 41-47. Armstrong T, Bauman A, Davies J. Physical activity patterns of Australian adults (AIHW Catalogue No. CVD 10). Canberra: Australian Institute of Health and Welfare, 2000. US Department of Health and Human Services. Physical activity and health: a report of the Surgeon General. Washington DC: Department of Health and Human Services, Centers for Disease Control and Prevention, 1996. Statistical package for the social sciences [computer program]. Version 10. Chicago, Ill.: SPSS Inc, 2000. Stephenson J, Bauman A, Armstrong T, et al. The costs of illness attributable to physical inactivity. Canberra: Commonwealth Department of Health, 2000. Blair SN, Kohl HW III, Barlow CE, et al. Changes in physical fitness and all cause mortality: a prospective study of healthy and unhealthy men. JAMA 1995; 273: 1093-1098. Watson W, Ozanne-Smith J. The cost of injury to Victoria. Report No. 124. Melbourne: Monash University Accident Research Centre, 1997. Ashby K. Dog bites. Hazard no. 26. Victorian Injury Surveillance System. Melbourne: Monash University Accident Research Centre, 1996: 7-13. Moloo J, Waller JL, McKeown RE, et al. Xenotransmission of the socioeconomic gradient in health? A population based study. BMJ 1998; 317: 1686-1686. Mathers C, Vos T, Stevenson C. Burden of disease and injury in Australia. (AIHW Catalogue no. PHE 17). Canberra: Australian Institute of Health and Welfare, November 1999. (Received 15 Oct, accepted 2 Nov, 2001) Authors' details School of Public Health and Community Medicine, University of NSW, Sydney, NSW. Adrian E Bauman, PhD, FAFPHM, Professor of Public Health; Susan E Furber, PhD, Senior Lecturer. Strathfield, NSW. Schroeder J Russell, Canine Walking Advocate. School of Population Health, University of Queensland, Herston, QLD. Annette J Dobson, PhD, Professor of Biostatistics. Reprints: Professor A E Bauman, Epidemiology Unit, Hugh Jardine Building, Locked Mail Bag 7017, Liverpool BC 1871, NSW. Make a comment Walking and total physical activity time, and percentages meeting recommended physical activity levels, according to dog ownership and dog-walking status Total hours Achieved 150 minutes per week Category Number Walked per week (mean [95% CI]) Physical activity per week (mean [95% CI]) By walking only By total physical activity Adjusted odds ratio†(95% CI) Non-dog owner 484 1.7 (1.4-1.8) 3.3 (2.9-3.6) 121 (25.1%) 229 (47.3%) 1.0 (reference) Dog owner* 410 2.0 (1.8-2.2) 3.5 (3.1-3.8) 105 (29.7%) 191 (46.9%) 0.95 (0.72-1.23) Does not walk dog Walks dog up to 1 h/week Walks dog 1-2.5 h/week Walks dog > 2.5 h/week 240 33 73 61 1.3 (1.0-1.5) 1.3 (0.9-1.7) 2.2 (1.8-2.5) 5.0 (4.3-5.6) 2.5 (2.0-3.0) 1.9 (1.3-2.5) 4.1 (3.4- 4.8) 7.0 (6.0-8.1) 39 (16.3%) 5 (15.2%) 16 (21.9%) 45 (100%) 76 (31.7%) 9 (27.3%) 45 (61.6%) 61 (100%) 0.55 (0.39-0.77) 0.45 (0.2-1.01) 1.89 (1.1-3.1) n/a * Data on dog-walking time were missing for three dog owners. † Odds ratios for meeting the recommended physical activity guidelines, adjusted for age, sex, education, marital status. n/a = not available. 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Adrian E Bauman · Schroeder J Russell · Susan E Furber · Annette J Dobson

Fitness and fads Estimating historical changes in physical activity levels Garry J Egger, Neeltje Vogels and Klaas R Westerterp MJA 2001; 175: 635-636 Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Psychiatry Abstract Objective: To compare activity levels between a simulated "historical" lifestyle and a "modern" lifestyle to try to validate earlier estimates of secular changes in activity. Design: Triaxial accelerometers (TRACMORs) were used to measure activity levels in a "historical" group of seven male actors who were paid to live like early Australian settlers at a theme park north of Sydney (eg, minimising the use of modern technology) for a week. Results were compared with those from a group of seven "modern" sedentary office workers. Results: Activity levels were up to 2.3 times greater in the historical group than the modern group. Calculations based on body weight and energy expenditure suggest the difference is the equivalent of walking up to 16 km per day more in the past than today. Conclusions: These findings accord with two previous estimates of changes in daily activity levels over time and suggest that recent public health guidelines for increasing physical activity may be inadequate. An inactive lifestyle has been linked to a range of diseases, many of which are mediated through obesity.1 Intuitively, it seems apparent that average activity levels have decreased with modern industrial development and have mirrored the worldwide rise in obesity. Proxy measures of inactivity, such as the sale of motor vehicles and television viewing time, show a clear relationship to the development of obesity in the presence of a declining food intake. For this reason, some obesity experts suggest that the modern phase of the obesity epidemic (from 1980 onwards) is probably mediated more by inactivity ("sloth") than overconsumption ("gluttony"). However, the quantitative dimensions of a change in physical activity are difficult to estimate.2 If they could be (even roughly) determined, they might provide valuable information against which to assess modern physical activity guidelines for weight loss and maintenance. A "back of an envelope" calculation suggested an average decline in energy expenditure in the United Kingdom from the years after World War II to 1995 of around 800 kcal/d.3 At an energy cost of around 50 kcal/km for a 70 kg man,4 this suggests a decline in activity levels equivalent to walking about 16 km less per day. More recently, a comparison of activity levels of hunter-gatherer populations with those of individuals in modern Western societies suggested that the average daily difference may be equivalent to walking about 19 km.5 In an attempt to validate these estimates, we recently mocked up a small experiment for a lifestyle television production (Burke's Backyard). Our experiment was designed to compare activity patterns in Australian settlers of 150 years ago with modern-day sedentary office workers. We then attempted to calculate differences in terms of distance walked daily to compare with the previous estimates. Methods Movement levels were monitored in two groups of men by use of a triaxial accelerometer (TRACMOR, Maastricht University, Maastricht, the Netherlands) worn around the waist during waking hours. This has recently been validated against doubly-labelled water,6 and is regarded as one of the most sophisticated modern ambulatory measurement monitors. The device measures movement in activity units on three axes (forwards, sidewards and upwards), and includes even relatively minor movements such as fidgeting and upper-body actions. Seven male actors aged 30-60 years who work at "Old Sydney Town", a historic theme park north of Sydney set around the early 19th century, were selected to represent a historically active group. The men are paid to play the role of early Australian soldiers, convicts and settlers for about eight hours every day. They agreed to wear a TRACMOR during waking hours for one week, and were asked to avoid the use of modern technology as much as possible when they were not working at the park during the week. In an attempt to further authenticate this process, five of the men lived on the premises in convict huts for up to four days and nights. A second group of seven male modern sedentary workers, aged 30-60 years, including accountants, information technology personnel, doctors, a taxi driver and an entertainer, were also given TRACMORs to wear during waking hours, and were asked to continue their normal lifestyle over the course of a week. All records were downloaded into a computer program developed by the developers of the TRACMOR at Maastricht University in the Netherlands for analysis of results. Results The mean activity level (arbitrary units) for the historical group was 88 533 (95% CI, 33 697-143 369; range, 62 204-129 924), compared with 54 920 (95% CI, 32 019-77 821; range, 38 322-70 399). Thus, the historical group were on average 1.6 times more active than the modern group. However, the task was taken more seriously by some in the historical group than others (eg, some still used cars and televisions to some extent during the week). Hence, the two main outliers in the group, who kept rigidly to the experimental requirements, may provide a better reference point for calculations. These two individuals (with activity levels of 129 924 and 125 800 units) were 2.3 times more active than the modern group. Using estimates derived from energy expenditure tables (see Box), it was calculated that the difference in activity levels between the means of the two groups was equivalent to walking about 8 km per day. However, when the two outliers in the historical group were compared with the mean of the modern group, the difference was equivalent to walking about 16 km per day. Discussion A difference in daily activity levels equivalent to walking 8-16 km per day between previous and modern times represents a huge secular change in daily energy expenditure. At the upper level, this coincides roughly with previous estimates.3,5 It probably also accords with the levels of movement required for foraging for survival throughout most of human evolution. Anthropological evidence suggests that early humans, like modern hunter-gathers, may have transported tools, weapons and game over a daily range of about 15 km.8 Given their other daily tasks, this would have added up to a substantial daily energy use which was rarely, if ever, likely to be exceeded by food intake over an extended period, thus reducing the chances of energy imbalance. As a result, human populations, up until the past 2-3 decades, have not been significantly overweight. The growth of time-saving and time-using technologies,9 however, means that these activity levels are unlikely ever to be reached without conscious effort. In the presence of an abundant (and energy-dense) food supply, obesity, at least at the population level, is almost an inevitable consequence of modernisation. More telling are the implications this has for physical activity recommendations for optimal health and weight management. Recent government recommendations suggest an added daily energy requirement of 30 minutes of accumulated mild- to moderate-intensity activity.10,11 However, for a 96 kg sedentary office worker, such as in this study, this would account for perhaps an extra 200 kcal/d, which is 300-800 kcal (the equivalent of walking 5-13 km) short of the 500-1000 kcal difference estimated here. These findings support the suggestion that, if the evolutionary perspective (which has dominated almost all of human existence) is indicative of requirements for optimal health, an increase in activity levels up to three times those recommended in modern guidelines may be necessary.5 Supporting this, data from the United States Weight Control Registry, a database of people who have lost more than 14 kg and maintained this for at least five years, have shown that people who achieve the greatest benefits are consciously active for up to 80 minutes a day.12 This is about three times greater than current recommendations.10,11 These figures are based on people who have been previously obese, and maintenance of weight loss may be more difficult than prevention of weight gain. Nevertheless, it is an awesome task, in the absence of a major environmental change, to expect these activity levels to be met in our society. The figures presented in this study should be interpreted with caution. Although we used a validated modern movement-sensing device,13 the results involve only small numbers under artificial conditions. In their present form, they merely add support to other attempts to calculate human activity levels over time and provide an indication of the activity requirements needed to correct these secular changes. References Powell KE, Blair SN. The public health burdens of sedentary living habits: theoretical but realistic estimates. Med Sci Sports Exerc 1994; 26: 851-856. Prentice A, Jebb S. Obesity in Britain: Gluttony or sloth? BMJ 1995; 311: 437-439. James WPT. A public health approach to the problem of obesity. Int J Obes Relat Metab Disord 1995; 19: S37-S45. Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc 2000; 32 (9 Suppl): S498-504. Cordain L, Gotshall RW, Eaton SB. Physical activity, energy expenditure and fitness: an evolutionary perspective. Int J Sports Med 1998; 9: 328-335. Bouton C, Verboeket-van de Venne WP, Westerterp KR. Physical activity assessment: comparison between movement registration and doubly labelled water. J Appl Physiol 1996; 81: 1019-1026. Movahedi A. Simple formula for calculating basal energy expenditure. Nutr Res 1999; 19: 989-995. Gowlett J. Mental abilities of early man: a look at some hard evidence. In Foley R, editor. Hominoid Evolution and Community Ecology. New York: Academic Press, 1984; 167-192. Bowden S, Offer A. Household appliances and the use of time: the United States and Britain since the 1920s. Econ Hist Rev 1994; XLVII: 725-748. United States Surgeon General. Physical activity and health: a report of the Surgeon General. US Department of Health and Human Services. Atlanta: Centers for Disease Control, 1996. Egger G. National physical activity guidelines for Australians: scientific background report. Canberra: Commonwealth Department of Health and Aged Care, 1999. Klem ML, Wing RR, McGuire MT, et al. A descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am J Clin Nutr 1997; 66: 239-246. Westerterp K. Pattern and intensity of physical activity. Nature 2001; 410: 539. (Received 25 Sep, accepted 22 Oct, 2001) Authors' details Deakin University, Melbourne, VIC, and GutBusters Pty Ltd, Sydney, NSW. Garry J Egger, MPH, PhD Adjunct Professor of Health Sciences. Masstricht University, The Netherlands. Neeltje Vogels, BBiolSc Student; Klaas R Westerterp, PhD, Professor of Human Energetics, Department of Biological Sciences. Reprints will not be available from the authors. Correspondence: Professor G J Egger, PO Box 313, Balgowlah, NSW 2094. eggergjATozemail.com.au Make a comment Calculation of distance equivalents Activity units measured by the TRACMOR are not readily convertible to energy units (kilocalories). However, an estimate of relative differences in activity levels can be made by assuming a total daily energy expenditure 1.4 times that of resting metabolic rate for the men in our modern group.5 With an average weight of 96 kg and age of 44 years, a mean resting metabolic rate of about 2000 kcal/d can be estimated.7 Therefore, total energy expenditure would be 1.4 x 2000 = 2800 kcal/d, of which 800 kcal represents daily physical activity. As activity counts in our historical group ranged from 1.6 times those of the modern group on average to 2.3 at the extremes, this implies a total daily physical activity level in this group of 1280-1840 kcal/d, or a net difference of about 500-1000 kcal/d between the groups. Using energy values for walking of 0.716 kcal/kg per kilometre (or about 61 kcal/km for a 90 kg man),4 this implies a net difference between the groups equivalent to walking about 8-16 km per day. Back to text

Garry J Egger · Neeltje Vogels · Klaas R Westerterp

Bites and stings Outbreak of caterpillar dermatitis caused by airborne hairs of the mistletoe browntail moth (Euproctis edwardsi) Caterpillars may be an under-recognised cause of skin and eye reactions. We report a four-month outbreak of recurrent papulourticarial rash among staff and visitors at a community centre. The cause was eventually diagnosed as airborne hairs from caterpillars of the mistletoe browntail moth (Euproctis edwardsi), which infested a eucalypt tree growing in front of the centre. To our knowledge, this is the first clear case of airborne caterpillar hairs causing dermatitis in an indoor environment. Corrine R Balit, Helen C Ptolemy, Merilyn J Geary, Richard C Russell and Geoffrey K Isbister MJA 2001; 175: 641-643 Clinical records - Discussion - Acknowledgements - References - Authors' details - - - More articles on Informatics and computers Lepidopterism refers to adverse effects from moths and butterflies (Lepidoptera), the most common arising from skin and eye contact with caterpillar hairs or spines.1 The pattern of reaction varies between caterpillar types.2 Caterpillar dermatitis can result not only from direct contact with the caterpillar, but also from airborne caterpillar hairs.3,4 Caterpillar dermatitis is probably far more common than previously realised.1,3,5-10 Patients often present with a rash of unknown origin, and the association with caterpillar exposure is often not recognised. We report an outbreak of caterpillar dermatitis related to an infestation of the caterpillar Euproctis edwardsi (Family: Lymantriidae), commonly known as the mistletoe browntail moth. The infestation occurred at a community centre, where staff and visitors experienced dermatitis and skin irritation for several months before caterpillar dermatitis was diagnosed. To our knowledge, these are the first clear cases of dermatitis caused by airborne caterpillar hairs in an indoor environment. Clinical records In February 2001, the Wentworth Public Health Unit, Sydney, NSW, was contacted about a local community centre where both staff and clients had been experiencing skin reactions and irritation. Seven of the 14 employees of the centre were affected, as were about 5% of clients seen at the centre. The reactions began in November 2000 and appeared while people were at the centre. They would settle or resolve while people were away from the centre on weekends and holidays and recur on their return to work. The skin reactions comprised a papulourticarial rash. Clinical effects in six patients are shown in Box 1, and further details of one patient in Box 2. The centre had been sprayed against a variety of pests on several occasions, without benefit. Each time, the pest control company reported no visible evidence of insects in the centre. Many staff sought medical advice, and various treatments were prescribed, including topical corticosteroids and oral antihistamines, with no benefit. The site was inspected by the Environmental Health Officer of the Population Health Unit (H C P). In front of the centre was an ironbark tree (Eucalyptus sideroxylon) which contained a mistletoe plant and, at its base, a large clump of caterpillars (pictured above). The tree was growing adjacent to the mail box, about 3 m from the front door of the centre and the window of the upstairs lunchroom, and 10 m from the intake vent of the air-conditioning system. Caterpillar samples were identified at the Department of Medical Entomology, Westmead Hospital, Sydney, as E. edwardsi, commonly known as the mistletoe browntail moth. Caterpillar-like hairs were also identified in samples of dust from inside the centre. Based on reports of successful use of sticky tape to sample affected areas for nematocysts in jellyfish stings,11 this method was tried on three affected individuals. Transparent sticky tape was applied to the affected area and then placed onto a glass slide. Caterpillar-like hairs were identified from two of the three people thus tested (Box 3). The caterpillars were treated with insecticide and removed along with the mistletoe, according to the recommendations of the environmental health officer. Although the officer also recommended re-inspection of the tree and removal of any mistletoe regrowth the following spring, the centre eventually removed the tree completely. The building was thoroughly cleaned to remove all caterpillar hairs. Follow-up of people at the centre a month later showed significant improvement in their conditions. Occasional episodes of skin irritation in two people were successfully treated by immediate application of sticky tape to the affected areas. Follow-up after six months revealed no further reports of irritation. Discussion This is the first case series that clearly demonstrates dermatitis resulting from airborne caterpillar hairs in an indoor environment. Although the cause of the dermatitis was not identified for months, once found treatment was straightforward — removal of the caterpillars and their food source to prevent re-exposure. We also demonstrated the usefulness of the sticky-tape technique in diagnosing, as well as treating, caterpillar dermatitis by removing caterpillar hairs from the skin.1E. edwardsi is reported to be the most important cause of caterpillar dermatitis in Australia.1 It occurs from Queensland to South Australia and is widely distributed in south-eastern Australia.12 Its food source is usually Amyema species of mistletoes.1 The incidence of caterpillar dermatitis peaks between December and March,3 with two generations of the moth each year, in early summer and autumn.1 The fully grown caterpillar is about 4 cm long and has golden tufts of spicules on its back. These spicules easily separate from the caterpillar, causing irritation on skin contact. The most common reaction is a papulourticarial rash, usually on exposed skin, but possibly more extensive if clothing is contaminated.1 The hairs are small enough to become airborne and affect people without direct contact with the caterpillar. In patients presenting with skin reactions and dermatitis of unknown cause, particularly recurrent rash, a careful history of location and seasonality is required. Caterpillar dermatitis should be considered in the differential diagnosis and can be confirmed by identifying the source of the caterpillar or its hairs. Microscopy of sticky-tape samples from the affected area may aid diagnosis. The use of sticky tape has been reported previously as a treatment option in caterpillar exposures, to remove fine hairs that may cause ongoing symptoms.5 This is the first report demonstrating the use of sticky tape as a simple and effective diagnostic tool. Once the source of exposure has been removed, treatment of caterpillar dermatitis is essentially symptomatic and supportive. Patient 1 allowed several treatment options to be assessed. Most effective was topical aspirin paste, with improvement within hours. Topical aspirin has previously been reported to be effective for histamine-induced rash.13 The paste is made by adding a few drops of water to a soluble aspirin tablet and applying it to the affected area. A topical preparation containing lignocaine offered some symptomatic relief but did not shorten the duration of symptoms. A topical hydrocortisone cream produced no noticeable change. Outbreaks of caterpillar dermatitis are not uncommon and may be difficult to diagnose. Sticky-tape sampling of the affected area may aid diagnosis. Topical aspirin paste appears an effective treatment, and topical lignocaine preparations and oral antihistamines may provide partial symptomatic relief. Acknowledgements We thank Dr James Isbister (Royal North Shore Hospital, Sydney, NSW) for providing digital images of the sticky tape slides and Mr Stephen Doggett (Department of Medical Entomology, ICPMR, Westmead Hospital) for taking the clinical photograph. We also thank Judith Kirby and all the staff at the NSW Poisons Information Centre for their support and assistance. References Southcott RV. Lepidopterism in the Australian region. Records of the Adelaide Children's Hospital 1978; 2: 87-173. Isbister GK, Whelan PI. Envenomation by the billygoat plum stinging caterpillar (Thosea penthima). Med J Aust 2000; 173: 654-655. Thompson JI. Mistletoe brown tail moth - a skin irritation caterpillar. AGFACTS. Sydney: NSW Department of Agriculture, 1984. Southcott RV. Some harmful Australian insects. Med J Aust 1988; 149: 656-662. Dunlop K, Freeman S. Caterpillar dermatitis. Australas J Dermatol 1997; 38: 193-195. Scholz A, Russell R, Geary M. Investigation of caterpillar dermatitis in school children. NSW Public Health Bull 1993; 4: 65-66. Blair CP. The browntail moth, its caterpillar and their rash. Clin Exp Dermatol 1979; 4: 215-222. Cleland JB. Papulo-urticarial rashes caused by the hairlets of caterpillars of the moth (Euproctis edwardsi Newm.). Med J Aust 1920; 1: 169-170. McKeown KC. Australian insects. An introductory handbook. Sydney: Royal Zoological Society of NSW, 1942. Lee D. Arthropod bites and stings and other injurious effects. Sydney: School of Public Health and Tropical Medicine, University of Sydney, 1975. Currie BJ, Wood YK. Identification of Chironex fleckeri envenomation by nematocyst recovery from skin. Med J Aust 1995; 162: 478-480. Musgrave A. Harmful moth caterpillars. Aust Museum Mag 1941; 7: 391-396. Yosipovitch G, Ademola J, Lui P, et al. Topically applied aspirin rapidly decreases histamine-induced itch. Acta Derm Venereol 1997; 77: 46-48.(Received 14 Jun, accepted 27 Sep, 2001) Authors' details NSW Poisons Information Centre, The Children's Hospital, Sydney, NSW. Corrine R Balit, BPharm, Pharmacist. Wentworth Population Health Unit, Sydney, NSW. Helen C Ptolemy, BAppSci, Environmental Health Officer. Department of Medical Entomology, ICPMR, Westmead Hospital, Sydney, NSW. Merilyn J Geary, DipAppSci, PestContCert, Laboratory Manager; Richard C Russell, MSc, PhD, Director, and Associate Professor, University of Sydney, NSW. Department of Clinical Toxicology and Pharmacology, Newcastle Mater Misericordiae Hospital, Newcastle, NSW. Geoffrey K Isbister, BSc, MB BS, Toxicology Registrar. Reprints will not be available from the authors. Correspondence: Ms Corrine R Balit, NSW Poisons Information Centre, The Children's Hospital, Locked Bag 4001, Westmead, NSW 2145. CorrineBATchw.edu.au Make a comment 1: Details of six people who developed a papulo-urticarial rash at the community centre Patient (sex, age in years) Affected areas Duration of rash Sticky tape sample 1. Staff (M, 24) Arms, legs Recurrent, Nov-Feb Positive 2. Staff (F, 26) Face, legs, hands, stomach Recurrent, Nov-Feb Negative 3. Staff (F, 38) Arms, chest, neck Recurrent, Nov-Feb Positive 4. Staff (F, late 30s) Arm, chest, face Recurrent, Nov-Feb Not available 5. Visitor (F, 23) Neck, chest, face, arms 5 days Not available 6. Visitor (F, 32) Neck, chest 24 hours Not available F = female. M = male. Back to text 2: Severe reaction to caterpillar hairs (Patient 5) A 23-year-old woman developed a moderately severe reaction after visiting the community centre for an hour. She had a past history of atopy, asthma and mild atopic dermatitis. On examination, exposed areas were affected, including the forehead, face, neck, upper chest and lower arms. The reaction began as an itchy red area within six hours of exposure, and over the next 24 hours developed into a papulourticarial rash with intense pruritus (pictured 24 hours after exposure). Initial dizziness and light-headedness were the only systemic effects. A number of treatments were tried in different affected areas, including topical hydrocortisone (1%), a topical combination of lignocaine, bufexamac and chlorhexidine, topical aspirin paste, and sedating and non-sedating antihistamines. Areas treated with aspirin paste showed marked improvement over four hours. Topical lignocaine and sedating antihistamines provided symptomatic relief, but other treatments produced minimal responses. The rash cleared completely over five days. Back to text 3: Caterpillar hairs from Patient 1 Sticky-tape sample from an area of papulourticarial rash in Patient 1, showing a human hair (centre) surrounded by numerous smaller, caterpillar-like hairs (original magnification, x 20). Inset shows a control slide of hairs from the caterpillar Euproctis edwardsi (original magnification, x 40). Back to text

Corrine R Balit · Helen C Ptolemy · Merilyn J Geary · Richard C Russell · Geoffrey K Isbister

Hazards and help in communications Books as carriers of disease In the early years of bacteriology, librarians, microbiologists and public health physicians were much exercised by the question of whether books could transmit infectious diseases. Mark J Ferson MJA 2001; 175: 663-664 Surveys and experiments on transmission - Attempts to sterilise books - Public health responses - Australian responses - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Given the current concern about transmission of anthrax spores via the mail, it may be instructive to revisit early research on whether books can transmit other infectious diseases. As the theory of spontaneous generation gave way to ground-breaking discoveries in the new science of bacteriology by Pasteur, Lister, Koch and others,1 it was perhaps not surprising that this question was posed at an 1879 meeting of librarians in Chicago.2 Although there was no evidence that bibliophiles had ever expressed a "fear of books as vehicles of pestilence",3 the question seemed to exercise greatly the minds of librarians, microbiologists and public health physicians, and numerous articles were published on the subject in medical and library journals over the succeeding 60 years. These articles sought to determine whether books could transmit infectious diseases and how library books could best be sterilised without damage. Surveys and experiments on transmission An early survey of United States boards of health elicited some notable and bizarre cases of infectious diseases acquired from books.4 These included scarlet fever transmitted by a book in which a young sufferer had inserted strips of his peeling skin as bookmarks, diphtheria in two children acquired through handling school books from a farmhouse where six cases of the disease had occurred 42 years previously, and smallpox in a man who borrowed books from a circulating library in a neighbouring town affected by a smallpox epidemic.4An 1896 issue of The Lancet drew attention to a French study demonstrating isolation of streptococci, pneumococci and Corynebacterium diphtheriae, but not Salmonella typhi or Mycobacterium tuberculosis, from books soiled with the secretions of infected patients.5,6 However, the obviously cynical author felt that fear of contagion would be insufficient to drive readers to buy rather than borrow books.5 A later study found that washings from library books which had been borrowed by people with tuberculosis failed to transmit infection when inoculated into the peritoneal cavity of guinea pigs.7 Attempts to sterilise books A 1911 report sought alternatives to gaseous methods of disinfection, which are unable to penetrate closed books, and to steam, which damages books. Immersing books for 20 minutes in petrol containing 2% carbolic acid sterilised all inoculated cultures of C. diphtheriae, S. typhi, Escherichia coli and Staphylococcus aureus, but did not reliably destroy the infectivity of books contaminated with sputum containing M. tuberculosis.8 Thankfully, the author provided a recipe for a mixture of essential oils to hide the strong odours of petrol and carbolic acid and, perhaps rather obviously, exhorted the reader "to keep . . . the book until dry away from the fire". The following year, an evidence-based review was published, drawing on references in English, German, Italian and French.9 On balance, formalin vapour was concluded to be ineffective, as the gas cannot penetrate the pages of a closed book. The author was unable to replicate the results of the previous study on petrol and carbolic acid, but supported earlier studies showing that the application of hot, moist air (78º-80ºC and 30%-40% humidity) to closed books for 32 hours destroys non-sporing bacteria and mycobacteria without injuring the books. For those not requiring immediate results, several studies found that storing books for a month in a warm, dry room minimised risk of transmission of tuberculosis,7,10 streptococci11,12 and staphylococci.12 Finally, there was concern about the lack of knowledge of virus survival, with a clear statement that books used by a smallpox sufferer should be burned.13 Public health responses In Britain, the government introduced specific provisions into public health legislation through the Public Health Act Amendment Act 1907. This required that a library book borrowed by a member of a household with a notifiable disease be returned to the local authority for disinfection or destruction, with failure to do so attracting a fine of up to £2. These provisions were continued in later versions of the Public Health Act and remain in force today. As the local authority was required to compensate the library for destroyed books, there was some incentive to disinfect them. However, well after introduction of the legislation, discussion continued among members of the Society of Medical Officers of Health as to whether books could transmit infectious diseases,14,15 with much difference of opinion. Australian responses In Australia, public health legislation does not specifically refer to libraries but does mention books. Regulations in the Victorian Health Act 1890 for preventing spread of contagious diseases require that "The room occupied by the patient . . . in all cases, whenever possible, all hangings . . . shall be removed, together with books . . . and sunshine and fresh air in current allowed full play."16 On the other hand, 1896 guidelines provided by the New South Wales Department of Public Health for householders concerned about diphtheria or scarlet fever stated that the "only articles which must always be burnt are books, papers and toys; they cannot be safely disinfected".17,18 Public health laws of the other States made no reference to books. This lack of official guidance did not prevent libraries making their own rules about the handling of books borrowed by individuals with infectious diseases. The clearest manifestation of this concern was the fashion for private lending libraries, particularly in Melbourne, to promote themselves as "hygienic" (Box) because of their practice of placing books in cabinets with formalin vapour (Dr Richard Travers, Rheumatologist, Royal Melbourne Hospital, VIC, personal communication, Sep 2001). This was despite the fact that formalin vapour had already been shown to be an ineffective disinfectant of books. By the 1950s and 1960s, the proliferation of public libraries had largely killed off private lending libraries, and the declining risk of infectious diseases and consequent public interest meant that the concept of books as transmitters of disease was no longer worthy of serious consideration. Acknowledgements I wish to thank Brenda Heagney and Donna Mendrawi of the History of Medicine Library of the Royal Australasian College of Physicians, Sydney, for assistance in obtaining historical references. References Lechevalier HA, Solotorovsky M. Three centuries of microbiology. New York: Dover, 1974. McClary A. Beware the deadly books: a forgotten episode in library history. J Library History 1985; 20: 427-433. Winterich JT. A primer of book-collecting. Revised edition. New York: Greenberg, 1935: 114-120. Reinick WR. Books as a source of disease. Am J Pharm 1914; 86: 13-25. Books as disseminators of disease. Lancet 1896; 1: 180. From our own correspondent. Paris. Lancet 1896; 1: 388. Kenwood H, Dove EL. The risks from tuberculous infection retained in books. Lancet 1915; 2: 66-68. Beebe WL. Carbo gasoline method for the disinfection of books. J Am Public Health Assoc 1911; 1: 54-60. Nice LB. The disinfection of books. Bull Med Library Assoc 1912; 1: 61-66. Smith CR. Survival of tubercle bacilli in books. Am Rev Tuberculosis 1942; 46: 549-559. Balmain AR. Recovery of Streptococcus scarlatinae from experimentally infected books. Lancet 1927; 2: 1128. Smiley HE. Books — shall they be sterilized? Rhode Island Med J 1933; 16: 5-6. McCartney JE. Infection by books. Lancet 1925; 2: 212. Society of Medical Officers of Health. Home Counties Branch. Public Health 1923-24; 37: 265-266. Society of Medical Officers of Health. North Western Branch. Public Health 1923-24; 37: 295-296. Cole HS, Morris H. The Health Act, The Infant Life Protection Act, The Margarine Act, with regulations, notes of English cases and index. Melbourne: Charles F Maxwell, 1894. Department of Public Health, New South Wales. Suggestions to householders for the prevention of scarlet fever (or scarlatina), on the domestic isolation and disinfection, and on the law on infectious diseases. (Public Health Act, 1896, part III.). Sydney: WA Gullick, Government Printer, 1898. Department of Public Health, New South Wales. Suggestions to householders for the prevention of diphtheria, on the law on infectious diseases, and on isolation and disinfection. (Public Health Act, 1896, part III.) Sydney: WA Gullick, Government Printer, 1898.(Received 23 Oct, accepted 29 Oct, 2001) Authors' details South Eastern Sydney Public Health Unit, Sydney, NSW. Mark J Ferson, MD, FRACP, FAFPHM, Director, and Conjoint Associate Professor, School of Public Health and Community Medicine, University of New South Wales, Sydney, NSW. Reprints will not be available from the author. Correspondence: Dr M J Ferson, South Eastern Sydney Public Health Unit, Locked Bag 88, Randwick, NSW 2031. fersonmATsesahs.nsw.gov.au Make a comment Bookplate for Stinton's Hygienic Library, Moonee Ponds, Melbourne, VIC, circa 1940s. Back to text

Mark J Ferson

Indigenous Health Household infrastructure in Aboriginal communities and the implications for health improvement Ross S Bailie and Myfanwy J Runcie MJA 2001; 175: 363-366 Abstract - Methods - Results - Discussion - Competing Interests - Acknowledgements - References - Authors' details - - - More articles on Aboriginal health Abstract Objective: To evaluate housing survey data, describe the state of household infrastructure in Aboriginal communities in the Northern Territory (NT), and to discuss implications for health improvement for people in these communities. Design: Quantitative analysis of survey data and qualitative analysis of the survey process. Setting: All NT houses funded for repairs and maintenance through the Indigenous Housing Authority of the Northern Territory (IHANT). Main outcome measure: Status of infrastructure necessary for four key "healthy living practices" (washing people, washing clothes and bedding, waste removal, and food storage and preparation). Results: 3906 houses (79% of all houses funded by IHANT) were surveyed. Infrastructure components most frequently identified as not functional or not present were those required for the storage and preparation of food (62% not functional). The facilities required for personal hygiene and safe removal of human waste were not functional in 45%-46% of houses. Conclusions: These findings highlight the significance of absent or non-functioning household infrastructure as a potential contributory factor in the poor nutritional status and high rates of respiratory, skin and gastrointestinal infections in Indigenous communities. The environmental health and housing survey in the NT is an important tool for monitoring progress on addressing a key underlying determinant of the health of Indigenous people, and potentially for facilitating research aimed at gaining an improved understanding of the relationship of the household environment to health in Indigenous communities. The most significant improvements in health in industrialised countries over the past two centuries have been attributed to improvements in living and working conditions. Adequate and safe water supply, sanitation, housing, nutritious food, waste disposal, drainage and crowding have all been shown to influence health.1,2 A number of Australian studies have described the inadequacy of housing and the association between the poor living environment and poor health in the Indigenous population.3-6The National Aboriginal Health Strategy, through the establishment of the Health Infrastructure Priorities Projects in 1993 and 1994 and the Environmental Health Program in 1996, provided for large-scale infrastructure development in communities where this would have maximal impact on health. Projects included ensuring adequate water supply, sanitation, housing and drainage, providing internal roads, and dust management.7 The Indigenous Housing Authority of the Northern Territory (IHANT) was established to ensure a coherent housing strategy, with a specific mandate to facilitate planning and allocation of housing programs and to increase Aboriginal consultation, self-determination and self-management. The NT Government Environmental Health Task Group has published Environmental Health Standards for remote communities in the NT that define a minimum set of functional components of household infrastructure for the building and maintenance of houses.8 These standards are based in part on work done in central Australia by the HealthHabitat group in defining a set of "healthy living practices". As the program manager for IHANT, the NT Department of Local Government introduced an annual Environmental Health Survey (EHS) in 1998. Important points in the background to the survey are presented in Box 1. The Menzies School of Health Research was contracted to evaluate the first round of survey data, with a view to advising on improvement in the conduct of the survey and reporting on the current status of housing in the NT.9 We report the findings of this evaluation. Methods The survey methods are described in detail in the survey evaluation report.9Briefly, the survey aimed to cover all houses funded by IHANT, and included all communities in the NT, including remote settlements and communities near or within the boundaries of towns and major centres. Surveys were conducted primarily by environmental health officers of Territory Health Services or community development officers of the Department of Local Government. A number of surveys were also conducted by Aboriginal environmental health workers or other community workers under the direction of the environmental health officers and community development officers, with the intention of ultimately handing over responsibility for the survey to community housing organisations. The survey form included components of infrastructure specified as essential in the Environmental Health Standards,8 with each component scored according to its presence or absence, and, if present, its condition and the level of maintenance required to render it fully functional. The data were entered into a database managed by the Department of Local Government. Evaluation and data analysis The design and conduct of the survey were examined through documentary evidence (held by the Department of Local Government); interviews with the project manager, field officers and database operators; and examination of the database. The data within the database were checked for data entry errors and completeness. Errors were corrected and a subset of the data containing observations for houses with entries in most data fields was downloaded and analysed using SPSS statistical software.10The proportions of houses for which each infrastructure component specified on the survey form was adequately functional (required no or minor repairs only), was not functional (required major repairs or replacement), was not present or for which data on that component were missing were calculated. Of the nine healthy living practices described by Pholeros et al,4 four that are directly dependent on components of household infrastructure examined in this survey were identified. These were washing people, washing clothes and bedding, waste removal, and food storage and preparation. A set of infrastructure components required to allow the effective conduct of each of these four healthy living practices was defined, and the four healthy living practices were expanded to six for the purpose of the analysis, as shown in Box 2. The proportion of houses which had all the infrastructure components required for each practice recorded as functioning was calculated, both overall and for individual communities with 10 or more houses included in the survey. Ethical approval This article is based on data collected primarily for the purposes of housing management and planning rather than for research. No individuals or communities are identified, so there are no issues relating to confidentiality or privacy that require ethical approval for publication. Results Complete data were recorded for 3906 (79%) of a total 4936 houses funded by IHANT. A number of inadequacies in survey conduct and quality control were found. These stemmed primarily from a lack of or inadequate protocols for the conduct of the survey and from inadequate training of surveyors. These inadequacies resulted in inconsistencies in identifying the most appropriate respondent for the survey, and in questioning, inspection and testing of infrastructure components, and may have restricted the survey coverage.9 The components of infrastructure most frequently identified as not functional or not present were the kitchen bench, the stove top and the oven (26%, 41%, and 42%, respectively) (Box 3). The cold water taps and supply to the kitchen sink, shower and laundry were clearly identified as functional in between 76% and 81% of houses. In the bathroom, 30% of houses were identified as having no functioning cold water taps, and 32% as having no functional basin. Hot water taps were functional in the laundry in 68% of houses, and in the shower in 74%. However, the hot water service was functional in only 62% of houses, not functional in 11% of houses and absent altogether in 14%. Electricity supply to switches, power points and lights was functional in different rooms for 72%-79% of houses. Between 63% and 78% of houses had the general structure of the kitchen, laundry, bathroom, bedroom, main toilet, exterior doors and windows and house exterior recorded as functional and not a threat to safety. The general structure was least commonly identified as functional or safe in kitchens. Forty-two per cent of houses were clearly identified as having a functioning refrigerator, 19% had functioning air-conditioning or evaporative cooling and 41% had a functioning washing machine. Thirty-three per cent had a functional fence around the boundary. The proportion of surveyed houses for which the components required to effectively conduct each of the six key "healthy living practices" ranged between 38% and 69%. Those components required for preparing and storing food were least likely to all be in a functional state and those required for removal of rubbish were most likely to be available (Box 2). The proportion of houses that had functioning infrastructure for conducting each of the healthy living practices varied widely between communities. In some communities, and for some healthy living practices, none of the surveyed houses had the required infrastructure functioning, whereas in other communities all of the surveyed houses had the required infrastructure functioning (Box 2). In 13% of all communities where 10 or more houses were surveyed, more than 50% of surveyed houses had the functional amenities to allow all six of the key healthy living practices (Box 4). In 44% of communities 50% of surveyed houses had functional infrastructure components necessary for three or less of the healthy living practices. Discussion Our analysis of the survey data describes for the first time the poor state of household infrastructure in Indigenous communities at a detailed level and across a wide jurisdiction. The findings confirm the poor state of housing previously described at a more localised level.4,5,11 Certain types of infrastructure are commonly in a poor state of repair, most notably the facilities for storage and preparation of food. This is of particular concern in light of the high rates of gastrointestinal infection, undernutrition and obesity in children and obesity in adults,12-14 the associated high rates of "lifestyle"-related disease among people living in these communities, and the now widely accepted evidence of the role of fetal nutrition in the development of chronic disease in adulthood.15 (We recognise that lifestyle is strongly determined by the social, cultural and physical environment.) The poor state of housing and access to adequate facilities for washing have been identified as key underlying factors in the high levels of morbidity and mortality from bacterial respiratory tract infections, and the significant contribution of such infections to the generally poor state of health of many Indigenous Australians.16 Providing sound household infrastructure is clearly important for improving the poor state of health among Indigenous people in Australia. The work of HealthHabitat in central Australia indicates that household infrastructure is used when it is available.4 However, providing a secure and good-quality food supply, and good hygienic and dietary behaviour, is also essential. Although there were concerns about the lack of quality control in the conduct of the survey between different communities and regions, the high level of coverage (it might more correctly be referred to as a census) and the consistency in coding items as not present and missing data across regions9 allay these concerns to some extent. Further, the findings need to be seen as representing the best-case scenario in the NT, as the survey was intended to target permanent dwellings only. An estimated 1000 temporary dwellings (caravans, tin sheds, improvised dwellings) occupied by close to 4000 people17 would not have been included in this survey. This suggests that the level of functional infrastructure reported in this survey overestimates the level for all dwellings in the NT by about 25%. Current infrastructure projects can be expected to contribute to improvements in health for the people they reach. However, projections indicate that, even with these projects, there will be significant unmet need for many years as population growth and aging housing stock tip the balance against the supply of new houses and repairs and maintenance to existing houses.18 Many more resources need to be committed if such projects are to influence health at the wider population level in the near future. The annual environmental health and housing survey introduced in the NT is an important tool for defining areas of greatest need, monitoring progress, and potentially for improving the understanding of the contribution of household infrastructure to a range of health, educational and social outcomes. Competing interests This article was based on an independent evaluation of a survey conducted under contract by the Menzies School of Health Research for the Northern Territory Department of Local Government. There was agreement at the start of the evaluation between the Department of Local Government and the evaluation team that the results of the evaluation could be the subject of articles published in the scientific literature. The authors have no conflict of interest in writing this article, and have not been subject to any undue influence. Opinions expressed are those of the authors and do not necessarily represent those of any employee of the NT Government. Acknowledgements Thanks to the Northern Territory Department of Local Government for its cooperation and funding of the work that led to this report. We acknowledge the decision of the Aboriginal Community Councils to agree to participate in the survey and the contribution of the many people involved in data collection and processing for the survey. We are grateful to a number of people for their cooperation in the survey evaluation, including Sallie Cairnduff, Graham Franklin, Steve Guthridge, Andrew Heath, Barbara Klessa, Esther Pearce, Phillipe Porigneaux, Danni Quickenden, Helen Secretary, Lynette Shields and Nicola Slaven. References Lindheim R, Syme SL. Environments, people and health. Ann Rev Public Health 1983; 4: 335-338. World Bank. World Development Report: Investing in health. New York: Oxford University Press, 1993. Nganampa Health Council Inc, South Australian Health Commission, Aboriginal Health Organisation of South Australia. Report of Uwankara Palyanku Kanyintjaku: an environmental and public health review within the Anangu Pitjantjatjara Lands. Adelaide: Nganampa Health Council, 1987. Pholeros P, Rainow S, Torzillo P. Housing for health: Towards a healthy living environment for Cape York Communities. Newport Beach: HealthHabitat; 1993. Pormpuraaw Community Council, Apunipima Cape York Health Council, Centre for Appropriate Technology, HealthHabitat. Pormpuraaw housing for health project report: Towards a healthy living environment for Cape York Communities. Cairns: Apunipima Cape York Health Council, 1997. Torzillo P, Kerr C. Contemporary issues in Aboriginal public health. In: Trompf P, Reid J, editors. The health of Aboriginal Australians. Sydney: Harcourt Brace & Co, 1997. Guthridge S, Cairnduff S, Gollow P, et al. Structure, function and health: a review of the health impact of infrastructure change in remote Aboriginal communities of the Top End — final draft. Darwin: Territory Health Services, 2000. Northern Territory Government Environmental Health Task Group. Environmental health standards for remote communities in the Northern Territory. Darwin: Northern Territory Government, 1998/1999. Runcie M, Bailie R. Evaluation of environmental health survey data — Indigenous housing. Darwin: Cooperative Research Centre for Aboriginal and Tropical Health, 2000. SPSS [computer program], version 10.0.5. Chicago: SPSS Inc, 1999. Hardy B. Ramingining Manymak Wanga project report. Darwin: Territory Health Services, 1998. Cunningham J, Makerras D. Overweight and obesity: Indigenous Australians. Canberra: Australian Bureau of Statistics, 1994. Ruben A, Walker A. Malnutrition among rural Aboriginal children in the Top End of the Northern Territory. Med J Aust 1995; 162: 400-403. Muller SM, Priestly JR, McComb JR. Malnutrition among rural Aboriginal children in the Top End of the Northern Territory. Med J Aust 1995; 163: 445. Harding JE. The nutritional basis of the fetal origins of adult disease. Int J Epidemiol 2001; 30: 15-23. Mathews JD. Historical, social and biological understanding is needed to improve Aboriginal health. Rec Adv Microbiol 1997; 5: 257-334. Housing and Infrastructure in Aboriginal and Torres Strait Islander communities. Canberra: Australian Bureau of Statistics, 1999. Strategic plan — 1996. Darwin: Indigenous Housing Authority of the Northern Territory, 1996. (Received 18 Apr, accepted 10 Aug, 2001) Authors' details Menzies School of Health Research and Flinders University Northern Territory Clinical School, Darwin, NT. Ross S Bailie, MB ChB, FAFPHM, Associate Professor of Public Health. CSIRO, Sustainable Ecosystems, Canberra, ACT. Myfanwy J Runcie, PhD, Research Scientist. Reprints will not be available from the authors. Correspondence: Professor R S Bailie, Flinders University Northern Territory Clinical School, PO Box 41096, Casuarina, NT 0811 ross.bailieATmenzies.edu.au Make a comment 1: Background to the housing survey The survey is the responsibility of the Indigenous Housing Authority of the Northern Territory (IHANT), the peak body for Indigenous housing issues in the NT. The two elected Zone Commissioners and seven elected Regional Chairs of the Aboriginal and Torres Strait Islander Commission (ATSIC) have a majority on the IHANT Board to ensure appropriate Indigenous representation. The housing survey's purpose is not just to document the condition of housing infrastructure, but to guide and monitor a substantial maintenance and building program. Feedback of information and developing capacity at local and regional levels are key strategies in the program. The survey aims to ensure the most appropriate use of funds and to improve health status. Back to text 2: Percentage of surveyed houses for which the infrastructure components required to effectively conduct each of six "healthy living practices" were functional Healthy living practice Infrastructure components % Functioning in all surveyed houses Median % functioning per community (range)* Wash people Shower hot tap; shower cold tap; shower drainage; bathroom basin; bathroom hot tap; bathroom cold tap 54% 41% (6%-95%) Wash clothes Laundry trough; laundry hot tap; laundry cold tap 68% 69% (14%-100%) Functioning toilet Main toilet pan; main toilet cistern; main toilet water supply; main toilet drainage 55% 58% (7%-95%) Remove waste water Shower drainage; main toilet drainage 61% 61% (9%-100%) Remove waste rubbish Rubbish bin 69% 72% (0-100%) Prepare and store food Kitchen cold tap; stove top; oven; dry place for food storage; kitchen bench 38% 33% (0-100%) *Includes only those communities where at least 10 houses were surveyed. Back to text 4: Funtionality ratings of 86 communities across the Northern Territory with 10 or more houses surveyed Back to text

Ross S Bailie · Myfanwy J Runcie

CLASS="LinkBox"> Viewpoint Losing the battle of the bulge: causes and consequences of increasing obesity Richard M Eckersley MJA 2001; 174: 590-592 For editorial comment see Baur; see also Magarey et al Abstract - The problem - Health consequences - Economic consequences - Social causes - Risk fatigue? - What can be done? - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract Increasing proportions of Australians are overweight or obese, a problem shared by all developed ...

Richard M Eckersley

Public Health Has the ban on smoking in New South Wales restaurants worked? A comparison of restaurants in Sydney and Melbourne Simon Chapman, Ron Borland and Anita Lal MJA 2001; 174: 512-515 Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract Objective: To evaluate compliance with a legislative ban on smoking inside restaurants by comparing smoking in Sydney restaurants (where it is legally banned) with smoking in Melbourne restaurants (not subject to a legal ban). Design and participants: Unobtrusive observational study of restaurant patrons, and interviews with restaurant staff, carried out by 159 volunteers. Setting: 78 Sydney restaurants with smoke-free indoor environments (as required by legislation) and 81 Melbourne restaurants not subject to legislation preventing smoking. The study took place from 20-31 October 2000. Intervention: Legislation to ban smoking in indoor areas of restaurants was introduced in New South Wales in September 2000 (about six weeks before our study). Outcomes: Observed incidents of smoking inside restaurants; staff attitudes to the ban; customer satisfaction as indicated by comments to staff; staff perceptions of restaurant patronage. Results: No restaurant patrons were seen smoking in 78 Sydney restaurants during 156 hours of observation of 2646 diners, compared with 176 smokers among 3014 Melbourne diners over 154 hours of observation. Thirty-one per cent (24/78) of Sydney restaurants had experienced smokers attempting to smoke indoors after the legislation was introduced; 6% (5/78) reported instances of smokers refusing to stop smoking when asked; 79% (62/78) of restaurants had received favourable comments from patrons about the smoke-free law; 81% (63/78) of restaurant staff interviewed either supported or strongly supported the law. Since introduction of the legislation, 76% of restaurants reported normal trade, 14% increased trade, and 9% reduced trade. Conclusions: Smoke-free restaurants do not require "smoking police" to enforce bans, present few ongoing difficulties for staff, attract many more favourable than unfavourable comments from patrons, and do not adversely affect trade. Throughout more than 15 years of advocacy for an Australia-wide ban on smoking in restaurants, opponents of smoke-free policies (principally the tobacco industry and the Australian Hotels Association1) have argued that such a ban would have serious negative consequences: patronage would be reduced; smoking tourists would choose other travel destinations; staff would be reluctant to enforce the ban; and without expensive government "smoking police" many smokers would ignore the ban.2,3Advocates of smoke-free restaurants have argued that bans not only bring public and occupational health benefit, but are very popular with diners4 and do not reduce trade.5-8 In June 2000, the New South Wales government introduced legislation to ban smoking inside all restaurants, cafes and other places where food is purchased and consumed indoors.9 The law took effect in September 2000, 10 days before the commencement of the Sydney Olympic Games. Smoking was still permitted in outdoor eating areas and in bar areas inside those restaurants that had a "reception" licence (ie, typically, a bar area where patrons are served drinks before a meal). The Victorian State government announced in May 2000 that a smoking ban, identical in most respects to that operating in New South Wales, would be introduced to take effect from 1 July 2001.10 Prior to the ban on indoor smoking in NSW restaurants, an increasing number of restaurants in both States had voluntarily introduced totally smoke-free dining, designated smoking areas or time restrictions (eg, smoking permitted only after 10 pm). The introduction of anti-smoking legislation in NSW prior to its introduction in Victoria afforded a unique window of opportunity to evaluate its implementation by comparing amount of smoking, staff acceptance of bans and customer numbers in restaurants in jurisdictions with and without a ban. Methods One hundred and fifty-nine volunteers (78 in Sydney, 81 in Melbourne), mainly employed by or studying at the University of Sydney or the VicHealth Centre for Tobacco Control, were recruited via email to be observers in our study. Over the period 20-31 October 2000, the observers were invited to dine in Sydney and Melbourne restaurants and were reimbursed $40 towards the cost of their meal. The restaurants (selected by us from dining guides) were restricted to locations within three kilometres of the suburb of residence of the volunteers. No attention was given in selection to the type of food served, the prices charged or whether the restaurant had banned smoking as restaurant policy before the legislative ban (in Sydney) or already, despite absence of a legal ban (in Melbourne). The restaurants selected in both Sydney and Melbourne were spread over a fairly broad geographical area. No restaurant was observed more than once. Observers, after familiarising themselves with a standard observer's protocol, were asked to go their allocated restaurant in the evening, request a table inside the restaurant, order a meal and eat at their leisure. During the evening they tallied the number of diners and patrons waiting to collect take-away meals in the same room as themselves; recorded any indoor smoking incidents and whether smoking occurred in any bar areas; noted whether ashtrays were present; and, before leaving, administered to their table waiter a brief eight-item questionnaire (designed by us) on experiences with the new law and attitudes toward smoking in restaurants. In Melbourne there were two different versions of the questionnaire, depending on whether a ban had already been implemented or whether staff were expressing expectations relating to a future ban. Any comments made by restaurant staff were also noted. Results Observation In Sydney, 78 restaurants were observed for a mean time of 120 minutes (range, 45-240 minutes). The mean number of diners per restaurant was 34 (range, 4-115). None of the 2646 diners in these restaurants were seen to smoke. Ashtrays were observed on tables in three restaurants (4%). In Melbourne, 81 restaurants were observed for a mean time of 114 minutes (range, 60-235 minutes). The mean number of diners per restaurant was 37 (range, 5-198). Of the 3014 patrons, 176 diners (6%) smoked in indoor eating areas during the observation period. Overall, 15% (12/81) of restaurants had voluntarily introduced total bans on smoking indoors, with another 7% (6/81) banning smoking in all eating areas, giving 22% (18/81) having management-initiated bans comparable to those in law in NSW. A further 30% (24/81) had bans in some areas or at certain times, leaving 48% (39/81) that did not provide some notionally smoke-free dining. Smoking practices were observed for compliance with individual restaurant policies on smoking (Box 1). It was noted that intrusion of smoke into smoke-free areas could be a problem, but there was no evidence of violation of management bans. Moreover, in areas where smoking was allowed, there were a considerable number of instances in which no smoking was actually observed. The presence of ashtrays in areas where smoking was allowed was associated with marginally more smoking -- smoking was observed in 20% (16/81) of restaurants with ashtrays versus 14% (11/81) of restaurants with no ashtrays. Staff interviews In Sydney, staff were asked about their experiences since the implementation of the mandated ban (Box 2). With the ban having been in place for about six weeks, 31% (24/78) of restaurants had experienced smokers attempting to smoke indoors since the ban, mostly in the first two weeks. Thirty-three per cent (26/78) had experienced at least one incident of smokers complaining or "making a scene" about not being allowed to smoke; however, only 6% (5/78) had experienced smokers refusing to stop smoking when asked. Most attempts to smoke occurred with people who were unaware of the new law. Sixteen restaurants (21%) reported that smokers, when told that they could not smoke indoors, had gone elsewhere before ordering. The frequency of this was not recorded, but no restaurant staff described it as a common occurrence. In contrast to the one-third of restaurants receiving complaints, 79% (62/78) of Sydney restaurants had received favourable comments from patrons about the ban, with over half receiving several or many comments since its implementation. Of restaurant staff who were questioned, 81% (63/78) supported the ban. Several of those who were against the ban commented that they were smokers themselves and resented being no longer able to smoke while working. While most businesses (76%) reported patronage in the current week to be normal, 14% of restaurants reported being busier than normal and 9% said business was slower. In Melbourne, in the 18 restaurants with eating area bans and seven of the restaurants with partial bans (25/81), staff were asked questions about implementation of bans. In restaurants with no bans, staff were asked about what they would expect to happen if bans were introduced (Box 2). In Melbourne restaurants, expectations and experiences of staff were generally similar, but staff in Melbourne observed or expected patrons to be more resistant to smoking bans than did staff in Sydney. It is notable that reports of patrons leaving without eating or saying they "won't be back" appear to be less frequent where bans are mandated. It is also notable that levels of positive comments were at least as high in Melbourne as Sydney. However, the small numbers preclude meaningful statistical analyses of differences. Discussion Our study shows that Sydney diners do not require "smoking police"11 to convince them not to smoke inside restaurants. Staff have dealt with smoking incidents by reminding patrons of the law, and only a small proportion of restaurants have experienced incidents of smokers refusing to put out their cigarettes when asked. While one in three restaurants reported incidents of smoking in the first weeks of the ban, compliance with the new law now appears to be exceptionally high. In Melbourne, while an encouraging number of restaurants have voluntarily introduced smoking bans, staff experience of people complaining, going elsewhere or generally "making a scene" appears to be more common than in Sydney, where the ban may have introduced a "level playing-field", whereby patrons threatening to "go elsewhere" find that all restaurants now have the same non-smoking conditions. Increasingly, Australian studies have demonstrated that a majority of restaurant patrons prefer to eat in situations where smoking is banned or meaningfully restricted,12 and that restaurateurs have for years severely underestimated the demand for smoke-free dining.13-16Economic game theory17 predicts that restaurant owners trying to introduce voluntary bans could be caught in a dilemma between complying with occupational health and safety laws and yielding to perceived competitive pressures to allow smoking. Under these circumstances, many would continue to put their (often erroneously) perceived economic interests first. Internal tobacco industry documents affirm that the industry has long been intensely concerned about the impact of smoking restrictions on tobacco sales.18 Just as smoke-free workplaces have dramatically reduced smoking frequency among continuing smokers,19 smoke-free dining also reduces smoking opportunities and so is likely to further reduce net tobacco consumption. The most immediate effect of such bans is to reduce the occupational exposure of restaurant staff to environmental tobacco smoke.20 Internal industry documents also reveal that the tobacco industry was aware that its public campaigns predicting dire economic consequences for restaurants were disingenuous. A 1994 Philip Morris internal document stated that "the economic arguments often used by the industry to scare off smoking ban activity were no longer working, if indeed they ever did. These arguments simply had no credibility with the public, which isn't surprising when you consider that our dire predictions in the past rarely came true."21 Our findings suggest that the Sydney restaurant trade has not declined, despite smoking bans — if anything, it may have increased slightly. However, our study had a number of limitations. Firstly, it was conducted over a very short period, during weather conditions that were warm and well suited to outdoor dining. About one-third of the restaurants observed had outdoor areas where smokers could eat and smoke. It will be important to reassess compliance with the legislation in the longer term and during colder months. Secondly, the selection of restaurants was not strictly random, but related to proximity to the homes of the volunteer observers. Selection from restaurant guides also meant that very low price cafes were not included, so our results can not be generalised to all commercial indoor eating venues. Thirdly, the reported perceptions of table waiters about customer reaction to smoke-free dining, although consistent with population-based surveys of dining preference,3,11-14 are unvalidated, as are their estimates of the volume of patronage. Proper validation of the impact of smoke-free legislation on restaurant and hotel trade would require the collection of longitudinal tax receipt data. In the United States, when tax receipts have been used as outcome measures, smoke-free laws have been shown to either have no effect on sales or to generate slightly increased patronage.5-8 Acknowledgements NSW Health funded the study. The New South Wales Cancer Council and Quit Victoria assisted in administering the grant. References Egan C. Where there's smoke, there's ire. The Australian 2000; 20 Dec. Rowbotham J. Restaurant, pub smoking ban stalled. Sydney Morning Herald 1999; 4 Feb: 6. Stevenson S. AHA to oppose new smoking ban moves. The Mercury (Hobart) 2000; 29 July: 9. Walsh RA, Paul CL, Tzelepis F. Overwhelming support for smoking bans. Aust N Z J Public Health 2000; 24: 640-641. Glantz SA. Effect of smoke-free bar law on bar revenues in California. Tob Control 2000; 9: 111-112. Glantz SA, Smith LRA. The effect of ordinances requiring smokefree restaurants on restaurant sales. Am J Public Health 1994; 84: 1081-1085. Chapman S, Lee NM, Monaem A. Smoking in restaurants [letter]. Med J Aust 1998; 168: 637. Glantz S, Charlesworth A. Tourism and hotel revenues before and after passage of smoke-free restaurant ordinances. JAMA 1999; 281: 1911-1918. Parliament of New South Wales. 52nd Parliament. Smoke-Free Environment Bill (Legislative Council). Hansard, 29 June 2000, p 7809. Government of Victoria. Department of Human Services, Public Health Division. Smoke free dining legislation — what does this mean for restaurants and cafes? Information Bulletin 1, May 2000. Available at <http://www.tobaccoreforms.vic.gov.au/cafes1.htm>. Jones A. Radio 2UE (Sydney) 30 Aug 2000; 06:41 am. Trotter L. Environmental tobacco smoke: surveys of restaurant patrons and hospitality industry personnel. Quit Evaluation Studies Vol. 9, Chapter 3. Available at: <http://www.quit.org.au/QE9/QE9Home.html>. Accessed 4 April 2001. Schofield MJ, Considine R, Boyle CA, Sanson-Fisher R. Smoking control in restaurants — the effectiveness of self-regulation in Australia. Am J Public Health 1993; 83: 1284-1288. Borland R, Hill D. Public attitudes to smoke-free zones in restaurants: an update [letter]. Med J Aust 1991; 154: 292-293. Mullins R. A survey of patrons of Melbourne restaurants on the provision of smokefree dining. Melbourne: Centre for Behavioural Research in Cancer, May 1991. Roberts C, Algert C, Chey T, Capon A. Community attitudes to smoking in restaurants [letter]. Med J Aust 1992; 157: 210. Shiel A, Chapman S. The inertia of self-regulation: a game-theoretic approach to reducing passive smoking in restaurants. Soc Sci Med 2000; 51: 1111-1119. Public smoking: the problem. Available at: <http://www.tobaccoinstitute.com/getallimg.asp?DOCID=TIMN0014554/4565>. Accessed 4 April 2001. Chapman S, Borland R, Brownson R, et al. The impact of workplace smoking bans on declining cigarette consumption in Australia and the USA. Am J Public Health 1999; 89: 1018-1023. Jarvis MJ, Foulds J, Feyerabend C. Exposure to passive smoking among bar staff. Br J Addict 1992; 87: 111-113. Laufer D. (Philip Morris USA) Presentation transcript. Available at: <http://www.pmdocs.com/getallimg. asp?DOCID=2041183751/3790>, p 28. Accessed 4 April 2001. (Received 2 Feb, accepted 27 Mar, 2001) Authors' details Department of Public Health and Community Medicine, University of Sydney, Sydney, NSW. Simon Chapman, BA(Hons), PhD, Professor of Public Health and Community Medicine. VicHealth Centre for Tobacco Control, Carlton, VIC. Ron Borland, PhD, Director; Anita Lal, BEc, GradDipPsych, Research Officer. Reprints will not be available from the authors. Correspondence: Professor S Chapman, Department of Public Health and Community Medicine, University of Sydney, Sydney, NSW 2006. simoncAThealth.usyd.edu.au Make a comment 1: Proportion of restaurants in Sydney and Melbourne in which various smoking behaviours were observed, correlated with individual restaurant policies on smoking Sydney Melbourne Observation Mandated ban (n = 78) Banned totally (n = 12) Banned in eating areas (n = 6) Partial bans* (n = 24) No restric- tions (n = 39) No smoking 100% 75% 50% 33% 21% Smoking, but not in eating areas 0 8% 50% 13% 8% Smoking in eating areas 0 0 0 50% 69% Ashtrays on tables 4% 0 0 38% 51% * Partial bans = arbitrary smoking and non-smoking sections. Back to text 2: Responses of restaurant staff in Sydney and Melbourne to questions about banning smoking in restaurants. Data are proportion of restaurants experiencing or anticipating problems/advantages by type of smoking ban Sydney Melbourne Observation/opinion Experience after introducing mandated ban (n = 78) Experience after introducing voluntary ban (n = 25) Expectations in restaurants without voluntary ban (n = 56) Patrons lighting up 31% 44% 49% Smokers complaining or "making a scene" 33% 56% 48% Smokers refusing to stop smoking when asked 6% 0 22% Smokers going elsewhere 21% 54% 51% Patrons saying they "won't be back" 4% 36% 24% Patrons stubbing out cigarettes on floor 0 12% 11% Patronage over past week Increased Normal Decreased 14% 76% 9% 24% 68% 8% 17% 72% 11% Increased number of non-smoker patrons qna 33% 49% Positive comments from patrons on ban None Once or twice Several times Many times Can't say 21% 23% 28% 28% 0 16% 16% 28% 36% 4% qna qna qna qna qna Staff support for bans Strong support Moderate support Neutral Against bans 49% 32% 14% 5% 76% 16% 4% 4% 41% 29% 18% 13% qna = question not asked. 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Simon Chapman · Ron Borland · Anita Lal

Research Iron deficiency in Australian-born children of Arabic background in central Sydney Margaret A Karr, Michael Mira, Garth Alperstein, Samia Labib Boyd H Webster, Ahti T Lammi and Patricia Beal MJA 2001; 174: 165-168 For editorial comment, see Couper and Simmer Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Public and environmental health Abstract Objectives: To determine the prevalence of iron depletion and deficiency, and iron-deficiency anaemia, along with risk factors for iron depletion, in Australian-born children aged 12-36 months of Arabic-speaking background. Design: Community-based survey. Setting: Central Sydney Area Health Service (CSAHS), NSW, April to August, 1997. Participants: All children born at five Sydney hospitals between 1 May 1994 and 30 April 1996, whose mothers gave an Arabic-speaking country of birth and resided in the area served by the CSAHS. Main outcome measures: Full blood count (haemoglobin, mean corpuscular haemoglobin, mean corpuscular volume), plasma ferritin concentration, haemoglobin electrophoresis, potential risk factors for iron depletion. Results: Families of 641 of the 1161 eligible children were able to be contacted, and 403 agreed to testing (response rate, 62.9% among those contacted). Overall, 6% of children had iron-deficiency anaemia, another 9% were iron deficient without anaemia, and 23% were iron depleted. Multiple logistic regression analysis showed three significant independent risk factors for iron depletion: < 37 weeks' gestation (odds ratio [OR], 5.88, P = 0.001); mother resident in Australia for less than the median time of 8.5 years (OR, 1.96, P = 0.016); and daily intake of > 600 mL cows' milk (OR, 3.89, P = < 0.001). Conclusion: Impaired iron status is common among children of Arabic background, and targeted screening is recommended for this group. Numerous studies have documented the adverse health effects of iron deficiency in infants and preschool children, including growth retardation,1,2 gastrointestinal changes,3 impaired immune function,4 impaired behavioural and mental development5,6 and decline in psychomotor development.7,8 In 1992-1994, a study of Sydney children aged 9-62 months found that 1.1% had iron-deficiency anaemia, while 2.8% were iron deficient without anaemia and another 10.5% were iron depleted.9 The prevalence of iron-deficiency anaemia appeared to be higher among children of Arabic-speaking background, but the small number of these children prevented firm conclusions, and the reasons for any difference were not clear. The most important determinants of iron status in infants are growth rate relative to iron endowment at birth, dietary iron content and bioavailability and gastrointestinal blood loss.10 Risk factors for iron deficiency in infancy and childhood include prematurity, low birth weight,11,12 exclusive breastfeeding beyond six months of age,13 introduction of whole cows' milk before 12 months of age,14 and high intake of cows' milk.15 We examined the prevalence of impaired iron status in a large group of Australian-born children of Arabic-speaking background and evaluated their risk factors for iron depletion. Methods The study was a community-based survey undertaken between April and August 1997. Participants Children were identified from the medical records of five Sydney hospitals, which, according to the Midwives Data Base, account for 92% of deliveries to mothers born in an Arabic-speaking country and residing in the area served by the Central Sydney Area Health Service (CSAHS).16 Eligibility criteria were: birthdate between 1 May 1994 and 30 April 1996; mother gave an Arabic-speaking country of birth on admission; postcode of mother's place of residence was in the area served by the CSAHS. Hospitals were asked to exclude stillbirths and neonatal deaths. Contact details were obtained from the medical records. Survey Parents of all eligible children were sent a letter about the study in both Arabic and English. Five days later, they were telephoned to discuss queries and to invite their child's participation. If they agreed, an appointment was made at a convenient early childhood health centre, or a home visit was arranged. Parents were asked to bring the child's Personal Health Record for assessment of birth weight and gestation. Demographic data were obtained using a structured questionnaire administered by an Arabic-speaking research assistant (S L). Questions were also asked about the child's feeding habits since birth and whether the child had had a fever in the two weeks before the blood test, as fever can elevate plasma ferritin concentration.17 Investigations About 0.75 mL of blood was collected by fingerprick and tested at the Royal Alexandra Hospital for Children (RAHC), Sydney, NSW. Haematological investigations (using a Coulter S+IV, Fullerton, Cal, USA) included measurement of haemoglobin and red cell indices. Plasma ferritin concentration was measured by immunoradiometric assay (Biorad, Hercules, Cal, USA). Haemoglobin electrophoresis was performed on all samples to detect haemoglobinopathies. Definitions of impaired iron status are shown in Box 1. All parents were notified of their children's results. Children with poor iron status or haemoglobinopathy were referred to their general practitioners (GPs). A copy of the laboratory report was sent to the GP and to the parents, if they so requested. Statistical analyses Children found to have a haemoglobinopathy were excluded from the analyses, which were performed using Stata (version 5).21 Statistical tests were performed after adjustment for possible cluster effects both within hospitals and within families (as some families contributed more than one child to the study). Confidence intervals were similarly adjusted. Adjusted χ2 tests were used to examine relationships between iron depletion and demographic and risk factors. Variables found to be significantly associated with iron depletion were then entered into a multivariate logistic regression model. Prevalence of impaired iron status was compared with prevalence in children from the general population of central Sydney assessed in 1992-1994.9 Data from that study were re-examined for children aged 12-38 months, using a ferritin level < 10 µg/L to define iron depletion. To test the representativeness of our sample group, demographic characteristics of the mothers were compared with those of all women who in the 1996 census gave an Arabic-speaking country of birth, resided in the area served by the CSAHS, were aged 15-45 years and had children aged 12-38 months. These data were obtained from the Australian Bureau of Statistics. Ethical approval for all components of this study was obtained from the CSAHS Ethics Review Committee. All participating parents gave informed written consent. Results We were able to contact families of 641 of the 1161 eligible children and tested 403 of these children (63% response rate among those able to be contacted). Haematological testing identified a haemoglobinopathy in 21 children, who were therefore excluded from analysis, although two had other haematological parameters consistent with iron depletion. This left 382 children with a plasma ferritin result, and 315 with complete haematological results (blood volume was insufficient for a complete examination in the other 67). Median age of the 382 children at the time of data collection was 25 months (range, 12-38 months). Age distribution was 12-23 months (149 children), 24-35 months (204), and 36-38 months (29). Just over half the children (53%) were male. Prevalence of impaired iron status Prevalence of impaired iron status is shown in Box 2. Overall, 38% of children with an Arabic background had impaired iron status, comprising 6% with iron-deficiency anaemia, a further 9% with iron deficiency without anaemia and a further 23% with iron depletion. The Box also shows prevalences found in 1992-1994 among children the same age in the general population of central Sydney.9 The proportion of children with impaired iron status was substantially higher among Australian-born children of Arabic-speaking background in 1997 than among children of the same age in the general community in 1992-1994. Among the children of Arabic background, those who were reported as having a fever in the two weeks before the blood test were statistically less likely to fulfil the criteria for iron depletion (19/122 versus 68/260; F1,339 = 5.07; P = 0.025). However, they did not differ significantly in rates of iron deficiency (11/108 versus 16/207; F1,282 = 0.49; P = 0.48) or iron-deficiency anaemia (8/108 versus 12/207; F1,282 = 0.31; P = 0.58). The rate of iron depletion among the 260 children reported not to have had a fever in the two weeks before the blood test was 26% (95% CI, 21%-32%). There were no significant differences in iron status between the sexes or between age groups. Risk-factor analysis Potential risk factors among the 382 children are shown in Box 3. Univariate analysis revealed that prematurity, mother resident in Australia less than the median time of 8.5 years, mother born in a country other than Lebanon, and daily intake of more than 600 mL of cows' milk were significantly associated with iron depletion (Box 4). None of the other variables tested, including age of introduction of cows' milk, were significantly associated with iron depletion. Multivariate logistic regression analysis determined that prematurity, mother resident in Australia less than the median time of 8.5 years, and daily intake of more than 600 mL of cows' milk, but not mother born in a country other than Lebanon, were independently associated with iron depletion (Box 4). Children who had been born prematurely were almost six times more likely to be iron depleted, while those who drank more than 600 mL cows' milk per day were almost four times as likely and those whose mothers had been in Australia less than the median time (8.5 years) were almost twice as likely. Representativeness of sample We compared post-secondary education and time in Australia between the sample group and all women who in the 1996 census gave an Arabic-speaking country of birth, resided in the area served by the CSAHS, were aged 15-45 years and had children aged 12-38 months. In the sample group, 29% (116/403) had post-secondary qualifications (95% CI, 24%-33%), compared with 30.2% in the census group (421/1392). Similarly, 30% (121/401) of our sample had been in Australia for six to 10 years (95% CI, 26%-35%), while the corresponding figure for the census group was 26.4% (368/1392). The 238 parents who declined a blood test for their child were questioned by telephone about the age and sex of the child and the volume of cows' milk consumed daily; 180 parents (76%) responded. There were no significant differences between their children and those who had blood tests in age (P = 0.7), sex (P = 0.6) or reported volume of cows' milk consumed daily (P = 0.17). Among the 382 children tested for iron depletion, 67 had moved place of residence since birth and 315 had not moved. The proportion with iron depletion did not differ between these two groups (OR, 1.31; 95% CI, 0.73-2.36). Nor did it differ between the 67 children who had only ferritin level estimated and the 315 who gave sufficient blood for a full haematological examination (OR, 1.03; 95% CI, 0.53-2.01). Discussion These results indicate a public health problem in Australian-born children of Arabic-speaking background in central Sydney that could indicate a nationwide problem. More than a third of these children had impaired iron status, including 6% with iron-deficiency anaemia and another 9% with iron deficiency without anaemia. These prevalences are higher than those found in children the same age in the general population of central Sydney in 1992-1994.9There are several potential sources of bias in this study. The first was the use of retrospective records and consequent failure to contact about 45% of mothers. This is a common problem in such retrospective studies.22,23 However, the mothers of the children studied did not differ significantly from all women in the 1996 census who were aged 15-45 years with children in the target age range, gave an Arabic-speaking country of birth and resided in the CSAHS, while prevalence of iron depletion did not differ between children who had moved residence since birth and those who had not. It is unlikely that our sample differed substantially from the total study population. A second potential source of bias was non-response. However, children whose parents refused a blood test did not differ significantly from those who had a blood test in age, sex and proportion who drank more than 600 mL cows' milk daily. Finally, children whose blood samples were insufficient for full haematological assessment did not differ significantly in prevalence of iron depletion from those who had a full assessment. In the group of children reported to have had a fever in the two weeks before the blood test, a significantly lower proportion fulfilled the criteria for iron depletion. Therefore, the rate of iron depletion reported may be an underestimate. The definition of iron deficiency used in this study was particularly stringent, requiring abnormal values for three laboratory indicators of iron status. Criteria used by the United States Third National Health and Nutrition Examination Survey were less stringent: individuals were diagnosed as iron-deficient if they had abnormal values for two of three laboratory indicators (serum ferritin, free erythrocyte protoporphyrin or transferrin saturation).18 Nevertheless, that survey found rates of iron deficiency and iron-deficiency anaemia among children aged one to two years less than half the rates found in our study (3% versus 6% in our study). The US rate was similar to the rate found in children in the general population of central Sydney in 1992-1994. Risk of iron depletion in our study was greater in children whose mothers had been in Australia for less than the median time of 8.5 years. About 79% of these mothers spoke Arabic, or mainly Arabic, in the home. Early childhood health centres in central Sydney have specific days on which an Arabic interpreter is present, but anecdotal reports suggest that many mothers do not avail themselves of this service. Newly arrived mothers should be targeted in hospital, immediately postpartum, and given information as to which days an Arabic interpreter will be at their local centre and strongly encouraged to attend on a regular basis. Prematurity is well documented as a risk factor for iron deficiency, and this should be kept in mind by GPs and other healthcare providers. Of particular interest is the risk associated with the volume of cows' milk consumed daily. The National Health and Medical Research Council recommends that children aged under 12 months should not receive cows' milk as the main source of milk, while those aged over 12 months should not receive more than 600 mL per day.24 In the multiple logistic regression model, children who consumed more than 600 mL per day were almost four times as likely to have iron depletion, and targeted screening is strongly indicated based on this dietary history. Cows' milk is a poor source of iron, displaces foods with greater available iron and may also increase gastrointestinal occult blood loss. GPs should be aware of the importance of a dietary history for children of Arabic-speaking background and should enquire particularly about the volume of cows' milk consumed per day after 12 months of age. Acknowledgements We wish to thank the parents and children who participated in this study, the haematology laboratory staff at the Royal Alexandra Hospital for Children, Sydney, and the nurses of the participating Early Childhood Health Centres. The blood collection skills of Mrs Rhonda Dryden were invaluable to this study. The study was funded by the National Health and Medical Research Council Public Health Research Development Committee, Grant No: 97-417-7. References Aukett MA, Parks YA, Scott PH, Wharton BA. Treatment with iron increases weight gain and psychomotor development. Arch Dis Child 1986; 61: 849-857. Prasad AN, Prasad C. Iron deficiency; non-hematological manifestations. Prog Food Nutr Sci 1991; 15: 255-283. Berant M, Khourie M, Menzies IS. Effect of iron deficiency on small intestinal permeability in infants and young children. J Pediatr Gastroenterol Nutr 1992; 14: 17-20. Thibault H, Galtn P, Selz F, et al. The immune response in iron-deficient young children: effect of iron supplementation on cell-mediated immunity. Eur J Pediatr 1993; 152: 120-124. Oski FA, Honig AS, Helu B, Howanitz P. Effect of iron therapy on behavior performance in nonanemic, iron-deficient infants. Pediatrics 1983; 71: 877-880. Lozoff B, Jiminez E, Wolf AW. Long-term developmental outcome of infants with iron deficiency. N Engl J Med 1991; 325: 687-694. Williams J, Wolff A, Daly A, et al. Iron supplemented formula milk related to reduction in psychomotor decline in infants from inner city areas: randomised study. BMJ 1999; 318: 693-697. Walter T, De Andraca I, Chadud P, Perales CG. Iron deficiency anemia: adverse effects on infant psychomotor development. Pediatrics 1989; 84: 7-17. Karr M, Alperstein G, Causer J, et al. Iron status and anaemia in preschool children in Sydney. Aust N Z J Public Health 1996; 20: 618-622. Dallman PR, Siimes MA, Stekel A. Iron deficiency in infancy and childhood [review]. Am J Clin Nutr 1980; 33: 86-118. Gorten MK, Cross ER. Iron metabolism in premature infants: 2. Prevention of iron deficiency. J Pediatr 1964; 64: 509-520. Friel JK, Andrews WL, Matthew JD, et al. Iron status of very-low-birth-weight infants during the first 15 months of infancy. CMAJ 1990; 143: 733-737. Calvo EB, Galindo AC, Aspres NB. Iron status in exclusively breast-fed infants. Pediatrics 1992; 90: 375-379. Penrod JC, Anderson K, Acosta PB. Impact on iron status of introducing cow's milk in the second six months of life. J Pediatr Gastroenterol Nutr 1990; 10: 462-467. Mills AF. Surveillance for anaemia: risk factors in patterns of milk intake. Arch Dis Child 1990; 65: 428-431. NSW Department of Health, NSW Midwives Data Collection, 1994. Sydney: NSW Department of Health, 1995. Elin RJ, Wolff SM, Finch CA. Effect of induced fever on serum iron and ferritin concentrations in man. Blood 1977; 49: 147-153. Looker AC, Dallman PR, Carroll MD, et al. Prevalence of iron deficiency in the United States. JAMA 1997; 277: 973-976. Dallman PR, Siimes MA. Percentile curves for hemoglobin and red cell volume in infancy and childhood. J Pediatr 1979; 94: 26-31. Dallman PR, Looker AC, Johnson CL, Carroll M. Influence of age on laboratory criteria for the diagnosis of iron deficiency anaemia and iron deficiency in infants and children. In: Hallberg L, Asp N-G, editors. Iron nutrition in health and disease. London: J Libbey, 1996: 64-74. Stata statistical software release 5.0 [computer program]. College Station, Texas: Stata Corporation, 1997. McBride WG, Black BP, English BJ. Blood lead levels and behaviour of 400 preschool children. Med J Aust 1982; 2: 26-29. Ranmuthugala G, Karr M, Mira M, et al. Opportunistic sampling from early childhood centres: a substitute for random sampling to determine lead and iron status of pre-school children? Aust N Z J Public Health 1998; 22: 512-514. National Health and Medical Research Council. Dietary guidelines for children and adolescents. Canberra: AGPS, 1995. (Received 2 Mar, accepted 1 Sep, 2000) Authors' details Central Sydney Area Health Service, Sydney, NSW. Margaret A Karr, MPH, MSc(Med), Senior Research Officer, Division of General Practice; Michael Mira, MB BS, PhD, Clinical Professor, Department of General Practice, University of Sydney; Garth Alperstein, FRACP, Paediatrician and Clinical Senior Lecturer, University of Sydney, and Conjoint Senior Lecturer, University of New South Wales, Sydney, NSW; Samia Labib, BA, MEd(Health), Senior Interpreter, Health Interpreter Service. Department of Haematology, Royal Alexandra Hospital for Children, Sydney, NSW. Boyd H Webster, FRCPA, Senior Staff Specialist; Ahti T Lammi, FRACP, FRCPA, Senior Staff Specialist; Patricia Beal, MSc, Senior Hospital Scientist. Reprints will not be available from the authors. Correspondence: Professor M Mira, General Practice Casualty, Balmain Hospital, Booth Street, Balmain, NSW 2041. michaelmira_auATyahoo.co.uk 1: Definitions of impaired iron status used in the survey of children of Arabic background Iron depletion18 Plasma ferritin level Iron deficiency19 Iron depletion plus Mean corpuscular volume plus Mean corpuscular haemoglobin Iron-deficiency anaemia20 Iron deficiency plus Haemoglobin level Back to text 2: Prevalence of impaired iron status among children aged 12-38 months of Arabic background in central Sydney in 1997 Arabic background General population9 Iron status* Number % (95% CI) Number % (95% CI) Iron depletion Iron deficiency Iron-deficiency anaemia 87/382 27/315 20/315 23% (19%-27%) 9% (5%-12%) 6% (4%-9%) 36/381 14/329 5/329 9% (7%-12%) 4% (2%-7%) 2% (0-3%) *Definitions of iron status in children of Arabic background are shown in Box 1. The same definitions were used for children in the general population, except that iron deficiency was defined as iron depletion plus mean corpuscular volume < 70fL (age, 12-23 months) or < 73fL (age, 24-38 months), or red cell zinc protoporphyrin level > 80µmol/mol haem. Back to text 3: Potential risk factors for iron depletion among 382 children aged 12-38 months of Arabic background in central Sydney, 1997 Children with Children without Potential risk factors iron depletion iron depletion P* Born before 37 weeks' gestation 12/87 (14%) 10/295 (3%) 0.001 Birth weight 7/86 (8%) 8/293 (3%) 0.05 Breastfed initially 70/87 (81%) 245/295 (83%) 0.59 Breastfed at time of data collection 4/87 (5%) 9/295 (3%) 0.49 Cows' milk introduced before age of 12 months 32/87 (37%) 76/295 (26%) 0.06 Cows' milk introduced before age of 9 months 15/87 (17%) 36/295 (12%) 0.20 Consume >600mL cows' milk per day 54/83 (65%) 109/287 (38%) Consume ≥1L cows' milk per day 23/83 (28%) 30/287 (11%) Iron-fortified cereal as first solid 38/87 (44%) 149/295 (51%) 0.27 Consume meat 42/87 (48%) 122/295 (41%) 0.26 Receiving vitamin supplement 3/87 (3%) 11/295 (4%) 0.90 Receiving iron-containing supplement 1/87 (1%) 4/295 (1%) 0.88 Mother not born in Lebanon 26/87 (30%) 49/295 (17%) 0.01 Arabic or mainly Arabic spoken at home 58/87 (67%) 180/293 (61%) 0.39 Mother resident in Australia less than median time (8.5 years) 53/86 (62%) 137/294 (47%) 0.02 *By adjusted χ2 test. Back to text 4: Risk factors significantly associated with iron depletion among children aged 12-38 months of Arabic background in central Sydney, 1997 Univariate analysis Multivariate analysis Risk factor Odds ratio (95% CI) P Odds ratio (95% CI) P Gestation ≥37 weeks 1.00 1.00 4.55 (1.70-12.50) 0.003 5.88 (2.22-20.0) 0.001 Years mother in Australia ≥8.5 years 1.00 1.00 1.82 (1.10-3.03) 0.02 1.96 (1.36-3.33) 0.016 Cows' milk consumed daily ≤600mL 1.00 1.00 >600mL 3.04 (1.80-5.13) 3.89 (2.22-6.80) Country of birth Lebanon 1.00 Country other than Lebanon 2.14 (1.18-3.88) 0.01 NS NS=Not significant. Back to text

Margaret A Karr · Michael Mira · Garth Alperstein · Samia Labib · Boyd H Webster · Ahti T Lammi · Patricia Beal

Research Use of fake tanning lotions in the South Australian population Kerri R Beckmann, Barbara A Kirke, Kieran A McCaul and David M Roder MJA 2001; 174: 75-78 Abstract - Methods - Results - Discussion - Conclusions - References - Authors' Details - - More articles on Public and environmental health Abstract Objective: To explore the relationship between the use of fake tanning lotions and repeated sunburn among South Australian adults, with a view to informing the Anti-Cancer Foundation of South Australia's (ACFSA) policy on fake tanning products. Study design: Population survey. Participants: 2005 South Australians aged 18 years or older, selected randomly from the electronic White Pages. Main outcome measures: Self-reported use of fake tanning lotions in the past 12 months; frequency of sunburn over summer; and various sun-protective behaviours. Results: 2005 of the 2536 eligible participants (79%) were surveyed by telephone. Fake tan use was most prevalent among women (15.9%), people aged 18-24 years (15.4%), and people with household incomes above $40 000 per year (11.9%). Fake tan users were more likely than non-users to use sunscreens (81.3% v 56.5%; P < 0.001), but less likely to take other precautions such as wearing hats (40.9% v 51.0%; P = 0.04) and protective clothing (22.3% v 34.1%; P = 0.005). They were also more likely to report having been burnt more than once over summer (26.2% v 16.5%; P = 0.025). Multivariate analysis indicates a statistically significant association between fake tan use and repeated sunburn (odds ratio, 2.07; 95% confidence interval, 1.17-3.69), which was independent of age, sex, skin type and sun-protection practices. Conclusion: Users of fake tanning products may be at greater risk of repeated sunburn. The ACFSA sees no justification at this stage for altering its present policy position of not actively promoting the use of fake tanning lotions as a means of reducing sunburn. Anticancer organisations in Australia have been conducting programs aimed at reducing Australia's high rate of skin cancer for over two decades.1 The main objective of these programs is to encourage people to reduce their exposure to solar ultraviolet radiation, the major contributing factor to the development of skin cancer.2In Australia public awareness about the dangers of overexposure to the sun is generally high. In spite of this, a suntan is still desired by some sectors of the community -- in particular, young, fashion-conscious people.3,4 Skin cancer prevention programs have attempted to change attitudes that value tanned skin as attractive and healthy with such messages as "there is no such thing as a safe tan" and "a tan is a sign of skin damage". Last year, Chapman challenged anticancer organisations to consider the role that fake tanning lotions might play in reducing sun exposure, suggesting that they should be assessed as a potential harm-reduction strategy.5 The Anti-Cancer Foundation of South Australia (ACFSA) has, for a number of years, provided information on fake tanning lotions. While not actively encouraging their use, the information suggests that, for those desiring a tan, using fake tanning lotions is preferable to exposure to artificial or solar ultraviolet radiation. In October 1999, the ACFSA included a question on the use of fake tanning lotions in a Health Monitor Survey along with questions on skin type, experience of sunburn and frequency of wearing hats, cover-up clothing, applying sunscreen and seeking shade. This article reports the findings of that survey and discusses them in relation to the position taken by the ACFSA regarding fake tanning lotions. Methods Questions relating to sun exposure and ultraviolet radiation protective behaviours, including one relating to the use of fake tanning lotions, were asked of a random sample of South Australians, by computer-assisted telephone interviewing. These questions (Box 1) were part of a larger health-related survey organised and conducted by the Department of Human Services, South Australia, in October 1999. Except for the question relating to fake tan use, these questions have been used routinely in monitoring sun-protection behaviours in South Australia and were originally validated as written questions in a national Secondary School Children's Survey conducted triennially since 1990.6 The question on fake tan use is a slightly modified version of a question asked in Victorian surveys in 1993 and 1995.7,8Ethical approval for the survey that incorporated the questions used in this study was obtained through the Department of Human Services, with legal authorisation under section 64d of the South Australian Health Commission Act (1976). A sample of 3400 residences from rural and metropolitan areas within South Australia was drawn from the electronic White Pages. One adult from each household (the person whose birthday was the most recent) was invited to participate. Two thousand and five interviews were conducted from the 2536 households that could be contacted after six callback attempts, giving a participation rate of 79.1%. All data were weighted by age, sex and region, and on the probability of selection within the household. The population profile for weighting was obtained from the Australian Bureau of Statistics' estimated population for South Australia, 1997. Geographical region was defined as either metropolitan or country region. Both descriptive analysis of the survey data and logistic regression modelling were undertaken using STATA version 6,9 as this software allows calculation of robust estimates of standard error using methods devised by Huber10 and White.11 Consequently, variance estimates are adjusted for the data weighting. The relationship between fake tan use and reported sunburn over summer was examined using logistic regression modelling, allowing adjustment for age, sex, skin type and sun-protective behaviours. We first constructed a model containing known risk factors for sunburn and then added fake tan use to this model to establish if this improved the fit of the model. "Having been burnt two or more times during the previous summer" was the dependent (outcome) variable. For each of the sun protective behaviour questions, respondents were coded as regular users if they indicated that they "usually, almost always, or always" took such precautions when out in the sun for an hour or more, and were coded as irregular users if they indicated that they "never, rarely or sometimes" took these measures. Results Based on results from this survey, the estimated prevalence of fake tanning lotion use during the past 12 months among South Australians aged 18 years or more was 8.7% (95% confidence interval [CI], 7.3%-10.5%). The prevalence of fake tan use among various subgroups of the population is shown in Box 2. The use of fake tanning lotions is most common among younger people, particularly women, with the peak prevalence being 28% among young women aged 18-24 years. Fake tan use is also more common among those who report that their skin burns before tanning, compared with those whose skin just tans or just burns. Fake tan use also appears to be related to household income, with those with relatively high household incomes (above $40 000 per year) more likely to use fake tanning lotions. Individuals who had used fake tanning lotions in the past year were more likely to report regularly using sunscreen with a sun protection factor (SPF) of 15+ or higher when in the sun than non-users (81% v 57%; P < 0.001). However, they were less likely to report regularly wearing hats (41% v 51%; P = 0.04) or protective clothing (22% v 34%; P = 0.005). They reported seeking shade at levels similar to those who had not used fake tanning lotions (80% v 76%, P = 0.4). Those who had used fake tanning lotions were also more likely to report having been burnt two or more times during the previous summer (26% v 17%; P = 0.025) (Box 3). Factors such as age, skin type, sex and regular sun-protective behaviours are likely to confound the association between fake tan use and risk of burning. Results of logistic regression modelling, which takes into account the effects of these potential confounders, indicate an increased risk among fake tan users of having been sunburnt more than once (odds ratio [OR], 2.07; 95% CI, 1.17-3.69), as shown in Box 4. As the use of fake tanning lotions was much more prevalent among women than men, we also undertook regression analyses for women and men separately. No association between fake tan use and sunburn was found among men (OR, 0.90; 95% CI, 0.14-5.97). This was most probably owing to the fact that only 12 men reported using fake tanning lotions. There was, however, a strong association between using fake tanning lotions and repeated sunburn among women (OR, 2.47; 95% CI, 1.38-4.42). Discussion While the overall prevalence of fake tan use among adult South Australians is low (8.7%; 95% CI, 7.3%-10.5%), the use of fake tanning lotions is fairly common in younger women, with more than one in four women aged 18-24 years reporting having used fake tanning lotions in the past year. These findings are consistent with the reported prevalence of use in Victoria.7,8Respondents who reported using fake tanning lotions were more likely to report regularly using SPF 15+ or higher sunscreen when out in the sun during summer, but were less likely to report wearing hats or protective clothing. Fake tan users were more likely to report being sunburnt two or more times over the past summer. When other known risk factors were taken into account, fake tan users had twice the risk of repeated sunburn over summer compared with non-users. The only previously reported findings in relation to the association between fake tan use and sunburn are from two surveys conducted in Victoria, one in 19937 and one in 1995.8 The first of these surveys found a higher prevalence of sunburn among fake tan users (66% v 46%), while the latter survey found no difference (39% v 40%). The inconsistency of these two reports may have been owing to the relatively small sample size of each survey (n < 700). Owing to the limited nature of the questions in this survey, we were unable to determine whether fake tanning lotions were used just at the start of the season to give a tanned look before a sun-induced tan could be achieved, or throughout the summer as a substitute for sunbathing. Given the timing of the survey (ie, spring), there may be some inaccuracy in people's recall of sunburn in the previous summer. However, it seems unlikely to us that one group would have been more or less likely to under-report having been sunburnt, so any recall effect would have been equivalent in both groups. Another limitation in relation to the timing and cross-sectional nature of the survey is the inability to establish a temporal relationship. In some cases, sunburn may have preceded the use of fake tanning lotions. We can not conclude that fake tan use contributes directly to an increased risk of sunburn. We can only suggest that the behaviours of fake tan use and sun exposure may be linked. A further limitation of this study is that we did not ask about the reason for or frequency of use. We do not know whether there are differences in the risk of sunburn among those who use fake tanning lotions only on special occasions (eg, theatrical performances) compared with those who use such products regularly to maintain a tanned appearance. This lack of detail does not negate the finding that, as a whole, those who use fake tanning lotions are at greater risk of sunburn. Regardless of when and why people use fake tanning lotions, the results of this survey do not offer any evidence that use of fake tanning lotions, as currently practised, protects against sunburn. However, since this is an observational study, we can not rule out the possibility that the use of fake tanning lotions may actually offer some protection. It is conceivable that, had users not been applying fake tanning lotions, sunburn levels could have been even higher in this group. Further clarification of this issue would require a longitudinal (experimental) study design. Our results suggest that, rather than reducing their sun exposure, fake tan users are more likely to be exposing their skin to damaging levels of ultraviolet radiation than non-users. The evidence also suggests that, in general, fake tan users take fewer precautions to protect their skin from the sun. While fake tan users are more likely to report using sunscreens, they appear to rely on sunscreens alone for sun protection rather than using multiple strategies, as recommended by the Anti-Cancer Foundation. Some fake tan users may believe that the tanned effect provided by fake tanning lotions offers protection against the sun. Further confusion may arise in cases where their chosen brand of tanning lotion contains sunscreen. An inspection of fake tanning lotions currently available in South Australia showed that most brands do not include a sunscreen, and many state on the label that the fake tan does not provide protection against solar ultraviolet radiation. Some brands also include the advice to use a regular SPF 30+ sunscreen when going into the sun. However, a few brands of fake tanning lotions do contain sunscreen, varying in their sun protection factor from 4 to 15. One commonly available product with an SPF 4 rating states on its label, "UV Protection: Protects you in the sun, providing 4 times your natural sunburn protection". While technically correct, the protection would apply only to the period immediately after application and not for the time that the tan remains visible on the skin. Such claims are obviously very misleading. Anticancer organisations advise that sunscreens need to be reapplied regularly, ideally two-hourly, to maintain adequate protection. If such advice was followed when using a fake tanning lotion containing a sunscreen, the colour of the tan would deepen with each application. Also, it may take up to four hours for the tan colour to fully develop. Most products recommend removal of dry or flaky skin before applying the fake tanning lotion. The need to do this and the effect of repeated applications on tan colour are likely to preclude regular reapplication of fake tanning lotions, thereby increasing the likelihood of users risking sunburn if they rely on the protection offered by one application. In our view, including a sunscreen in a fake tanning lotion offers no obvious benefit. On the contrary, it has the potential to generate a false sense of protection which may lead to sunburn in fake tan users. Conclusions In response to the discussion posed by Chapman5 in relation to the use of fake tanning lotions as a "harm minimisation" approach, the ACFSA was prompted to review its policy in relation to the promotion and sale of fake tanning lotions. The results of this study do not point to a reduced risk of harmful sun exposure among fake tan users. Rather, they suggest an elevated risk of sunburn. In the light of these findings, the ACFSA sees no justification for altering its current position on the use of fake tanning lotions. The use of fake tanners is not actively promoted by the ACFSA. However, where there is a strong desire for a tan, people are advised that the use of fake tanning lotions is a better alternative than sunbathing or using a solarium. They are also advised that a fake tan does not provide protection against the sun and are warned about the limited protection offered by products that contain a sunscreen. More in-depth investigation of why and when fake tanning lotions are used, and the extent to which fake tan users believe they are protected from the harmful effects of the sun while using such products, is needed to inform education strategies and guide any policy change by organisations such as the ACFSA. The potential of the labelling of fake tan products containing sunscreens to be misleading needs to be brought to the attention of the relevant authorities. References Gray N. Report of the Chairman of the Education Committee. Australian Cancer Society Annual Report, 1979. Sydney: ACS, 1979: 9. Armstrong BK. Stratospheric ozone and health. Int J Epidemiol 1994; 23: 873-885. Arthey S, Clarke V. Suntanning and Sun protection: A review of the psychological literature. Soc Sci Med 1995; 40 (2): 265-274. Clarke V, Williams T, Arthey S. Skin type and optimistic bias in relation to the sun protection and suntanning behaviors of young adults. J Behav Med 1997; 20: 207-222. Chapman S. Faking it: should cancer control agencies promote fake tanning lotions? Med J Aust 1999; 170: 603-604. Broadstock M, Borland R, Hill D. Knowledge, attitudes and reported behaviours relevant to sun protection and suntanning in adolescents. Psychol Health 1996; 11: 527-539. Purchase M, Borland R. Public reaction to the 1992/93 SunSmart campaign: results from a representative survey of Victorians. SunSmart Evaluation Studies 3. Melbourne: Anti-Cancer Council of Victoria, 1994: 93. Dixon H, Cappiello M, Borland R. Reaction to the 1994/95 SunSmart campaign: results from a representative household survey of Victorians. SunSmart Evaluation Studies 5. Melbourne: Anti-Cancer Council of Victoria, 1997: 64. Stata version 6 [computer program]. College Station, TX: Stata Corporation, 1999. Huber PJ. The behavior of maximum likelihood estimates under non-standard conditions. Proceedings of the Fifth Berkeley Symposium on Mathematical Statistics and Probability 1967; 1: 221-233. White H. A heteroskedasticity-consistent covariance matrix estimator and direct test for heteroskedasticity. Econometrica 1980; 48: 817-830. (Received 21 Mar, accepted 31 Jul, 2000) Authors' Details Anti-Cancer Foundation of South Australia, Adelaide, SA. Kerri R Beckmann, BSc(Hons), MPH, Program Evaluation Officer; Barbara A Kirke, DipN, MPHC, Skin Cancer Prevention Project Officer. Collaborative Research Centre for Asthma, University Department of Medicine, Sir Charles Gairdner Hospital, Perth, WA. Kieran A McCaul, BSc, MPH, Biostatistician. Epidemiology Branch, South Australian Department of Human Services, Adelaide, SA. David M Roder, AM, MPH, DDSc, Director. Reprints will not be available from the authors. Correspondence: Ms K R Beckmann, Anti-Cancer Foundation of South Australia, PO Box 929, Unley, SA 5061. kbeckmannATcancersa.org.au Make a comment Back to text Back to text Back to text 4: Factors associated with being burnt more than once over summer All respondents Women only Adjusted Adjusted odds ratio 95% CI P odds ratio 95% CI P Fake tan use Non-users Users 1.00 2.07 - 1.17-3.69 0.013 2.47 1.38-4.42 0.002 Sex Female Male 1.00 2.99 - 2.09-4.29 - - - Age (group years) 65+ 18-24 25-34 35-44 45-54 55-64 1.00 13.70 5.83 4.72 2.46 1.27 - 7.00-26.78 3.19-10.65 2.66-8.38 1.34-4.53 0.61-2.66 0.004 0.529 15.46 4.40 5.12 3.56 0.40 5.34-44.77 1.71-11.34 2.04-12.86 1.37-9.23 0.09-1.65 0.002 0.001 0.009 0.203 Skin type Just tan Burn then tan Just burn 1.00 2.07 2.47 - 1.20-3.56 1.47-4.16 0.009 0.001 1.86 2.12 0.69-5.01 0.83-5.39 0.222 0.117 Sunscreen use Irregular Regular 1.00 1.03 - 0.72-1.48 0.876 0.82 0.44-1.49 0.509 Hat wearing Irregular Regular 1.00 0.69 0.48-0.98 0.038 0.91 0.52-1.59 0.746 Protective clothing Irregular Regular 1.00 0.63 - | 0.44-0.91 0.014 0.95 0.56-1.61 0.856 Shade seeking Irregular Regular 1.00 0.91 - 0.62-1.32 0.604 0.55 0.30-1.01 0.056 *Logistic regression modelling using forced entry of all variables. Separate models for all respondents and women only. Back to text

Kerri R Beckmann · Barbara A Kirke · Kieran A McCaul · David M Roder

Conference Report XIII International AIDS Conference, Durban, 9-14 July, 2000 Nelson Mandela argues for urgent action against HIV in Africa John B Ziegler and Rosemary A Ffrench Let us not equivocate: a tragedy of unprecedented proportions is unfolding in Africa. AIDS today in Africa is claiming more lives than the sum total of all wars, famines and floods, and the ravages of such deadly diseases as malaria . . . Economic growth is being undermined and scarce development resources have to be diverted to deal with the consequences of the pandemic . . . Decades have been chopped from life expectancy and young child mortality is expected to more than double in the most severely affected countries of Africa. AIDS is clearly a disaster, effectively wiping out the development gains of the past decades and sabotaging the future. Earlier this week we were shocked to learn that within South Africa one in two, that is half, of our young people will die of AIDS. The most frightening thing is that all of these infections, which statistics tell us about, and the attendant human suffering, could have been, can be, prevented. Something must be done as a matter of the greatest urgency. And with nearly two decades of dealing with the epidemic, we now do have some experience of what works.-- Nelson Mandela1 MJA 2000; 173: 572-574 Prevention - Mother-to-child transmission - Vaccines - Treatment strategies - Hope - References - Authors' details Box 1: HIV in African countries, 1999 Box 2: Trends in mortality among children under five Nelson Mandela's closing address to the conference1 was a welcome contrast to the opening address by Thabo Mbeki, President of South Africa, who disappointed delegates by failing to resolve their concerns about his view that HIV does not cause AIDS. In his plenary address, David Ho (Director, Aaron Diamond AIDS Research Center, New York) noted that Mbeki would be judged harshly by history. Judge Ed Cameron, a gay white South African living with HIV, in a moving address, pointed out that his government had consistently mismanaged the epidemic, and that he was only alive because his income allowed him to purchase antiviral drugs not available to most South Africans with AIDS. Prevention Box 3: Probability of a Zimbabwean boy aged 15 dying before age 50 Box 4: Projected population structure, Botswana 2020 While news of the explosive spread of HIV in the Republic of South Africa highlighted the urgency of effective preventive strategies, there was relatively good news from some countries where decisive action by pragmatic governments was paying off: the HIV infection rate has stabilised at a relatively low level in Senegal; Uganda has brought its estimated prevalence rate down to about 8% from a peak of close to 14% in the early 1990s; Thailand's "100% condom use" campaign among female sex workers has contributed to falling prevalence in military recruits and antenatal clinic patients.2 In the opening plenary session, Professor Roy Anderson (Director, Centre for the Epidemiology of Infectious Disease, Oxford) explained that interventions to interrupt the spread of HIV in populations would have relatively little impact once prevalence was high. Targeting individuals engaging in high risk behaviours was only effective early in an epidemic; unfortunately, few governments have been prepared to invest resources in the early stages, when such efforts are most cost-effective. There was hope that relatively inexpensive strategies to prevent heterosexual transmission of HIV might emerge from the conference. Unfortunately, the results of a study of a vaginal microbicide containing nonoxynol-9 among sex workers in Côte d'Ivoire showed a higher infection rate in the experimental arm. This suggests that the microbicide's detergent action caused ulceration that enhanced HIV transmissibility. Mother-to-child transmission Amid the gloom of the inexorable spread of HIV in Africa and emerging epidemics in Eastern Europe, delegates were virtually unanimous that there should be no delay in implementing cost-effective measures to prevent mother-to-child transmission of HIV, especially with some drug companies offering to provide free drugs in less developed countries. Data from a prospective observational study in the USA showed that, with optimal maternal combination antiretroviral treatment, the risk of mother-to-child transmission falls to as low as 1%. In breast feeding populations treated with only one drug the gains were less dramatic, but nevertheless very impressive, with the potential to prevent the infection of 25 000 infants a year in South Africa alone. Data presented at the conference reinforced concern that the benefit of perinatal antiviral therapy would be lost when mother-to-child transmission occurred during subsequent breast feeding. However, analysis of the HIVNET 012 trial (mother and infant each received a single dose of nevirapine in labour and by Day 3, respectively) at 18 months showed that an absolute 8% reduction persisted despite prolonged breast-feeding.3 These interventions prevent only about a third of mother-to-child transmission, but they point to cost-effective strategies relevant in resource-poor settings. Implementation will be challenging; it was clear that many women attending African antenatal clinics do not accept HIV screening, do not return for results or do not accept antiretrovirals if HIV positive; attrition rates of 80% were reported. The role of breast feeding in perinatal transmission of HIV was firmly established by a randomised, controlled trial in Nairobi, Kenya.4 While observational data suggested that exclusive breast feeding may be safer than mixed feeding, bottle feeding provides the best protection against HIV infection. The Nairobi investigators reported that the mode of feeding did not affect survival to 24 months, either in the infected or uninfected infants. Surprisingly, breast feeding was associated with three times as much maternal mortality at two years as formula feeding. Vaccines New candidate HIV vaccines presented at the conference provided some hope for the future control of the pandemic. After the disappointing immunogenicity of the recombinant protein vaccines, which were designed to elicit antibody responses, it was thought that strategies for eliciting cellular immunity, particularly cytotoxic T lymphocyte (CTL) activity, may be more successful. The trials of vCP205 (a canarypox virus expressing HIV genes), both alone or with a recombinant protein boost, showed very few vaccine recipients with detectable CTL activity, and these few responses were not sustained. However, it was shown that responses were detected more frequently when vaccine recipients received higher doses of vCP205, so more antigen expresssion may be necessary to achieve the desired levels of immunity. Results of a Phase II trial of the whole, killed HIV vaccine, Remune, in HIV-positive individuals in Thailand were presented. The subjects who received the therapeutic vaccine had a small but significant increase in the CD4+ cell count (P = 0.05) of about 46 cells/µL, with increased antibody levels but no change in viral load. Probably the most controversial decision relating to HIV vaccines in the past few years was to take the AIDSVAX recombinant envelope protein into Phase III clinical trials (in Phase I/II trials the vaccine did not induce antibodies that would neutralise circulating strains of HIV). It was reported in Durban that enrolment in the Phase III trials had been completed in Thailand (n = 2100) and the USA (n = 5400). Efficacy data will not be available until early 2003. There are many new vaccine concepts currently undergoing preclinical testing and some impressive data were presented on experiments in mice and macaques. Stephen Kent (Principal Research Fellow, HIV Vaccines Laboratory, University of Melbourne) presented further evidence that a prime-boost vaccine strategy using DNA vectors, followed by fowlpox virus recombinant for gag and pol simian immunodeficiency virus genes, produced very high levels of cellular immunity in macaques, and that these responses could be increased by the co-expression of the cytokine gene IFN-g. This candidate vaccination strategy, for which the University of New South Wales was recently awarded $27 million by the US National Institutes of Health (NIH), will be tested in Phase I/II human clinical trials in Australia within two years. Another vaccine that has generated considerable interest was presented by Dr Robert Johnson (Director, Alphavax, Professor of Virology, University of North Carolina). The vector for the vaccine, a Venezuelan equine encephalitis replicon, was shown to target dendritic cells, one of the most powerful inducers of cellular immune responses. Testing of this vaccine will begin in South Africa early next year. Dr B. Ensoli (Virologist, Instituto Superiore di Sanità, Rome) also presented some convincing data on preclinical macaque studies of a vaccine targeting immune responses to the tat gene of HIV. She found that five of seven macaques were protected from infection with pathogenic simian/human immunodeficiency virus challenge, and that these monkeys had developed good cellular immune responses to tat protein. Clinical trials are due to begin with this vaccine in Italy and Africa. Thus, although HIV vaccines tested to date have produced somewhat disappointing results, there was optimism at Durban that the next generation of vaccines are promising. Treatment strategies Clinicians and patients have recently become excited by the concept of structured treatment interruptions, which have been suggested to enhance immune responses to HIV while providing relief from the cost, inconvenience and toxicity of complex antiretroviral regimens. Dr Tony Fauci (Director, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland) presented a pilot study of five patients selected because they had achieved undetectable viral levels with potent therapy. They then interrupted therapy for one week in two. During seven such interruption cycles the patients' viral levels remained undetectable and their immune function was preserved. However, because the cohort was small, the subjects highly selected (with extremely well controlled viral replication) and the period of observation was too short, the results did not provide reassurance that such a strategy would not be associated with the risk of induction of drug-resistant variants. It is thus much too early to recommend this strategy in clinical practice. Hope Overall, the conference was hugely successful. Despite talk of boycotts because of Mbeki's views, the conference was well attended. The colourful national costumes of delegates, signage, art and craft displays and street theatre all provided a celebratory atmosphere. There was a mood of optimism that the problems of access to treatments in resource-poor countries were at last beginning to be addressed. Simple, cost-effective, population-based prevention strategies are working in those countries which have implemented them. The hope is that an affordable preventive vaccine that is active against strains of HIV in areas of high prevalence is not too far off. References Closing address by former President Nelson Mandela at the 13th International AIDS Conference, 14 July 2000, Durban. <http://www.aids2000.com/> Accessed 1 November 2000. UNAIDS. Report on the global HIV/AIDS epidemic, June 2000.<http://www.unaids.org/epidemic_update/report/index.html> Accessed 1 November 2000. Guay LA, Musoke P, Fleming T, et al. Intrapartum and neonatal single-dose nevirapine compared with zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda: HIVNET 012 randomised trial. Lancet 1999; 354: 795-802. Nduati R, John G, Mbori-Ngacha D, et al. Effect of breastfeeding and formula feeding on transmission of HIV-1: a randomized clinical trial. JAMA 2000; 283: 1167-1174. Authors' details Department of Immunology, Sydney Children's Hospital, Sydney, NSW. John B Ziegler, MD, FRACP, Associate Professor. Rosemary A Ffrench, PhD, Senior Scientist, Research Laboratory. Reprints will not be available from the authors. Correspondence: Associate Professor J B Ziegler, Department of Immunology, Sydney Children's Hospital, High Street, Randwick, NSW 2031. j.zieglerATunsw.edu.au 1: Seroprevalence of HIV in African countries in 1999 Over the last decade HIV has spread dramatically in sub-Saharan Africa, the fastest increases in prevalence occurring in Eastern and Southern Africa. (Reproduced by kind permission of the Joint United Nations Progamme on HIV [UNAIDS].) Back to text 2: Trends in mortality among children under five years old, with reference to adult HIV prevalence rate at the end of 1999 During the 1980s there were impressive improvements in child mortality attributable at least in part to improved immunisation rates, better management of diarrhoeal and respiratory disease and economic development. However, those gains are being lost and the increased child mortality rates are attributable to increasing incidence of perinatally acquired HIV. (Source: Demographic and Health Surveys, Macro Intenational, USA.) Back to text 3: Probability of a Zimbabwean boy aged 15 years dying before age 50 Trends are shown according to data from various national surveys. In high prevalance countries, a teenager has a greater than 50% chance of dying of AIDS before age 50. (Source: Feeney G, unpublished data, 1999.) Back to text 4: Projected population structure with and without the AIDS epidemic, Botswana 2020 The population chimney graph shows the dramatic impact that AIDS is predicted to have on the structure of the population of Botswana, where over a third of the 775 000 adults are now infected with HIV. The red pyramid shows the population structure as it would be in the absence of an AIDS epidemic. More children would be born (because more mothers would survive and remain fertile throughout their reproductive years) and fewer would have died because they acquired the virus from their mothers. Far fewer young adults would die before old age. The yellow areas show that the burden of AIDS will be greatest in children and in the most economically productive years of adult life. The implications of this change in population structure are shocking. The United States Census Bureau projects that in 20 years' time there will be more adults in their 60s and 70s in Botswana than in their 40s and 50s. This is based on the assumption that patterns of new infection will not change greatly over the next decade; however, as changes in future infection rates will principally affect men and women under 40 in 2020, the demographic chimney pattern for older adults is hardly affected by this assumption. The "missing adults" -- men and women who should have reached their 40s and 50s in 2020 -- are now in their 20s and 30s, although some have already died. Many more are already infected with HIV and will die before they reach their 50s.2 (Source: US Census Bureau, World Population Profile 2000.) Back to text

John B Ziegler · Rosemary A Ffrench

Responding to Crisis Malaria in the Australian Defence Force during and after participation in the International Force in East Timor (INTERFET) Scott J Kitchener, Alyson M Auliff and Karl H Rieckmann Malaria in Australian Defence Force members has been far more common in East Timor than in other recent overseas deployments. By six months after all 5500 members of the International Force in East Timor had returned to Australia, 267 malaria infections had been reported to the Army Malaria Institute. Only 64 of those affected had their first clinical episode during their 4-5 months in East Timor, and about two-thirds of these infections were caused by Plasmodium falciparum. The remaining 212 soldiers developed their first symptoms after returning to Australia, and all but two infections were caused by P. vivax. After treatment, 44 soldiers had relapses of their vivax infections; 11 had a second relapse and two had a third relapse. These findings raise several issues about prevention and management of malaria in the ADF. MJA 2000; 173: 583-585 Antimalarial measures - High malaria rates in two battalions - Notification of malaria infections - Malaria infections with onset in East Timor - Malaria infections with onset in Australia - Parasite resistance to drugs? - References - Authors' details - - More articles on Infectious diseases and parasitology On 12 September 1999, President Habibie of Indonesia invited an international peace-keeping force to help restore peace in East Timor after significant civil unrest. The United Nations Security Council Recommendation 1264 (15 September 1999) directed the formation of an International Force in East Timor (INTERFET). On 20 September, lead elements of INTERFET from the Australian Defence Force (ADF) landed in Dili and were soon followed by approximately 5500 ADF personnel assigned to serve in different parts of East Timor. INTERFET concluded on 23 February 2000, when most ADF personnel came under the command of the Peace Keeping Force of the United Nations Transition Administration for East Timor (UNTAET). Antimalarial measures ADF personnel used various personal protection measures against mosquitoes, including insect repellents and permethrin-treated mosquito-nets. Preventive medicine units also carried out mosquito control measures. Personnel were given doxycycline (100 mg daily) for prophylaxis, starting one or two days before departure for East Timor and continuing for two weeks after return to Australia. Weekly doses of mefloquine (250 mg) were used as an alternative if doxycycline prophylaxis was not tolerated or contraindicated. In addition, terminal prophylaxis with primaquine (7.5 mg three times daily) was given for two weeks after return to Australia. In general, chemoprophylaxis was not taken under supervision. High malaria rates in two battalions On 23 October 1999 -- approximately one month after deployment -- the first malaria infection was diagnosed in a soldier serving with the Second Battalion, Royal Australian Regiment (2RAR). During the four months of the battalion's deployment on the northern border region, mainly during the wet season, 17 members of the battalion developed malaria (monthly rate, 0.71%). Most of these cases were traced to exposures in Batugade (see Box 1). The Third Battalion (3RAR), deployed to the Oecussi (Ambino) enclave for five months, reported 24 cases of malaria (monthly rate, 0.73%). These malaria attack rates were the highest observed during the ADF involvement in INTERFET. Based on data from ADF units deployed to other areas of East Timor, other high risk areas were the mouth of the Komoro River in Dili (near the international airport) and the southern border regions near Suai. Within 7-8 months after returning to Australia, a further 127 soldiers from 2RAR and 3RAR had developed malaria. Combined with the 41 cases with onset overseas, this equates to nearly three (2.96) of every 100 soldiers from these two battalions acquiring malaria for every month's deployment to East Timor. This rate is higher than that experienced by Australian military forces deployed recently to Southeast Asia and Africa1 and Bougainville (unpublished), but lower than that observed during some military deployments to Papua New Guinea.2 Notification of malaria infections That malaria was a health problem was obvious during the five-month duration of INTERFET, and this became even more noticeable after the return of troops to Australia. Clinical episodes of malaria were reported to the Central Malaria Register of the ADF, which is managed by the Army Malaria Institute (AMI). The AMI records clinical and epidemiological data, and, whenever possible, confirms the diagnosis by microscopic examination of blood films or polymerase chain reaction (PCR). Malaria infections with onset in East Timor During deployment of the entire Australian contribution to INTERFET, 64 ADF members developed malaria while in East Timor (Box 2a). About two-thirds of these infections were caused by Plasmodium falciparum and the remainder by P. vivax. This 2:1 ratio reflects the relative prevalence of these two species in the local communities,3 and suggests that there was inadequate compliance with doxycycline prophylaxis or that there were other factors resulting in lower drug concentrations, such as drug deterioration under adverse environmental conditions or reduced bioavailability. The falciparum infections were treated with either a one-day course of mefloquine, or quinine (3 days) combined with doxycycline (10 days). One patient tolerated mefloquine poorly and received atovaquone and proguanil (3 days). None of the patients had a recurrence of clinical symptoms and were presumably cured of their infections. The vivax infections were treated with a combination of chloroquine (3 days) and primaquine (14 days). All affected patients responded well to treatment, but a few had a recurrence of clinical symptoms and parasitaemia (relapse) a few weeks to months later (Box 2b). Malaria infections with onset in Australia Many more malaria infections had their onset after soldiers had left East Timor, with the first clinical episode of malaria occurring in 212 ADF members after their return to Australia (Box 2a). They all had vivax malaria, except for two soldiers who developed falciparum malaria within two weeks of their return. This indicates that doxycycline prophylaxis effectively prevented the development of the blood stages of P. vivax, but that dormant parasites (hypnozoites) in the liver reactivated, entered the bloodstream, and initiated acute attacks of malaria after doxycycline prophylaxis was discontinued. Such initial episodes of vivax malaria could occur many months after return to Australia, with most ADF personnel involved in INTERFET leaving East Timor between December and March 2000 (Box 2b). A few more initial infections will undoubtedly emerge up to 12 months or longer after return from East Timor. It was obvious that terminal prophylaxis with primaquine had not been successful in eradicating all the residual hepatic parasites. As primaquine is the only drug capable of eliminating such parasites, the 210 patients hospitalised with vivax malaria received primaquine again (22.5 mg or 30 mg daily) in addition to a standard course of chloroquine (3 days). Compliance with treatment courses was undoubtedly better than with terminal prophylaxis. Forty-four soldiers had relapses 22-180 days (median, 77 days) after treatment. Although most soldiers were cured after a second course of chloroquine and primaquine, 11 had a second relapse 28 to 157 days (median, 82 days) after treatment and two had a third relapse 145 to 159 days after the third course of treatment. Apart from the distress caused by these recurrent acute episodes of malaria, the overall effect on operational capability was quite substantial. Clearly, there is an urgent need for more effective malaria prophylaxis. Parasite resistance to drugs? Doxycycline has proven to be very effective in the past for prophylaxis of both falciparum and vivax malaria. In combination with any rapid-acting drug, it also cures falciparum infections provided it is taken for 7-10 days. All the falciparum infections in East Timor were cured after treatment with doxycycline, indicating that the parasites had not developed resistance to doxycycline. Primaquine tolerance is a well-recognised phenomenon in Papua New Guinea2 and other Melanesian countries, but it has not been well documented in East Timor. The surprisingly large number of soldiers who developed vivax malaria after returning to Australia obviously had their infections suppressed effectively by doxycycline while they were in East Timor. Their delayed malaria attacks after their return were the result of either deteriorating drug compliance or primaquine-tolerant hepatic parasites. The fact that 44 (21%) of the 210 patients with vivax malaria had a relapse of their infections (a quarter on more than one occasion), under more closely supervised drug administration, indicates that primaquine-tolerant parasites are present in East Timor. Efforts currently being made to reduce the many malaria casualties in East Timor are summarised in Box 3. References Shanks GD, Roessler P, Edstein MD, Rieckmann KH. Doxycycline for malaria prophylaxis in Australian soldiers deployed to United Nations Missions in Somalia and Cambodia. Milit Med 1995; 160: 443-445. Rieckmann KH, Yeo AET, Davis DR, et al. Recent military experience with malaria chemoprophylaxis. Med J Aust 1993; 158: 446-449. World Health Organization. East Timor epidemiological profile, September 1999 <http://www.who.ch/eha/> (accessed November 2000). Authors' details Army Malaria Institute, Gallipoli Barracks, QLD. Scott J Kitchener, FAFPHM FACTM, Officer Commanding Clinical Field Section; Alyson M Auliff, BSc(Hons), Scientific Officer, Clinical Field Section; Karl H Rieckmann, MD, Director. Reprints: Major S Kitchener, AMI, Gallipoli Barracks, Milpo, QLD 4152. scott.kitchenerATdefence.gov.au Make a comment 1: East TimorMap showing Batugade and the Oecussi (Ambino) enclave, identified as sources of infection for the Secound and Third Battalions, Royal Australian Regiment. Back to text 2: Pattern of malaria infections during the deployment of the International Force in East Timor (INTERFET) (a) Distribution of malaria type and place of onset for the 267 infections among INTERFET peronnel deployed from September 1999 to March 2000. (Data collected up to September 2000). (b) Time of onset of 210 initial vivax malaria infections and 57 relapses after return to Australia (between December 1999 and March 2000). Back to text 3: Improvement of malaria control measures Increased vigilance for malaria in the border areas of East Timor, and continued surveillance of malaria infections after redeployment to Australia; Assessment of the effectiveness of personal protection measures and remedial measures to improve compliance; Evaluation of higher doses of primaquine for eradicating parasites from the liver; and Appraisal of the effectiveness of alternative control measures, including new prophylactic drug regimens. Back to text Plasmodium falciparum Plasmodium vivax

Scott J Kitchener · Alyson M Auliff · Karl H Rieckmann

Editorial Domestic violence The healthcare sector could become agents of change MJA 2000; 173: 513-514 The recent series of review papers on domestic violence in the Journal has dealt with a number of important themes: the impact of domestic violence on individuals;1 characteristics of perpetrators;2 presentation of domestic violence in clinical settings;3 and what can be done about domestic violence.4 The prevalence of domestic violence is difficult to estimate because of the variability of definitions and ways of measuring it and the lack of systematic epidemiological studies. Rates tend to be high among patients presenting to general practitioners,5 antenatal clinics,6 emergency departments7 and mental health services,8 but in each of these settings detection is poor. While studies are often developed within a feminist frame of reference and have mostly emphasised the impact on women, men may also be subject to violence from women, as may partners in same-sex relationships. Its impact on children is also substantial, both through witnessing violence and experiencing the effects of abused and abusing parents.9 Focusing on physical abuse as the key indicator may fail to identify far more damaging emotional abuse. There are major health and economic costs of domestic violence.10 Both physical and mental health are affected, increasing the risk of suicide-related behaviours, the drain on healthcare resources and negative perceptions of health status.8,10 Domestic violence in a cultural context Cultural factors have an important impact on the prevalence of domestic violence. These include stereotyped attitudes about "ownership" of women and their value and place in the family and in society; attitudes that define social status in terms of power over others; and the belief of some people that violence is a normal and acceptable way to resolve conflict. The phenomenon of psychological "splitting" is relevant in many situations of domestic violence: people in relationships may unconsciously separate their own good and bad qualities, projecting the hated parts of themselves onto their partner, who is then abused. Understanding violence in families should always encompass an understanding of the importance and complexity of intimate relationships, the making and breaking of affectional bonds and the basic human needs they reflect. These attachments are central to human well-being. It is also vital to take into account social determinants and the particular adversities of social disadvantage that will add cumulative risk. Domestic violence and clinical care Patients are more likely to disclose domestic violence if they receive clear signals that their doctor does not condone violence and will approach the problem in a sensitive way.3,4 A number of questionnaires, including one that has been tested in Australian general practice,5 have been developed to screen for domestic violence. However, they tend to focus only on women, and some are too long to serve as a practical screening tool. In some cases, a single question or a few queries may be all that is required to bring about disclosure of domestic violence if the clinician is alert to its possibility. A high index of suspicion is appropriate if a patient presents with low self-esteem, vague somatic complaints, signs of bruising or other injury and a level of defensiveness. The doctor should question the patient about fear, abuse, depression, and suicidal thoughts. Some victims of domestic violence may even be suffering from a form of post-traumatic stress disorder.11,12 Support, protection, and treatment of acute problems are the first priorities. Effective mental health interventions are available, but should not be provided until the person is in a safe situation. It is also important to remember that children are often traumatised by domestic violence, even if not directly subject to abuse. Feelings of powerlessness, helplessness, and shame often make it difficult for victims of violence to speak of their experience, and they may feel that they are somehow to blame or have "deserved" the abuse. The review of perpetrator issues2 highlights the complexity of this behaviour, the lack of adequate data and the need for evidence of effective interventions. Joint counselling for the couple is usually not recommended because of the late recognition of most cases of domestic violence, the entrenched damaging behaviours and the critical requirement for safety. However, partner programs involving early intervention to reduce negative interaction and interpersonal hostility in relationships could be beneficial.13 Barriers to effective clinical identification and management of domestic violence by health professionals include lack of training, fears for the safety of the victim, or even of the self, identification with victims or perpetrators from the doctor's own social group and, above all, deeply entrenched social attitudes about the privacy of the family.4 Health services and social policy Health services have responded to domestic violence with a range of policies.14 The highest priority for health services is to ensure that victims are protected from further harm. Health professionals need to know about the relevant State legislation, contact details for refuges, and local protocols for appropriate responses when domestic violence is suspected or confirmed. They must be well informed about how to make timely and appropriate referrals.15 The effectiveness of current and proposed programs needs to be evaluated. There are a number of social and health-related policies and programs that could potentially influence the prevalence of and response to domestic violence. Policies that focus directly on domestic violence include: The National Campaign Against Violence and Crime.16 This has programs aimed at preventing violence in schools, rural communities and domestic settings, and programs for dealing with perpetrators. Partnerships Against Domestic Violence.17 This is an agreement between the Federal Government and the States and Territories to work together to prevent domestic violence across Australia. Legislation relating to child protection, family law and orders against violence. Specific policies of States and Territories relating to women's services and the provision of care and protection for women and children who are victims of violence. Other, more general initiatives that may have an effect on domestic violence include National Crime Prevention's "Pathways to Prevention",18 the National Action Plan for Mental Health Promotion and Prevention,19 the Stronger Families and Communities Strategy,20 national policies on alcohol and other drugs, and policies aimed at preventing child abuse and neglect. The complex interface of social policy and health is very relevant in this field. Social variables may far outweigh other factors in the aetiology of domestic violence, but the healthcare sector could become the driving force for change. Beverley Raphael Professor, and Director, Mental Health Services New South Wales Health Department, Sydney, NSW Astbury J, Atkinson J, Duke JE, et al. The impact of domestic violence on individuals. Med J Aust 2000; 173: 427-431. Romans SE, Poore MR, Martin JL. The perpetrators of domestic violence. Med J Aust 2000; 173: 484-488. Hegarty K, Hindmarsh ED, Gilles MT. Domestic violence in Australia: definition, prevalence and nature of presentation in clinical practice. Med J Aust 2000; 173: 363-367. Mazza DM, Lawrence JM, Roberts GL, Knowlden SM. What can we do about domestic violence? Med J Aust 2000; 173: 532-535. Hegarty K. Measuring a multi-dimensional definition of domestic violence: prevalence of partner abuse in women attending general practice. Brisbane: Department of Social and Preventive Medicine, University of Queensland, 1999: 246. Webster J, Sweett S, Stolz T. Domestic violence in pregnancy: a prevalence study. Med J Aust 1994; 161: 466-470. Roberts GL, O'Toole BI, Lawrence JM, Raphael B. Domestic violence victims in a hospital emergency department. Med J Aust 1993; 159: 307-310. Roberts GL, Lawrence JM, Williams GM, Raphael B. The impact of domestic violence on women's mental health. Aust N Z J Public Health 1998; 22: 796-801. Campbell JC, Lewandowski LA. Mental and physical health effects of intimate partner violence on women and children. Psychiatr Clin North Am 1997; 20: 353-374. Resnick HS, Acierno R, Kilpatrick DG. Health impact of interpersonal violence. 2: Medical and mental health outcomes. Behav Med 1997; 23: 65-78. Kemp A, Green BL, Hovanitz C, Rawlings EI. Incidence and correlates of posttraumatic stress disorder in battered women: shelter and community samples. J Interpersonal Violence 1995; 10: 43-55. Herman JL. Complex PTSD: a syndrome in survivors of prolonged and repeated trauma. J Trauma Stress 1992; 5: 377-391. Halford WK. Marriage and the prevention of psychiatric disorder. In: Raphael B, Burrows G, editors. Handbook of studies on preventive psychiatry. Amsterdam: Elsevier, 1995: 121-137. Review of NSW Health domestic violence policy. Discussion paper. NSW Health Department, 1999. Roberts GL, Lawrence JM, O'Toole BI, Raphael B. Domestic violence in the emergency department. 2: detection by doctors and nurses. Gen Hosp Psychiatry 1997; 19: 12-15. National Campaign Against Violence and Crime (NCAVAC). Canberra: Attorney-General's Department, 1998. Partnerships Against Domestic Violence. Information available at: <http://padv.dpmc.gov.au>. Accessed 11 October 2000. Pathways to prevention. Canberra: National Crime Prevention, Attorney General's Department, 1999. Mental Health Promotion and Prevention National Action Plan. Canberra: Commonwealth Department of Health and Aged Care, 1998. Stronger Families and Communities Strategy. Canberra: Commonwealth Department of Family and Community Services, 2000. Make a comment

Beverley Raphael

For editorial comment, see Saunders & Richards Abstract - Methods - Results - Discussion - Conclusions - Acknowledgements - References - Authors' details Abstract Objective: To estimate the prevalence of dependent or daily heroin users in Australia, and to compare the prevalence in Australia with that in other developed countries. Design: We applied three different methods of estimation (back-projection, capture-recapture, and multiplier) to data on national opioid overdose deaths in Australia, first-time entrants to methadone maintenance treatment, and heroin-related arrests in New South Wales. We compared our estimates with estimates derived by similar methods in countries of the European Union. Data sources: Data on national opioid overdose deaths were obtained from the Australian Bureau of Statistics. Data on methadone entrants in NSW were extracted from a database maintained by the NSW Department of Health. Data on arrests for heroin-related offences were supplied by the NSW Police Service. Results: The best estimates of the number of dependent heroin users in Australia in 1997-1998 from the three methods of estimation were between 67 000 and 92 000 and the median estimate was 74 000. The population prevalence was 6.9 per 1000 adults aged 15-54 years. The prevalence of heroin dependence in Australia is the same as that in Britain (7 per 1000) and within the range of recently derived estimates in the European Union (3-8 per 1000 adults aged 15-54 years). Conclusions: Although the exact figures need to be interpreted with caution, our estimates suggest that Australia has a substantial public health problem with dependent heroin use that is of a magnitude similar to that in comparable European societies. In Australia, dependent heroin users are typically daily, or near-daily, injectors of heroin, and of other opioid and sedative drugs when heroin is not available. They continue to use heroin despite the risks of being arrested for drug or property crimes, imprisoned for heroin-related offences, contracting infectious diseases, and overdosing.1Credible estimates of the number of dependent heroin users are needed to plan appropriate public policy responses to the consequences of dependent heroin use.2 These consequences, which have negative effects on the community and public health,3 include bloodborne virus transmission,4 premature death from overdose,5 and crime.6 The need for credible estimates is especially pertinent now, because an increased rate of fatal overdoses over the past five years4 has prompted claims in the popular media that there has been a substantial increase in heroin use in Australia in recent years. Household surveys of drug use are not well suited to estimating the prevalence of dependent heroin use, for several reasons. First, heroin use is likely to be under-reported in household surveys because it is an illegal and stigmatised behaviour.7 Second, dependent heroin users' lifestyles also make them less likely to live in conventional households and less likely to participate in household surveys, because of either their unavailability at the time the interviewer calls or their reluctance to be interviewed.8 Third, household surveys may underestimate the number of dependent heroin users in the population, because heroin users are heavily concentrated in a small number of geographic areas where heroin is most readily available.8 When these areas are represented in national samples in proportion to the contribution to the total population, the estimated population rates of heroin use are usually underestimated in national surveys.9 There is no widely accepted "gold standard" method for estimating the size of the "hidden population" of dependent heroin users. The most widely used approach has been to look for a convergence of estimates derived by applying a number of different indirect methods of estimation to data on the consequences of dependent heroin use, such as overdose death and persons seeking treatment.10 We used this strategy to estimate the number of dependent heroin users in Australia. Our aims were: to estimate the number of dependent heroin users in Australia; and to compare the estimated population prevalence in Australia with that in comparable European societies. Methods Data sources Estimates were derived from secondary analyses of the following datasets: national data on the number of fatal opioid overdoses per year between 1964 and 1997 compiled by the Australian Bureau of Statistics; the NSW Health Department's methadone client database between 1987 and 1998, provided by the Pharmaceutical Services Branch (PSB); and data on arrests for heroin offences in the period 1997-1999 from the NSW Police Service. Each of these datasets is likely to be incomplete to different degrees and in different ways. The number of opioid overdose deaths may be underestimated if the cause of death is not recognised as opioid-related. Data on methadone entrants are more likely to be complete because methadone can not be prescribed in NSW until a registration form is completed and identity checks are undertaken to prevent a person registering more than once. Data on arrests for heroin-related offences do not include heroin-dependent people who are arrested for non-drug-related offences, such as property offences. The aim of the study was to look for convergence of estimates derived from "multiple measures of independent imperfection".11 Methods of estimation Three indirect methods were used to estimate the number of dependent heroin users in NSW and Australia. Multiplier methods used the number of national opioid overdose fatalities and NSW methadone maintenance therapy (MMT) clients. For mortality, we used both the conventional multiplier of 100 (which assumes an annual overdose mortality rate of 1%),12 and a multiplier of 125, derived from a meta-analysis of cohort studies of treated heroin users (which suggests an annual mortality rate of 0.8%).9 The multiplier of 3 for MMT was derived from a study of demand for this type of treatment in Australia.13 Capture-recapture estimates were based on the numbers of individuals entering MMT (1995-1998) and arrested for heroin offences (1997-1998), using methods described elsewhere.9 The capture-recapture estimates were across periods of one year, rather than capture-recapture across different data sources in the same time period.14 Back-projection methods were applied to data on national fatal opioid overdose and first-time entrants to MMT in NSW to estimate the incidence and prevalence of heroin dependence. The form of back-projection used was that suggested by Becker and colleagues15,16 (see ref. 17 for details). The current study examined the degree of convergence between the back-projection estimates derived from the two different data sources. A national estimate was derived directly from national opioid overdose deaths. NSW estimates were derived from NSW MMT and arrest data. The NSW estimates were doubled to produce national estimates. This was done because NSW has consistently accounted for just under half of all opioid overdose deaths in Australia since 1979,5 and for just over half of the number of people enrolled in MMT in Australia.6 Results National estimates The estimates produced by the various methods are shown in Box 1. The best estimate for each method for Australia varied between 67 000 and 92 000, with a median of 74 000 and a mean of 77 000. The range of individual estimates was much wider, between 39 000 and 120 000. The degree of consistency between the best estimates derived from different methods from different data sources was reassuring, especially the agreement between the trends in the two back-projection methods over the period 1970-1997 (Box 2). This consistency provides some reassurance that the true estimate of the number of dependent heroin users in Australia is within our range of estimates. In the absence of any consensus on differential weighting of the estimates, we have taken the median national estimate of 74 000 as the best estimate. This represents a population prevalence of dependent heroin use in Australia of 6.9 per 1000 adults aged 15-54 years, with a range of 5.8-8.6 per 1000. Crude estimates of the number of heroin-dependent people in each of the Australian States and Territories can be derived by allocating the estimated number of heroin users in Australia as a whole (74 000) to each jurisdiction in proportion to the contribution that each jurisdiction made to national opioid overdose deaths in the period 1994-1998. On this basis, NSW is estimated to have 35 400 dependent heroin users, just under half of the national estimate (48%). The estimated number of 19 600 heroin-dependent persons in Victoria accounted for 27% of the national estimate. NSW and Victoria therefore account for 75% of all the estimated number of heroin-dependent persons in Australia. The smaller States accounted for the remaining 25%. The estimated numbers of dependent heroin users in the smaller States, particularly Queensland and Tasmania, appear to be underestimates in that they imply that an implausibly high proportion of dependent heroin users are currently receiving treatment. Because better local estimates need to be derived by applying our methods to data in each of the smaller States, we have not reported these estimates here. Discussion Several methods of estimating the size of the population of people who are heroin dependent in Australia have produced estimates that vary between 67 000 and 92 000 people. The median estimate is 74 000, which equals a population prevalence of 6.9 per 1000 population aged 15-54 years. Each estimation method makes assumptions that are of uncertain validity. Although these uncertainties mean that the estimates presented here should be interpreted with caution, there are a number of reasons why our estimates provide a better basis for public policy than more speculative estimates in the popular media. Firstly, there is reassuring convergence between estimates produced by different methods. The two back-projection estimation methods, applied to two very different datasets (new entrants to methadone treatment and opioid overdose deaths), produced estimates that were in close agreement. The ranges of estimates derived by plausibly varying the assumptions also substantially overlapped.17 The estimates produced by the mortality and treatment multiplier methods and the capture-recapture estimates were similar to those produced by the back-projection methods. Secondly, the estimated national prevalence rate is in the middle of the range of estimates of problem drug use derived recently by similar methods in Europe (3-8 per 1000 adults aged 15-54 years).18 The Australian prevalence is the same as the estimated prevalence of heroin dependence in the United Kingdom (7 per 1000 adults aged 15-54 years).18 Several factors explain the discrepancy between our estimates and media estimates of 200 000 Australian heroin users. Our estimate is of dependent heroin users, who are highly visible in a small number of geographic areas in Sydney and Melbourne. This means that they often attract media attention out of all proportion to their numbers. Within these areas, intoxicated dependent heroin users are often highly visible, dealing and using drugs, and leaving discarded injecting equipment in public places. Dependent heroin users who are involved in criminal activities engage in high rates of breaking and entering houses.19 The national estimate for 1997 (74 000) represents a doubling of the 34 000 estimated in 1984-198720 and a 25% increase on the estimate of 59 000 in the period 1988-1993.13 During this time, there was a corresponding increase in the rate of heroin dependence from 3.7 per 1000 in 1984-1987 to 5.9 per 1000 in 1988-1993 and to 6.9 per 1000 in 1997. The back-projection estimates produce trends in numbers that are consistent with these earlier estimates (Box 2). There are three plausible reasons why the number of dependent heroin users has increased in Australia over the past decade. First, there has been a substantial increase in the availability of very pure and very cheap heroin in Australia in the past two decades. The very limited historical data indicate that the purity of street heroin in Sydney has increased from 10% in 197921 to a mean of 60% in 1993-1995.22 The nominal price has remained stable at $30 for a street "cap", but the effective price per ounce of pure heroin has declined from about $16 000 in 1979 dollars to $5000 in 1999 dollars; the difference is even greater when account is taken of inflation.9 Second, the high purity and low price have meant that it has been easier for new users to initiate heroin use by non-injecting routes, such as smoking or inhaling the fumes of heroin heated on aluminium foil. This may have permitted more naive users to begin heroin use before making a transition to injecting.19 Third, the rise in heroin use in birth cohorts born in the latter half of the 20th century is paralleled by similar trends in a range of psychosocial disorders among young adults,23 including depression, suicide, antisocial behaviour and eating disorders. These trends and the reasons for them have been extensively reviewed by Rutter and Smith,23 who conclude that the increases are real. Conclusions Our estimated prevalence of heroin dependence in Australia (74 000 people; a population rate of 6.9 per 1000 adults aged 15-54 years) is similar to that in countries of the European Union. The media attention given to opioid overdose deaths in Australia in recent years has created a false impression that the prevalence of heroin dependence is unusually high in Australia. Other data suggest that, in Australia, dependent heroin use causes a substantial public health5 and public order problem,9 but the current estimates suggest that the number of dependent heroin users is of the same order of magnitude as in Britain and other European societies from which Australia's population has largely derived. Acknowledgements Both the National Centre in HIV Epidemiology and Clinical Research and the National Drug and Alcohol Research Centre are funded by the Commonwealth Department of Health and Aged Care. References Hall W, Lynskey M, Degenhardt L. Heroin use in Australia: its impact on public health and public order. NDARC Monograph No. 42. Sydney: UNSW, 1999. Stimson GV, Judd A. Estimating the scale and nature of drug problems: the relationship between science, policy and drug strategy. In: European Monitoring Centre for Drugs and Drug Addiction. Estimating the prevalence of problem drug use in Europe. EMCDDA Scientific Monograph No. 1. Luxembourg: Office for Official Publications of the European Communities, 1997; 19-26. Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. Canberra: AIHW, 1999. National Centre in HIV Epidemiology and Clinical Research. HIV/AIDS, hepatitis C and sexually transmissible infections in Australia. Annual Surveillance Report. Sydney: NCHECR, 1999. Hall W, Degenhardt L, Lynskey M. Opioid overdose mortality in Australia, 1964-1997: birth cohort trends. Med J Aust 1999; 171: 34-37. Hall W. Methadone maintenance treatment as a crime control measure. Crime Justice Bull 1996; 29: 1-12. Griffiths P, Farrell M, Howe S. Local prevalence estimation: can an inner city prevalence survey produce useful information? In: European Monitoring Centre for Drugs and Drug Addiction. Estimating the prevalence of problem drug use in Europe. EMCDDA Scientific Monograph No. 1. Luxembourg: Office for Official Publications of the European Communities, 1997; 67-72. Darke S, Ross J, Zador D, Sunjic S. Heroin-related deaths in New South Wales, Australia, 1992-1996. Drug Alcohol Depend 2000; 60: 141-150. Hall W, Ross J, Lynskey M, et al. How many dependent opioid users are there in Australia? NDARC Monograph No. 44. Sydney: UNSW, 2000. Hartnoll R. Cross-validating at local level. In: European Monitoring Centre for Drugs and Drug Addiction. Estimating the prevalence of problem drug use in Europe. EMCDDA Scientific Monograph No. 1. Luxembourg: Office for Official Publications of the European Communities, 1997; 247-161. Cook TD, Campbell DT. Quasi-experimentation: design and analysis issues for field settings. Chicago: Rand McNally, 1979. Frischer M. Estimating the prevalence of drug abuse using the mortality multiplier method: an overview. In: European Monitoring Centre for Drugs and Drug Addiction. Estimating the prevalence of problem drug use in Europe. EMCDDA Scientific Monograph No. 1. Luxembourg: Office for Official Publications of the European Communities, 1997; 113-126. Hall W. The demand for methadone maintenance treatment in Australia. NDARC Technical Report No. 28. Sydney: UNSW, 1995. Hook EB, Regal RR. Capture-recapture methods in epidemiology: methods and limitations. Epidem Rev 1995; 17: 243-264. Becker NG, Watson LF, Carlin JB. A method of non-parametric back-projection and its application to AIDS incidence data. Stat Med 1991; 10: 1527-1542. Becker NG, Watson LF, Marschner IC, et al. Assessing the extent of the Australian HIV epidemic from AIDS surveillance data. Aust J Pub Health 1993; 17: 226-231. Law M, Ross J, Lynskey M, Hall W. Back projection estimates of the number of dependent heroin users in Australia. Addiction 2000; in press. European Monitoring Centre for Drugs and Drug Addiction. Extended annual report on the state of the drugs problem in the European Union 1999. Luxembourg: Office for Official Publications of the European Communities, 1999. Maher L, Dixon D, Lynskey M, Hall W. Running the risks. Heroin, health and harm in South Western Sydney. Sydney: UNSW, 1998. National Drug Abuse Data System NDADS. How many heroin users are there in Australia? Statistical Update No. 5. March 1988. Williams ES. Australian Royal Commission of Inquiry into Drugs. Canberra: AGPS, 1980. Weatherburn D, Lind B. Drug law enforcement policy and its impact on the heroin market. Sydney: NSW Bureau of Crime Statistics and Research, 1995. Rutter M, Smith DJ, editors. Psychosocial disorders in young people: time trends and their causes. Chichester: John Wiley and Sons, 1995. (Received 5 Jun, accepted 25 Aug, 2000) Authors' details University of New South Wales, Sydney, NSW. Wayne D Hall, PhD, Professor and Executive Director, National Drug and Alcohol Research Centre; Joanne E Ross, PhD, Lecturer, National Drug and Alcohol Research Centre; Michael T Lynskey, PhD, Lecturer, National Drug and Alcohol Research Centre; Matthew G Law, PhD, Senior Lecturer, National Centre in HIV Epidemiology and Clinical Research; Louisa J Degenhardt, BA(Hons), Senior Research Assistant, National Drug and Alcohol Research Centre. Reprints: Professor W D Hall, National Drug and Alcohol Research Centre, University of New South Wales, Sydney, NSW 2052. w.hallATunsw.edu.au 1: Estimates of the number of dependent heroin users in New South Wales and Australia (rounded to nearest 1000) Method of estimation Estimate for Australia Range of estimates Back-projection National overdose deaths NSW methadone maintenance therapy entrants 67000 71000 39000-120000* 47000-109000* Capture-recapture Methadone maintenance therapy episodes Arrests for heroin offences 82000 86000 68000-109000† 78000-102000† Multiplier estimates Overdose fatalities (x 100) (x 125) MMT entrants (x 3) 74000 92000 68000 - - - Median estimate 74000 - *Ranges from sensitivity analyses. †95% confidence intervals around estimates. Back to text Back to text

Wayne D Hall · Joanne E Ross · Michael T Lynskey · Matthew G Law · Louisa J Degenhardt