Environmental health

We report a series of cases of thyroid dysfunction in adults associated with ingestion of a brand of soy milk manufactured with kombu (seaweed), and a case of hypothyroidism in a neonate whose mother had been drinking this milk. We also report two cases of neonatal hypothyroidism linked to maternal ingestion of seaweed made into soup. These products were found to contain high levels of iodine. Despite increasing awareness of iodine deficiency, the potential for iodine toxicity, particularly from sources such as seaweed, is less well recognised. Clinical recordsCases of thyroid dysfunction associated with ingestion of soy milkIn November 2008, a 36-year-old woman (Patient 1, Box 1) presented with a mildly elevated serum thyroid-stimulating hormone (TSH) level detected during screening for in vitro fertilisation. As she tested negative for thyroid antibodies, her urinary iodine level was measured to exclude iodine deficiency; this level was markedly elevated at 4445 μg/L (reference range [RR], < 200 μg/L). The source of the excess iodine was unclear until the patient did an internet search and identified that the soy milk she had been drinking (Bonsoy) contained kombu1,2 — a type of seaweed. The patient ceased drinking the soy milk, which resulted in rapid normalisation of her TSH level. Three months later, a 38-year-old man (Patient 2, Box 1) presented with florid thyrotoxicosis. Minimal uptake of technetium on a thyroid scan and absence of TSH receptor antibodies essentially excluded Graves disease. The scan result, in combination with his elevated urinary iodine level (1278 μg/L), indicated that iodine toxicity was the most likely cause of the thyrotoxicosis. He drank brands of soy milk other than Bonsoy, but also drank Bonsoy in takeaway coffee. After he ceased drinking all soy milk, his symptoms rapidly abated and his serum TSH level normalised 3 months later. No further cases of suspected iodine toxicity were seen until approximately 1 year later, when six additional patients presented to one of us (B A C) over a 6-week period (Patients 3–8, Box 1). These patients presented with thyroid conditions ranging from subclinical hyperthyroidism to florid thyrotoxicosis. Patient 3 had already been diagnosed with thyrotoxicosis due to underlying iodine toxicity (urinary iodine level, 11 427μg/L); however, the source of excess iodine was not identified until she sought a second opinion. One month after she ceased consuming Bonsoy milk (which she had been consuming for the previous 8 years), her serum TSH level normalised. An aliquot of Bonsoy milk was analysed for iodine content using a plasma mass spectrometer (Department of Biochemistry, Royal Prince Alfred Hospital, Sydney, NSW), which showed an iodine concentration of 25 000 μg/L. In comparison, the levels of iodine in other soy milks that were analysed ranged from 15 μg/L to 281 μg/L (Box 2). Two weeks later, the same laboratory received a second aliquot of Bonsoy milk for analysis, due to a case of neonatal hypothyroidism. The newborn screening program had identified a baby with an elevated TSH level (28 mIU/L; RR, < 20 mIU/L; heel-prick blood sample). Additional testing 19 days after birth showed further elevation of the baby’s serum TSH level (163 mIU/L), as well as a low level of serum free thyroxine (3.7 pmol/L; RR, 10–25 pmol/L). Exposure to exogenous iodine from a maternal source was suspected because of the marked rise in serum TSH level. Urinary iodine levels were subsequently found to be elevated in both the mother (5415 μg/L) and the baby (9797 μg/L). During the last trimester of pregnancy, the mother had been drinking about 500 mL of Bonsoy milk daily. She had been breastfeeding since delivery. The iodine concentration of the second aliquot of this soy milk (27 580 μg/L) was similar to that of the previously analysed sample. The baby was initially treated with thyroxine but, after the mother ceased ingesting the soy milk, the baby’s thyroid function normalised. Independent analysis of the soy milk (Division of Analytical Laboratories, NSW Health, Sydney, NSW) again revealed an extremely high iodine concentration (31 000 μg/L). Cases of neonatal hypothyroidism associated with maternal ingestion of seaweed soupTwo cases of neonatal hypothyroidism related to maternal ingestion of seaweed have been reported recently by two of us (P J E and M M J).3 The first case involved a Korean mother who, during pregnancy and the puerperium, consumed soup made with overseas-bought dried seaweeds. Her baby, born at 36 weeks’ gestation, had a normal TSH level at the time of newborn screening (heel-prick blood sample). However, the baby subsequently developed jaundice and, at 3 weeks of age, a repeat TSH test showed elevation of the baby’s serum TSH level (39 mIU/L; RR, 0.4–5.0 mIU/L) as well as a low level of serum free thyroxine (9.7 pmol/L; RR, 13–30 pmol/L) and an elevated urinary iodine level (690 μg/L). The baby was initially treated with thyroxine but, after the mother ceased ingesting seaweed soup, the baby’s thyroid function normalised. Dried samples of two different seaweed compounds, analysed by a commercial pathology company (Sullivan Nicolaides Pathology, Brisbane, QLD), showed iodine concentrations of 291 μg/g and 424 μg/g. The second case involved an infant born at 27 weeks’ gestation who had a normal TSH level at the time of newborn screening, and an elevated serum TSH level (24 mIU/L; RR, 0.06–7.14 mIU/L) when a routine repeat TSH test was carried out at 1 month of age. This infant’s mother had also been ingesting seaweed soup — made with Heng Fai seaweed, imported from China, to increase her breast milk supply. The baby’s urinary iodine level at the time of maternal seaweed ingestion was elevated (454 μg/L). The iodine concentration in the mother’s breast milk at the time of seaweed ingestion was elevated at 878 μg/L; 4 weeks after she ceased consuming the seaweed, the concentration dropped to 188 μg/L. NSW Health was notified and testing of the Heng Fai seaweed by the NSW Food Authority revealed high levels of iodine (4450 μg/g), which resulted in voluntary withdrawal of Heng Fai seaweed by the importers in March 2010.4 DiscussionIodine toxicity causes a spectrum of thyroid disorders, ranging from hyperthyroidism to hypothyroidism.5,6 Reasons for the variable effects are unclear, but may relate to age, pre-existing autoimmune thyroid disease, and amount and duration of iodine ingestion.5,6 The adults described here did not appear to have underlying nodular goiters or Hashimoto disease (Box 1). In iodine toxicity, thyroid technetium uptake scans usually show absent or low technetium uptake in thyrotoxicosis and increased technetium uptake in neonatal hypothyroidism. Graves disease and autonomous nodular thyroid disease are more common causes of thyrotoxicosis but can be excluded primarily by scan results, lack of a goitre and absence of TSH receptor antibodies. However, as urinary iodine levels are not routinely measured in clinical practice, iodine toxicity may be underdiagnosed. This series of cases of thyroid dysfunction led to a national recall of Bonsoy milk on 24 December 2009,7 and the distributer agreed to voluntary withdrawal of the product from sale in Australia. This brand of soy milk was fermented in seaweed, which is thought to improve the flavour, and is promoted as having wide-ranging health benefits.1 The NSW Health alert for Bonsoy milk stated that in a child, ingestion of only 5 mL, and in an adult, only 30 mL, would exceed the safe upper limit of iodine intake.8,9 It is unclear whether changes to the manufacturing process of the Bonsoy product may have increased its iodine content. However, after removal of kombu from the manufacturing process, the iodine content was reduced markedly (15 μg/L) and the product returned to the Australian market in April 2010. The World Health Organization was notified of the iodine toxicity of the Bonsoy milk, which was withdrawn from sale in a number of other countries.10 Between January and June 2010, 48 retrospective Australian cases of thyroid dysfunction associated with this brand of soy milk were also notified to local public health authorities (Katrina Knope, Coordinating Epidemiologist, OzFoodNet, Office of Health Protection, Department of Health and Ageing, June 2010, personal communication). A cluster of cases of thyrotoxicosis, linked to iodine toxicity from an unidentified soy milk, was also reported in New Zealand in 2005.11 The common practice by women from Japan and Korea of ingesting seaweed made into soup, sometimes in large quantities, to promote wellbeing in the mother and stimulate breast milk supply, does not appear to be widely known in the medical community. However, due to iodine transmission through breast milk, transient or even persistent hypothyroidism has been reported in neonates born to mothers who undertake this practice.12,13 If left undiagnosed and untreated, neonatal hypothyroidism can have devastating clinical consequences, including impaired intellectual development. Although newborn screening tests will help to identify hypothyroidism during the first week of life, there is no subsequent routine screening of thyroid function in term babies whose TSH level may not increase until after 1 week of age, as seen in one of the neonatal cases described here and in a Korean study of preterm infants.12 Our findings demonstrate the importance of: considering iodine toxicity in patients who present with thyrotoxicosis in the absence of TSH receptor antibodies and low or absent uptake on a thyroid technetium uptake scan; measuring urinary iodine level in cases where thyrotoxicosis is not explained by conditions such as autoimmune or nodular thyroid disease; and actively seeking a history of maternal seaweed consumption during pregnancy and lactation in cases of neonatal hypothyroidism. Finally, although iodine deficiency is a documented and serious concern in Australia,14,15 these cases highlight the risks of excess iodine intake from dietary sources. The food industry is not strictly regulated (eg, imported products are not usually tested to confirm their contents), and contamination of food and drink is only detected when unusual or severe clinical events ensue. There is a strong public health argument for monitoring iodine levels in imported foods and commercially available seaweed preparations. 1 Characteristics of a cluster of eight adult patients in whom thyroid dysfunction was attributed to consumption of Bonsoy, a brand of soy milk manufactured with seaweed, November 2008 to December 2009* Sex; age (years) SerumTSH level (mIU/L) Serum fT4 level (pmol/L) Serum fT3 level (pmol/L) Serum TRAb test result Serum TPO/Tg Ab test result Technetium uptake on thyroid scan Urinary iodine level (μμg/L) Thyroid ultrasound result RR 0.4–3.5 9–19 2.5–5.7 0.5%–3.5% < 200 Patient 1 F; 36 4.63 9.7 Not done Not done Negative Not done 4 445 Not done Patient 2 M; 38 < 0.02 59.4 16 Negative Negative Negligible 1 278 Normal size, single nodule (3 mm diameter), normal vascularity Patient 3 F; 46 < 0.005 50 39 Negative Negative < 0.5% 11 427 Mild enlargement, reduced vascularity Patient 4 F; 36 < 0.04 30 12 Negative Negative 0.5% 777 Normal Patient 5† F; 37 < 0.0005; 12.4 29; < 5 5.6; 3.4 Negative Negative Not done 6 208 Normal Patient 6‡ F; 29 0.04 16 4.9 Negative Negative 0.5% 48 Tiny nodules (< 3 mm diameter) Patient 7 F; 33 0.08 18 6.6 Negative Negative 1.3% 5 022 Normal Patient 8 M; 47 0.07 17 4.9 Negative Negative 0.1% 320 Single nodule (5 mm diameter) TSH = thyroid-stimulating hormone. fT4 = free thyroxine. fT3 = free triiodothyronine. TRAb = TSH receptor antibody. TPO/Tg Ab = thyroid peroxidase and thyroglobulin antibodies. RR = reference range. F = female. M = male. * Reported daily intake of Bonsoy milk ranged from < 100 mL/day to 1000 mL/day. † Patient 5 had blood tests for thyrotoxicosis performed at 5.5 months postpartum, and repeated at 7 months postpartum (when she had developed hypothyroidism). ‡ Patient 6 ceased consumption of the Bonsoy milk about 2–3 months before testing. 2 Iodine concentration in various milks, assayed in December 2009* Brand Iodine (μμg/L) Soy milks Bonsoy 25 000, 27 580 Sanitarium So Nice 27 Vitasoy 19 Coles Soy Drink 19 So Natural Original 15 Other milks Woolworths Lite (low-fat cows milk) 281 Pura Milk (full-fat cows milk) 215 So Good Rice Milk 29 * All testing was carried out at the Department of Biochemistry, Royal Prince Alfred Hospital, Sydney, NSW.

Bronwyn A Crawford PhD, MB BS, FRACP · Christopher T Cowell MB BS, FRACP · Phillip J Emder BSc(Med), MB BS, FRACP · Diana L Learoyd PhD, MB BS, FRACP · Elizabeth L Chua PhD, MB BS, FRACP · John Sinn MB BS, MMed(ClinEpi), FRACP · Michelle M Jack PhD, MB BS, FRACP

To the Editor: We report a case of measles in a 24-year-old man who returned from the Fédération Internationale de Football Association (FIFA) World Cup in South Africa in July 2010. Despite Australian health alerts about measles in South Africa,1 the patient had received no pretravel medical advice or vaccinations. Six days after returning home to the Northern Territory, the patient developed fever, headache and myalgia. The following day he developed vomiting, diarrhoea, and productive cough, with a widespread rash appearing the subsequent day. He visited two general practitioners, was prescribed doxycycline and then admitted to hospital on Day 6 of his illness. On examination, his temperature was 38.9ºC; pulse, 112 beats per minute; blood pressure, 133/72 mmHg; and oxygen saturation, 96% on room air. He had conjunctivitis, a widespread blanching maculopapular rash involving his face, trunk, limbs, hands and feet (Box) and cervical lymphadenopathy. He had bilateral basal lung crackles and tender hepatomegaly. Investigations showed thrombocytopenia (platelet count, 148 × 109/L; reference range, 150–450 × 109/L); hyponatraemia (sodium concentration, 131 mmol/L; reference range, 132–142 mmol/L); and abnormal liver function test results (alanine transaminase concentration, 417 U/L [reference range, < 40 U/L]; alkaline phosphatase concentration, 236 U/L [reference range, 39–117 U/L]). His chest x-ray was normal. The following day, measles virus RNA was detected from a throat swab, and the patient was put into respiratory isolation and therapy with doxycycline ceased. He made a full recovery. The patient reported receiving childhood vaccinations, and while he thought he may have received one measles, mumps and rubella vaccination, he had not had two. Follow-up was required for 84 identified contacts, with no measles cases subsequently notified in the NT. The FIFA World Cup is the world’s largest single-sport event, with an attendance this year of over 3 million people. Mass gatherings may be associated with outbreaks of communicable diseases such as meningococcal disease, measles and pandemic (H1N1) 2009 influenza, in addition to an increased risk of sexually transmitted diseases.2 These risks should be considered when seeing patients who have travelled to such events, in addition to country-specific health risks. Recent data from the GeoSentinal surveillance network showed that a systemic febrile illness was the most common presenting syndrome among travellers returning from South Africa. Most of these cases of illness (54.5%) were due to spotted fever group rickettsiosis.3 The risk of acquiring rickettsiosis increases among travellers visiting game parks, with an incidence of African tick bite fever (Rickettsia africae) among short-term safari tourists of 4.0%–5.3%.4 Measles has rarely been reported in travellers returning from South Africa,2 but the country is in the midst of a measles epidemic, with 17 354 confirmed cases between January 2009 and 12 August 2010.5 Measles presents with fever, cough, rhinorrhoea and conjunctivitis, followed by a widespread rash. The incubation period is usually 7–10 days, but may be up to 18 days. The virus is highly infectious, from 5 days before to 4 days after the onset of rash. Young adults from non-endemic countries such as Australia are at particular risk, as they may only have had one childhood vaccination for measles, with consequent inadequate protection. Although measles has been eliminated in Australia,6 sporadic outbreaks continue to occur,7 and travellers returning from overseas create an ongoing potential for the re-establishment of endemic measles. Given the public health implications of a delayed diagnosis, doctors must be alert to possible cases of measles in travellers returning from endemic countries. The patient’s widespread maculopapular blanching rash

Bridget E Barber · Krispin M Hajkowicz · Vicki L Krause · Kevin G Freeman · Bart J Currie

To the Editor: In their recent editorial, Bower and colleagues effectively summarised the problem of apparent governmental indifference to congenital anomalies.1 This is not unique to Australia and probably exists worldwide. National systems to collect congenital anomalies data were set up in many countries in the mid 1960s, including the National Congenital Anomaly System in the United Kingdom and the Canadian Congenital Anomalies Surveillance System. This followed the thalidomide tragedy and exemplified that it often takes an acute crisis to stimulate politicians into action. However, due to a lack of leadership, foresight and finances,2-4 these systems gradually declined to the extent that they became of very little value, lacking in accurate ascertainment and pregnancy termination data. As a result, regional registries were set up in England and Wales, and Canada was left with only two provinces (British Columbia and Alberta) collecting data. Prevention is one of the new driving forces for collecting good data, and the advent of using folic acid to effectively reduce neural tube defects brought a new urgency to the need for comprehensive useable data. Accordingly, the Canadian government set up a task force and formed a new entity in 2002, the Canadian Congenital Anomalies Surveillance Network, with a mandate to provide logistical and financial help to all 10 provinces and three territories. While progress has been slow, it has been very encouraging, with three additional provinces and one territory developing new surveillance systems this fiscal year (April 2010 – March 2011). The Network has set up guidelines and standards to enable all provinces and territories to collect data in a comparable format,5 which can then be forwarded to a central database in the national capital, Ottawa. The quality of the data should be improved because they are gathered at a local level. This model could be adapted for use in Australia because, according to Bower et al,1 a nucleus of good data from at least three states already exists.

R Brian Lowry

To the Editor: Costello and Murphy’s lament1 about the discoverer of prostate-specific antigen (PSA), Richard Ablin, describing PSA testing as a “hugely expensive public health disaster”2 contains several egregious claims that require correction. They write that “since the introduction of PSA testing in the 1980s, we have seen a 25% reduction in mortality” from the disease. Thirty years ago (in 1980), before PSA testing was possible, the age-adjusted mortality rate from prostate cancer in Australia was 33.4/100 000. In 2007, it was 31.0/100 000, a decline of 7.2%. Over the same period, prostate cancer incidence rose 110%, from 80.8/100 000 to 170/100 000,3 thanks to the aggressive promotion of PSA testing. Recent New South Wales data show that 3 years after radical prostatectomy, 77.4% of men are impotent and 12.3% have urinary incontinence, compared with 22.3% and 1.0%, respectively, of controls.4 Many of these men are, to use Costello and Murphy’s word, “overtreated”1 — they underwent unnecessary surgery and now live with the consequences. From a 2009 European trial,5 the take-home message for a man being tested today is: There is a one in 50 chance that, in 2019 or later, he will be spared death from a cancer that would otherwise have killed him. And there is a 49 in 50 chance that he will have been treated unnecessarily for a cancer that was never a threat to his life.6 This is what Ablin called a public health disaster. With reference to this European trial,5 Costello and Murphy claim that “PSA testing has led to greatly reduced mortality”. This “great reduction” was from 4.2 to 3.3 deaths per 10 000 person-years. Costello and Murphy propose that “those with a PSA level well below the median for men in their 40s . . . (the vast majority at this stage) could be reassured . . .”, but below the median lie half the men, not the vast majority. This policy would mean that the other half of men aged 40 (not the small minority, as implied by Costello and Murphy) would be above the threshold. They would not be reassured; presumably they would be offered more frequent testing and follow-up. Labelling half the population of men aged 40 as higher risk has enormous implications for the men (anxiety, inconvenience, cost) and the health system that would be called on to fund more appointments and tests. Such a proposal does indeed sound like a public health disaster.

Simon Chapman · Alexandra Barratt

In reply: Chapman and Barratt’s statements about prostate cancer highlight the dramatic difference between the views of sociologists and the views of clinicians who deal daily with the burden of prostate cancer diagnosis, treatment and mortality. In 1851, prostate cancer was considered a rare disease.1 Chapman and Barratt’s views seem to remain consistent with this thesis. However, in 2010 in Australia, prostate cancer is the most common cancer diagnosed in men, and the most common cancer causing death in men. Our own data do not support the contention that treatment for prostate cancer produces dreadful outcomes. We can reassure men that there is a high likelihood of cure through early treatment for prostate cancer, with a less than 5% chance of becoming incontinent and a 70% chance of retaining erectile function.2 Clearly, Chapman and Barratt have not taken into account a recently reported Swedish study which showed that in 20 000 men randomly allocated to prostate-specific antigen (PSA) screening or a control group between 1994 and 2008, there was a 50% reduction in mortality from prostate cancer for men in the screened arm.3 The numbers needed to screen (293) and treat (12) from this study are almost exactly the same as those from breast cancer screening studies. We repeat our recommendation for the early use of a single PSA test4 in men aged in their 40s. This is most beneficial because the background noise from benign prostatic hyperplasia development does not occur, and PSA level is very discriminatory for detecting those who go on to develop significant prostate cancer.

Anthony J Costello · Declan Murphy

From 1967, the Australian Human Pituitary Hormone Program offered treatment for short stature and infertility using human cadaver-acquired pituitary hormones (human growth hormone [hGH] and human pituitary gonadotrophin [hPG]). The program was suspended in 1985 when a growth-hormone recipient in the United States developed Creutzfeldt–Jakob disease (CJD), an incurable and rapidly progressive neurodegenerative disorder. Since this time, recipients have lived with the significant anxiety that they have an elevated risk of developing CJD. Furthermore, additional CJD infection control measures are required when recipients undergo some types of surgery. As it is 20 years since the last Australian pituitary hormone recipient developed CJD, we evaluated the risk for Australian recipients of developing iatrogenic CJD, and compared Australian data with data from New Zealand and selected other countries who had pituitary hormone programs. Our evaluation indicates that pituitary hormone recipients in Australia have the lowest risk of developing iatrogenic CJD, and that Australia is the only country not to have experienced ongoing CJD-related deaths. Thus, we believe that: in the Australian hGH recipient cohort, the risk of developing CJD is sufficiently low for this cohort to no longer require additional infection control measures in the health care setting; and in the Australian hPG recipient cohort, if another 5 years elapses with no further occurrence of CJD in this group, the hPG recipient cohort could also be considered as not requiring additional infection control measures in the health care setting. These recommendations should not be misunderstood as implying that there is no ongoing risk, but that the risk is acceptably low and generally in keeping with guidelines that stratify the risk.

Alison Boyd DipAppSci(Nursing), GradDipGenCoun · Genevieve M J A Klug BSc(Hons), PostGradDipEpiBioStat · Lawrence B Schonberger MD, MPH · Amelia McGlade BSc · Jean-Philippe Brandel MD · Colin L Masters MD · Steven J Collins MD

To the Editor: National best practice guidelines recognise that accurate data on the health of Indigenous Australians are crucial to improving health service delivery.1 The draft revision of the RACGP Standards for general practices acknowledges the need for improvement and requires that a practice demonstrates how it routinely records, in active patient health records, self-identified Aboriginal and Torres Strait Islander status.2 This is a commendable improvement but should be further strengthened, requiring that Indigenous status be recorded for at least 90% of active patients, the level required for a history of allergies. Improved record keeping in general practice has resulted in the potential to improve Indigenous identification among patients notified with a communicable disease. This enables the documentation of health disadvantage, and allows evaluation of measures aimed at closing the gap in health outcomes between Indigenous and non-Indigenous people. Demographic data in the NSW notifiable diseases database (NDD) were audited for all 258 Hunter New England (HNE) Salmonella infection notifications in 2007 by interviewing patients and their referring general practitioners. Interviews were completed for 83% of patients. Indigenous status was poorly recorded. The NDD listed three patients with salmonellosis as Aboriginal, but showed an unknown status for 87%. Among patients who had attended a GP during their illness (66%), practice records listed two as Aboriginal, but Indigenous status was unknown for 70%. Most GPs (95%) reported using electronic medical records, and 89% completed pathology requests with practice software. Many GPs (60%) requested information on how to appropriately ask about a patient’s Indigenous status. Interviews with patients who had been notified as having had salmonellosis identified 13 as Aboriginal, and no resistance to identification was encountered. The crude salmonellosis notification rates per 100 000 population were 42.2 (95% CI, 19.3–65.1) for Aboriginal HNE residents and 25.5 (95% CI, 21.7–28.6) for non-Aboriginal HNE residents which, while not statistically significant for this small sample, suggests a differential salmonellosis burden, consistent with studies elsewhere.3 The true burden of disease was likely to have been substantially higher, as many infections are not notified.4 The differential burden may also be an underestimate if Aboriginal HNE residents were less likely to be notified than non-Aboriginal residents due to, for example, reduced access to health services. The widespread availability of electronic practice software for generating pathology requests provides a new opportunity to substantially improve Indigenous identification in communicable disease notifications.3 Indigenous status should be routinely recorded by GPs and automatically included on their pathology request forms and subsequent laboratory notifications. There is now a need for a coordinated national approach to ensure consistent inclusion of Indigenous status on all laboratory notification data.

Anthony D Merritt · April R Roberts-Witteveen · David N Durrheim

Australia should support international bans on asbestos trade The adverse health effects of asbestos are well known, with all forms of asbestos recognised as human carcinogens, causing malignant mesothelioma, lung, laryngeal and ovarian cancers1 as well as the debilitating non-malignant diffuse lung disease, asbestosis, and pleural plaques. Although use, import and export of asbestos and asbestos-containing materials is banned in Australia and 51 other countries,2 an estimated 125 million people around the world are still exposed to asbestos in their home and work environments.3 Crocidolite (blue asbestos) and amosite (brown asbestos), two forms of asbestos that were heavily used in the past, are no longer in use. Chrysotile (white asbestos) accounts for 95% of the asbestos produced and used globally since 1990. There is no safe level of exposure to asbestos4 and no discernible threshold below which there is no risk of mesothelioma.5 Given the clear dangers, why are workers and their families in many parts of the world still being exposed to asbestos? Exposure comes from two main sources: residual asbestos-containing materials remaining in buildings constructed before the mid-1980s (when asbestos-containing cement sheet was removed from the market); and continuing mining and use of asbestos in some parts of the world. In Australia, the legacy of asbestos remains a problem. In most cases, asbestos is in a non-respirable form, and is not a hazard to human health if undisturbed. However, if damaged, it can become friable and change to a respirable form. The issues central to this global problem are education and research. Education about when asbestos exposure may occur, and how to avoid it, remains important. In this respect, the recent survey by Safe Work Australia6 is reassuring, with most tradespeople reporting awareness of asbestos-related health risks and demonstrating an understanding of how exposures occur. However, there was a general lack of understanding about which materials may contain asbestos, and there are no data on the level of awareness among people doing their own renovations. Asbestos will be with us for decades, so targeted and contextually appropriate education programs for at-risk populations are required. The effects of such programs should be monitored for their impact on risk, mortality and morbidity. As most of the people who will die from asbestos-related cancers in Australia already have asbestos in their lungs, research aimed at preventing or curing these cancers is also vital. Globally, the major problem is with continued mining and use of asbestos, with over 2 million tonnes produced in 2008.7 Developing countries, especially in Asia and Eastern Europe, are mining or importing asbestos for domestic use, and now account for the majority of the world’s exposure to asbestos. Thousands, if not millions, of people are likely to die in these countries as a result of continued asbestos exposure.8 Chrysotile is the only form of asbestos that is being traded in the 21st century; it is mostly used in the manufacture of asbestos cement sheets and pipes. There is a mistaken belief that this form of asbestos is less harmful than other forms, but overwhelming scientific evidence refutes this assertion.9 All forms of asbestos are classed as human carcinogens by the United States Environmental Protection Agency, and cancer is seen in workers who have only been exposed to chrysotile asbestos.9 There is also a mistaken view that chrysotile can be handled safely. Reports from the National Public Health Institute of Quebec show a failure to achieve “controlled use”, even in Quebec. In many developing countries, exposure is uncontrolled, and education of workers is, at best, minimal, and often non-existent. Tobacco smoking is also widespread in Asia, and is synergistic with chrysotile in increasing the risk of lung cancer. International organisations such as the World Health Organization and the International Labour Organization have called for a global ban of all forms of asbestos, with the goal of eliminating asbestos-related diseases.10 The Collegium Ramazzini, an international academic society independent of commercial interests that examines critical issues in occupational and environmental health, has just renewed its call for such a ban. This could, in part, be achieved via the Rotterdam Convention (http://www.pic.int), an international treaty intended to regulate global trade in chemicals that have been banned or severely restricted because of the hazards they pose to human health or the environment. The Convention was enacted in 2004, and 131 nations, including Australia, are current partners. The goal of the Convention is to protect the world’s most vulnerable countries from importing hazardous pesticides or regulated chemicals without prior knowledge or consent. Repeated efforts to include chrysotile asbestos under the Rotterdam Convention have failed, due to opposition from countries which mine and manufacture asbestos, including Canada. The Canadian Medical Association, Canadian Cancer Society and Canadian Public Health Association oppose exporting asbestos to developing countries, yet their government officially condones this activity. We, personally and on behalf of our respective professional affiliations, call for Australia and Australians to strongly support the latest international effort to ban the mining and manufacture of all forms of asbestos; to increase efforts, at home and abroad, in effective education of the dangers of asbestos both in the workplace and in the environment; and urge our legislators to redouble their efforts to rid the world of asbestos-related diseases.

Peter D Sly MB BS, FRACP, DSc · Robin Chase MB BS, DPH, FAFOEM · John Kolbe MB BS, FRACP · Philip Thompson MB BS, FRACP · Leena Gupta MB BS, MPH, FAFPHM · Mike Daube BA(Hons), HonDSci · Ian Olver MD, FRACP · Deborah Vallance BMedSci, MB BS, MPH

Objective: To describe changes in the incidence of hospitalised injury for New South Wales residents involved in non-traffic crashes for the period 1 July 1998 to 30 June 2007.Design, setting and participants: This study identified 37 480 NSW residents admitted to hospitals for injuries resulting from non-traffic crashes from the NSW Admitted Patients Data Collection during the study period. Injury rates were calculated by applying 2001 census-derived estimates of NSW population figures as the denominator, and directly adjusting to the age distribution of the 2001 Australian population. The significance of trends in rates was assessed by the per cent change annualised estimator.Main outcome measures: Age-standardised rates of hospitalisation for injuries, and trends by inpatient demographics, travel mode and severity of injuries.Results: The annual rate of hospitalisation for injury showed a significant increase of 0.7% per annum (95% CI, 0.2% to 1.2%) for NSW residents involved in non-traffic crashes over 10 years. Annual hospitalisation rates for serious injuries increased by 2.2% (95% CI, 0.9% to 3.6%). The hospitalised injury rate for motorcyclists and pedal cyclists increased significantly by 3.3% per annum (95% CI, 2.4% to 4.2%) and 3.7% (95% CI, 2.6% to 4.9%), respectively, but the rate declined significantly for car occupants and pedestrians by – 8.3% per annum (95% CI, – 9.5% to – 7.0%) and – 2.2% (95% CI, – 4.2% to – 0.2%) respectively.Conclusions: The rate of hospitalisation for injury from non-traffic crashes increased significantly over time for NSW residents from 1998–99 to 2007–08, especially for serious injuries and injuries to motorcyclists and pedal cyclists. These findings call for continuing and specific effort to prevent road non-traffic injuries.

Shanley Chong PhD, MAppStat, BA(Stats) · Wei Du PhD, MPH, MB BS · Julie Hatfield PhD

To the Editor: Blecher correctly asserts that alarm is not the appropriate reaction to the potential dangers of computed tomography (CT) scans.1 Such alarm risks discouraging patients from having the CT scans they need. Appropriate CT scans are good; inappropriate ones are bad. Blecher is also correct in stating that the linear, no-threshold (no dose is entirely safe however small) model of radiation risk is theoretical.2 However, the advice of all international regulatory radiation protection authorities is to assume that the model is correct. To do so is prudent, even if overly conservative. And while these authorities hold this position, it would be professionally irresponsible to ignore it. Notwithstanding the Health Physics Society statement that the risk of ionising radiation below 100 mSv is negligible,3 the risk is thought to be cumulative. Furthermore, a single CT scan of the chest, abdomen and pelvis may expose a patient to 30 mSv or more, and the risk in children and young adults is considered to be 2–3 times greater than the average.4 The atomic bomb data are based on radiation dose levels as low as 5 mSv,5 with the cohort exposed to doses between 5 and 20 mSv showing an 85% chance that the risk is worse than we think and a 15% chance that it is better than we think. Although not statistically significant at the 95% confidence level, these figures indicate that great care is needed. The dimensions of the risks of low-dose radiation are contentious, but are we willing to ignore the danger of accepting Blecher’s argument? It is a Pascal’s wager. Providing we do not spook patients from having necessary scans (and this requires better communication with patients), our possibly over-cautious approach should result in more appropriate use of diagnostic imaging. The benefits go beyond those of limiting unnecessary radiation. Blecher finds it ironic that concerns about the dangers of CT are rising as radiation doses are falling. Doses may be falling, although that depends on where the baseline is drawn. When multidetector CT scanning was introduced, doses rose,6 but if, since then, doses have been falling, there is nothing ironic about this. Doses are falling because of the concern. Whether a patient undergoes an imaging procedure should be subject to the process of justification mandated in the Australian Radiation Protection and Nuclear Safety Agency code of practice.7 If the potential benefit outweighs the risk, the procedure is justified and the examination should proceed, but optimised to ensure that the lowest possible dose of radiation is used to provide diagnostic images — the ALARA principle (As Low As Reasonably Achievable). In summary: If a CT scan is clinically justified, then it should be performed and we should certainly avoid alarming our patients. If a scan is not justified, it should not be performed. We should adhere to the ALARA principle. Whenever appropriate, a non-ionising alternative to CT scans should be considered, particularly for children and young patients.

Richard M Mendelson · Richard A Fox · Nicholas H de Klerk

Blood lead levels in children in Mount Isa are substantially elevated, and a purported lack of knowledge of the lead source is no longer tenable Environmental lead levels and blood lead concentrations in children at Mount Isa, in north-western Queensland, are substantially elevated compared with background values1-3 and, as a consequence, there is a public health risk. This problem is exacerbated by the reluctance of stakeholders, including Xstrata Mount Isa Mines Ltd, operator of Mount Isa Mines (MIM), and Queensland environmental and health authorities to acknowledge and respond effectively to the fact that the main environmental lead source is mining and smelting activity.1,2 It is frequently claimed that the lead source is natural surface mineralisation;4-6 this is not the case. Mount Isa city, located immediately adjacent to MIM, is a major lead, zinc and copper producer, and Australia’s largest atmospheric emitter of sulfur dioxide, lead and other metals.7 The emissions are likely to have had an impact on the blood lead level (BLL) of a significant proportion of the city’s population of about 21 000. The causal link between smelter lead emissions and an increased risk of adverse health effects has been convincingly documented elsewhere,8 and responded to, albeit with varying degrees of urgency, at smelting sites around Australia (Box).9 In Mount Isa, the link has been routinely questioned and remedial action delayed. In recent decades, considerable evidence has emerged showing lifelong negative health, intellectual and sociobehavioural effects associated with childhood BLLs above 10 μg/dL, the level widely regarded as the threshold above which intervention is necessary. However, there is emerging evidence of adverse effects occurring at 5–10 μg/dL, and even at levels as low as 2 μg/dL.8-11 In 2008, Queensland Health reported that Mount Isa children aged 1–4 years had a mean BLL of 5 μg/dL, with 37% having levels > 6 μg/dL and 11.3% having levels > 10 μg/dL.3 Recent data from Fremantle, Western Australia, an urban centre with no major industrial lead source, showed a mean BLL in children of 1.8 μg/dL, with no individual readings exceeding 10 μg/dL.12 This is similar to the mean BLL of 1.9 μg/dL (with only 1.6% of readings ≥ 10 μg/dL) for children aged 1–5 years in the United States in 1999–2002.10 Compared with these figures, BLLs remain substantially elevated in many of Mount Isa’s children and, as shown by numerous studies elsewhere, the level of lead exposure is likely to correlate with neurocognitive impairments.8-11 Lead exposure places children on an abnormal developmental trajectory that may result in reduced social and educational achievement and unmet life potential. Assuming that the Mount Isa BLL data are representative of all 1–4 -year-olds in the city (of whom 27% were sampled),3 then, on average, every nine days a child will exceed the BLL threshhold of > 10 μg/dL. Research commissioned during a Queensland government-led inquiry a decade ago,1 as well as subsequent peer-reviewed studies,2 have unequivocally demonstrated widespread contamination of soil and airborne dust in and around Mount Isa, as a result of both historic and ongoing mining and smelting activity by MIM. Contaminants include lead, copper and other metals and metalloids. Frequent claims that natural mineralisation of soils is the main cause of increased lead levels4-6 are incorrect, and have stymied an appropriate response to the Mount Isa lead problem. The “gossans” (ridges of lead-bearing surface rocks) initially discovered west of Mount Isa are now largely covered by mining operations, and cannot be a major source of environmental lead. Furthermore, there is no substantial natural exposure of copper ore, which was discovered “accidentally” during deep drilling. These observations are supported by data published by several of MIM’s own geologists over the past 60 years.13 Numerous soil profiles in and around Mount Isa show that it is usually only the surface layers that are contaminated with lead and copper.1,2 Concentrations of these metals correlate significantly with each other and are up to 20 times higher at 0–2 cm depth than at 10–20 cm depth. This shows that (1) soil contamination with both lead and copper can only have come from particles emitted into the atmosphere from MIM, as there is no other common source for both metals, and (2) that the surface soil metal enrichment can only have come from aerial deposition of contaminated particles. Lead isotope fingerprinting, used as a tracer, shows that surface soil — but in most cases not deeper soil — contains lead from the Mount Isa lead ore body due to aerial deposition.1 The capture by MIM of smelter fumes (sulfur dioxide and associated metal-bearing particles) is inefficient, as shown by the ongoing high emission levels that, for some compounds, have been rising in recent years.7 The Queensland Government’s air quality data for Mount Isa14 show 10 breaches of the guideline level for sulfur dioxide between September 2009 and February 2010, and that lead concentrations in air increased substantially during these breaches. However, the current legal standard for lead concentrations in air in Mount Isa is higher than the Australian national lead-in-air standard of 0.5 μg/m3, and therefore was not breached.15,16 More importantly, the current Mount Isa standard is an order of magnitude greater than the recently revised US lead-in-air standard,8 which was lowered by the US Environmental Protection Agency after assessing about 6000 studies related to the health impacts of lead exposure.8 The lower standard was deemed necessary to properly protect the health and wellbeing of children.8 The evidence is clear. There is a single primary source of environmental lead in Mount Isa: the historic and ongoing mining and smelting activity. Acceptance of this patent fact by all stakeholders will lead to a more targeted remedy to the lead problem, and better health and environmental outcomes for the community of Mount Isa. A purported lack of knowledge of the lead source is no longer a tenable response and provides no long-term resolution for Xstrata, the government or the children of Mount Isa whose futures are at risk. Australian mining- and smelting-related blood lead levels and government and industry responses9 Port Pirie, South Australia Early 1980s: high blood lead levels (BLLs) confirmed 1984 onwards: decontamination and demolition of residences, slag dumps covered, emissions controlled 2004: BLLs decreased but remain elevated Broken Hill, New South Wales Early 1990s: high BLLs confirmed 1994 onwards: land and home evaluation and remediation 2006: BLLs decreased but remain elevated Boolaroo, NSW Early 1990s: high BLLs confirmed 1991 onwards: emissions controlled 1997: lead abatement of homes 2003: smelting operations ceased 2005: BLLs decreased substantially after smelter closure Mount Isa Mines, Queensland 1994: high BLLs confirmed 1997: Mount Isa lead emission limits set above Australian national limits (national limits written into law in 2009, to apply in Mount Isa from 2012) 2000: partial emission capture 2007: Xstrata Mount Isa Mines “lead pathways” study initiated (not completed June 2010) 2008: BLLs lower than in 1994 but remain elevated 2009: Queensland government lead management report 2010: highest lead emissions in Australia

Niels C Munksgaard PhD · Mark P Taylor BSc(Hons), PhD · Alana Mackay BEnvMgt

Objectives: To determine the extent to which children with a hospital admission related to assault or maltreatment or to a notified sexually transmitted infection (STI) have contact with the Western Australian Department for Child Protection (DCP), and to investigate injuries and conditions often associated with child maltreatment and subsequent contact with the DCP.Design, participants and setting: Retrospective cohort study using de-identified, record-linked child protection and hospital morbidity data to identify all children aged 0–17 years in Western Australia between 1 January 1990 and 31 December 2005, and a subcohort of children born in WA between these dates, admissions of these children to public and private hospitals in WA, and their contact with the Western Australian DCP.Main outcome measures: Annual trends in notifications and substantiations of child maltreatment; proportion of children with assault-related and maltreatment-related hospital admissions resulting in notifications, substantiations, or out-of-home care.Results: Most children admitted for maltreatment-related reasons (90%) had contact with the DCP, with 81% of these children being notified, 68% having maltreatment substantiated, and 50% entering out-of-home care. Specific injuries and conditions were associated with children who had greater contact with the DCP, including retinal haemorrhage, rib fractures, multiple injuries, STIs at under 14 years of age, and malnourishment.Conclusions: The health system effectively identifies and notifies real cases of maltreatment, and a high proportion of these are substantiated. Health data play an important role in improving maltreatment surveillance, providing opportunities to make valid comparisons over time and between jurisdictions, as well as to monitor conditions and injuries associated with child maltreatment.

Melissa O’Donnell GradDipEd, MPsych, PhD · Natasha Nassar BEc, MPH, PhD · Helen M Leonard MB ChB, MPH · Richard P Mathews BPsych, MA · Yvonne G Patterson BSc, MPsych, MBA · Fiona J Stanley MB BS, MSc, MD

To the Editor: At the risk of appearing self-serving, we refer to our recently published article in which we recommended that there should be “greater uniformity in [food] packaging design, colour and descriptions”.1 In light of the Australian Government’s recent mandate on plain packaging for tobacco products,2 we can see no reason why this should not be extended to processed foods possessing no redeeming nutritional qualities. This would include soft drinks, potato chips, a great many of the so-called foods offered as replacements for fruit in children’s school lunches, biscuits and sweets. We challenge the Prime Minister and Minister for Health to do this, or explain why they won’t.

Bebe Loff · Brad R Crammond

MMR, Wakefield and The Lancet: what can we learn? Julie Leask, Robert Booy and Peter B McIntyre MJA 2010; 193 (3): 192 Missing text: In “MMR, Wakefield and The Lancet: what can we learn?” in the 5 July 2010 issue of the Journal (Med J Aust 2010; 193: 5-7), a line of text was omitted in the third-last paragraph (page 6). The text, from the beginning of the paragraph, should be “Second, public communication about vaccine risk, particularly regarding responses to adverse events following vaccination in new vaccine programs, needs to be planned, and should involve multiple stakeholders, as new issues can arise with little warning. This occurred as recently as 23 April 2010, when Australia’s Chief Medical Officer advised a temporary suspension of the 2010 trivalent seasonal influenza vaccine to children 5 years of age and under.15”

Julie Leask · Robert Booy · Peter B McIntyre

Vaccine scares are inevitable and we need to plan accordingly Twelve years after The Lancet published the study by Wakefield and colleagues1 that suggested a link between measles–mumps–rubella (MMR) vaccination, inflammatory bowel disease and autism, the journal has fully retracted the article. The retraction followed the findings of the Fitness to Practise Panel of the UK General Medical Council, released 28 January 2010, that certain statements in the article were false — namely, that children were “consecutively referred” and that investigations were “approved” by the local ethics committee.2 Wakefield’s theory had a significant impact on MMR vaccination rates in the United Kingdom. Looking at why Australia was relatively unaffected provides insights into how to better manage vaccine scares in the future. After publication of the article, many readers had written without delay to The Lancet regarding methodological deficiencies of the original research.3 Subsequent studies overwhelmingly supported the safety of MMR vaccination, but the accumulation of this evidence took years to achieve, with considerable opportunity costs, including time and resources spent on investigations which could have been better directed elsewhere.4 In the UK, the MMR vaccination rate fell from 91% in 1997–98 to 80% in 2003–04.5 Notably, there has been no decline in coverage for other vaccines for children in the UK. Despite a recovery in the MMR vaccination rate to 85% by 2008–09,5 there was a large upsurge in measles occurrences in the UK, beginning in 2002.6 In 2009, 1144 laboratory-confirmed measles cases were reported in England and Wales.6 The impact was also felt in the United States, where Wakefield’s theory augmented unsubstantiated fears about thiomersal (a mercury-based preservative) in some vaccines leading to autism. A recent survey found that one in four US parents believed that some vaccines cause autism in healthy children.7 Vaccine scares are typically depicted as conflicts between science and dogma; between the informed and the misinformed.8 The publication of Wakefield et al’s article in The Lancet breached the boundary between the two: here was a well credentialled specialist at a highly regarded teaching hospital whose findings were published in a renowned journal. These signifiers of prestige may have overshadowed the relatively poor quality of the science in the original article. Fortunately, in the years since the article was published, Australia’s MMR vaccine uptake has been relatively stable, as measured by the Australian Childhood Immunisation Register9 (Box). However, there were other consequences of Wakefield et al’s article, including the time and resources needed to address parents’ concerns.11 Some health professionals appeared to accept Wakefield’s theory. A 2006 survey of doctor and nurse vaccination providers in regional New South Wales found that 12% believed there was an association between MMR and autism, with a further 29% being unsure.11 Despite this, Australian MMR coverage remained essentially unaffected. The fact that Australian MMR vaccination rates remained stable may be related to some key differences between Australia and the UK: (i) in Wakefield, the UK had a “home-grown champion” for the MMR–autism theory; (ii) the extensive and sustained coverage of this issue in the UK media continually exposed new cohorts of parents of MMR-eligible children to the theory, while Australian television only sporadically reported the story; (iii) there is bipartisan political support for immunisation in Australia, whereas there was grandstanding by a member of the UK Conservative opposition and a refusal by the nation’s Labour Prime Minister to reveal whether his own son was immunised;12 and (iv) a foundation of mistrust in UK government assurances was perpetuated by public perceptions of the management of the Creutzfeldt–Jakob disease issue.13 The child vaccination program is held in high regard by most Australians, and, for this reason, the media have traditionally sidelined our small but vocal antivaccination lobby. This high level of public confidence has been helped by the structural support originating from the first National Immunisation Strategy in 1993, followed in 1997 by the federal Immunise Australia: Seven Point Plan, including financial incentives for parents and providers to adhere to the national vaccination schedule.14 What can the world learn from the Wakefield experience? First, we should accept vaccine scares as inevitable and plan accordingly. There remains the potential for vaccine safety scares to lead to large-scale opting out of vaccination, exacerbated by dwindling familiarity with the severe effects of vaccine-preventable diseases, and a groundswell of dissent from the antivaccination movement. Second, public communication about vaccine risk, particularly regarding responses to adverse events following vaccination in new vaccine programs, needs to be planned, and should involve multiple stakeholders, as new issues can arise with little warning. This occurred as recently as 23 April 2010, when Australia’s Chief Medical Officer advised a temporary suspension of the 2010 trivalent seasonal influenza vaccine to children 5 years of age and under.15 This suspension followed an increase in febrile convulsions among young child vaccine recipients reported in Western Australia. Third, the current level of trust in vaccine programs that we enjoy in Australia is a precious resource and must be continually fostered with good communication. Such communication is more than a didactic one-way process — it requires an interactive engagement between professionals, the public and the media. Clearly, this will be important and challenging after the recent suspension of the trivalent influenza vaccine, because professional and public concern generated by this suspension could spread to concern about influenza vaccination for other age groups.16 Australian federal, state and territory governments are now developing a new national vaccination strategy. Essential considerations in this strategy will be how the postmarketing surveillance of adverse events following vaccination is to be conducted, and authoritative and timely communication about vaccine safety with professionals and the public. MMR, DTP, OPV, Hib and hepatitis B vaccine coverage for Australian children at 24 months of age, 2000 to 2009*10 MMR = measles–mumps–rubella. DTP = diphtheria–tetanus–pertussis. OPV = oral polio vaccine. Hib = Haemophilus influenzae type b. Hep B = hepatitis B. * Figure updated with 2008–2009 data (Brynley Hull, Epidemiologist, National Centre for Immunisation Research and Surveillance, personal communication).

Julie Leask PhD, MPH, DipAppSci · Robert Booy MD, FRACP, FRCPCH · Peter B McIntyre PhD, FRACP, FAFPHM

Bowel cancer kills over 4000 Australians each year. From the late 1980s to October 2005, research evidence guided the development of bowel cancer screening policy proposals, but political, financial and institutional constraints restricted implementation options. Since 2006, the Australian Government has provided a limited bowel cancer screening program, based on what the government deems it can afford, rather than on evidence of what is required to implement a successful population-based screening program. Even a partial program can be implemented in an evidence-based way, and failure to do so threatens to undermine the potential public health gains of a national bowel cancer screening program. To realise the expected public health gains from a national bowel cancer screening program, bowel cancer screening policy should return to its evidence-based beginnings, starting with an analysis of Australian age-specific cost-effectiveness data.

Kathy L Flitcroft BBSc, MA(Govt), GradCertHealthPolicy · Glenn P Salkeld GDipHealthEconomics, MPH, PhD · James A Gillespie PhD · Lyndal J Trevena MB BS(Hons), MPhilPH, PhD · Les M Irwig MB BCh, PhD, FFPHM

To the Editor: We report the case of a 19-year-old female veterinary student who presented with a 2-week history of a rapidly growing mass on the lateral side of the deltoid area of her left arm. On examination, the mass was soft, freely movable, slightly warm and non-tender. There was no regional lymphadenopathy. The patient was afebrile, with no signs of systemic illness. Ultrasound showed a 3.2 × 2.3 × 1 cm, low-echogenic, lobulated lesion in the subcutaneous fat, with surrounding increased echogenicity suggestive of inflammation. Magnetic resonance imaging showed a poorly defined lesion throughout the deep and superficial fascia, with infiltration into the underlying deltoid muscle (Box 1). A provisional diagnosis of sarcoma was made, but an ultrasound-guided core biopsy sample showed non-necrotising epithelioid granulomas (Box 2). Two weeks after presentation, the patient noticed a smaller raised lump, about 1 cm in diameter, on the volar aspect of her left forearm. Four months before presentation, following negative results of both Q fever serological testing and a Q fever skin test administered on the volar aspect of her left forearm (at the site of the smaller lump), the patient had received a Q-VAX (CSL, Melbourne, Vic) vaccination in the left deltoid (at the site corresponding to the larger mass). Three months after this, and about 3 weeks before the deltoid mass first appeared, the patient received a Fluvax (CSL, Melbourne, Vic) influenza vaccination at the same left-deltoid site as the Q fever vaccination. This raises the possibility that the influenza vaccination may have been associated with the subsequent Q fever granuloma reaction. Q fever, a disease caused by the zoonotic rickettsial organism Coxiella burnetii, is an occupational hazard for many Australians in animal-related professions. The disease is characterised by an acute, self-limiting febrile illness, with pneumonia and hepatitis being infrequent complications. In 2001, an Australian national Q fever vaccination program was initiated, which led to a 50% decline in the incidence of Q fever.1 Side effects are normally rare and minor; during 2001–2004, only 86 adverse reactions were reported from about 49 000 vaccinations.2 Development of non-necrotising granulomas following Q fever vaccination is uncommon, with only six cases previously described.3-5 To explore the possibility of a causal association between influenza vaccination, Q fever vaccination, and development of a granuloma, we traced four of these six patients with Q fever granuloma by contacting the authors of the previous reports. One patient had been vaccinated against influenza 2 months before the time of Q fever vaccination, and another had influenza vaccination afterwards (as in our case). Of the five cases (including our case) for which clinical history was available, three had a temporal association between influenza vaccination and Q fever vaccination, followed by the development of the non-necrotising granuloma. The indurated lesion at the separate Q fever skin-test site on the volar forearm, found in two other patients5 as well as ours, supports the notion of a systemic immune reaction rather than simply a local reaction at the vaccination site. The Naranjo score in this case was 7, indicating a “probable” adverse drug reaction. Although the granuloma was self-limited in all known cases, this case shows that there is significant risk of misdiagnosis on clinical grounds. It seems prudent to be aware of the possible association between these two vaccinations. Magnetic resonance images of lesion Axial (top) and coronal T1-weighted fat-saturated post-contrast (bottom) images demonstrate a poorly defined enhancing lesion (red arrows) in the subcutaneous fat, which superficially infiltrates and extends in a plaque-like manner in relation to the underlying deltoid muscle (white arrows). 2 Ultrasound-guided core biopsy sample of lesion The core biopsy of fibroadipose tissue shows numerous well formed non-necrotising epithelioid granulomas (arrows). The granulomas are composed of epithelioid histiocytes and a few multinucleated giant cells, surrounded by numerous lymphocytes (a mixture of B and T cells, with a greater proportion of T cells). (Original magnification × 100; haematoxylin–eosin stain.)

Deborah Burnett · Leslie Burnett

Objective: To assess women’s compliance with different Australian guidelines on alcohol intake during pregnancy and examine factors that might influence compliance.Design, setting and participants: We analysed prospective, population-based data on women aged 22–33 years who were pregnant before October 2001, when guidelines recommended zero alcohol (n = 419), or were first pregnant after October 2001, when guidelines recommended low alcohol intake (n = 829). Data were obtained from surveys conducted in 1996, 2000, 2003 and 2006 as part of the Australian Longitudinal Study on Women’s Health.Main outcome measures: Relative risks (RRs) for zero alcohol intake, low alcohol intake and compliance with alcohol guidelines, estimated by a modified Poisson regression model with robust error variance.Results: About 80% of women consumed alcohol during pregnancy under zero and low alcohol guidelines. Compliance with zero alcohol guidelines or low alcohol guidelines (up to two drinks per day and less than seven drinks per week) was the same for women who were pregnant before October 2001 and women who were first pregnant after October 2001 (20% v 17% for compliance with zero alcohol guidelines, P > 0.01; 75% v 80% for compliance with low alcohol guidelines, P > 0.01). Over 90% of women drank alcohol before pregnancy and prior alcohol intake had a strong effect on alcohol intake during pregnancy, even at low levels (RR for zero alcohol, 0.21 [95% CI, 0.16–0.28]; RR for low alcohol, 0.91 [95% CI, 0.86–0.96]). RR for compliance with guidelines was 3.54 (95% CI, 2.85–4.40) for women who were pregnant while low alcohol intake was recommended, compared with those who were pregnant while zero alcohol guidelines were in place.Conclusion: The October 2001 change in alcohol guidelines does not appear to have changed behaviour. Risks associated with different levels of alcohol intake during pregnancy need to be clearly established and communicated.

Jennifer R Powers BSc, MMedStat · Deborah J Loxton BPsych(Hons), PhD · Lucy A Burns MPH, PhD, GradCertHlthPol · Anthony Shakeshaft BA, MA, PhD · Elizabeth J Elliott MD, MPhil, FRACP · Adrian J Dunlop MB BS, PhD, FAChAM

To the Editor: We describe here some of the difficulties in managing and investigating outbreaks of viral respiratory infection in aged care facilities (ACFs) in the context of an influenza pandemic. This adds to the previous report on logistics in a hospital setting.1 On 12 June 2009, NSW Health received a call from a surveillance officer in a remote town regarding a possible pandemic (H1N1) 2009 influenza outbreak in an ACF. On 9 June, a 77-year-old female resident had become unwell, without specific symptoms of influenza-like illness. From 7 to 10 June, nine of the other 27 residents developed influenza-like illness. On 10 June, nasal swabs were taken from the 10 unwell residents by the local general practitioner for influenza nucleic acid testing (NAT). On 12 June, the index case tested positive for pandemic influenza, while the other residents tested negative. Due to concern that there might be a pandemic influenza outbreak in the facility, the index case and the nine residents with influenza-like illness were given oseltamivir (75 mg twice a day for 5 days) from 13 June; the other 18 residents and the 27 staff were given oseltamivir prophylaxis (75 mg daily for 10 days). A formal outbreak investigation and further laboratory testing (NAT, serological testing) revealed a dual outbreak dominated by rhinovirus (10 cases), with two cases of pandemic influenza and one case of untyped influenza A. All 28 residents and 26 of the 27 staff had received seasonal influenza vaccine in early 2009. This outbreak illustrates that more than one respiratory virus may co-circulate in ACFs during winter outbreaks of respiratory infection. We followed Department of Health and Ageing policy guidelines for oseltamivir use in ACFs2 and the facility was closed to visitors from 12 to 18 June. However, as all residents had received seasonal influenza vaccination, and given that older people are generally at lower risk of pandemic (H1N1) 2009 influenza,3 we could have had a higher threshold for oseltamivir use. The total estimated cost of treatment and prophylaxis was $2750 (55 residents and staff at $50/person) for oseltamivir alone. Co-infection with respiratory viruses may be more common than thought in ACFs; a recent Canadian study found two and three different pathogens in 15% and 4% of respiratory infection outbreaks, respectively, from a total of 83 outbreaks (of which 91% occurred in long-term care facilities).4 If many ACF outbreaks have more than one respiratory virus involved, laboratory investigations should take a multiplex approach that covers common respiratory viruses. As many patients as practical (at least five) should be swabbed and tested to guide treatment, prophylaxis and other investigations. Community influenza surveillance should ideally include information on sensitivity to oseltamivir, and on other circulating respiratory viruses.

Gulam Khandaker · Bridget Doyle · Dominic E Dwyer · Robert Booy

Objective: To compare clinical oral health outcomes between a birth cohort of young Australian Aboriginal adults and age-matched, national-level counterparts.Design, setting and participants: Comparison of outcomes between the dental component of Wave-3 of the Aboriginal Birth Cohort (ABC) study — a cross-sectional study conducted between January 2006 and December 2007, nested within a prospective longitudinal investigation in the Northern Territory’s Top End — and the 2004–06 National Survey of Adult Oral Health (NSAOH), a representative survey of the Australian population. Data were analysed for 442 ABC study participants and 202 NSAOH participants aged 16–20 years.Main outcome measures: Severity and prevalence of clinical oral health outcomes.Results: The mean number of decayed teeth was 8.0 times higher among ABC study participants than NSAOH participants, while the prevalence of untreated decayed teeth was 3.1 times higher. ABC study participants experienced 10.8 times the prevalence of moderate or severe periodontal disease of NSAOH participants, and 1.9, 4.1 and 4.5 times the prevalence of calculus, plaque and gingivitis, respectively.Conclusion: Adverse clinical oral health outcomes were 2–11 times higher in a cohort of young Australian Aboriginal adults than their age-matched, nationally representative counterparts.

Lisa M Jamieson PhD · Susan M Sayers PhD · Kaye F Roberts-Thomson MPH

Objective: To compare bloodstream infection (BSI) rates, pathogens and mortality among Indigenous and non-Indigenous adults in central Australia.Design, participants and setting: Retrospective study of adult patients (aged ≥ 15 years) admitted to Alice Springs Hospital (ASH) between 1 January 2001 and 31 December 2005. Patients were followed up until 30 June 2008.Main outcome measures: Admission-based and population-based BSI rates and mortality rates for Indigenous and non-Indigenous adults.Results: During the study period, there were 824 BSI episodes (Indigenous, 753; non-Indigenous, 71). The admission-based BSI rate for Indigenous patients was 26.5 (95% CI, 26.4–26.6) per 1000 adult admissions, compared with 5.2 (95% CI, 5.1–5.2) per 1000 adult admissions for non-Indigenous patients (infection rate ratio [IRR], 5.13 [95% CI, 5.10–5.18]). The population-based BSI rate was 1354.7 (95% CI, 1256.3–1460.8) per 100 000 persons per year among Indigenous patients and 69.9 (95% CI, 55.1–88.6) per 100 000 persons per year among non-Indigenous patients (IRR, 19.4 [95% CI, 15.1–24.9]). These differences were not explained by higher comorbidity levels among Indigenous patients. Human T-cell lymphotropic virus type 1 and Strongyloides stercoralis infected 43% and 35%, respectively, of Indigenous patients tested. The risk of death during the follow-up period was 32.1% for Indigenous and 13.4% for non-Indigenous patients (hazard ratio [HR], 2.69 [95% CI, 1.38–5.25]; P = 0.004). Mortality rates were higher among Indigenous patients who had more than a single BSI (HR, 1.86 [95% CI, 1.32–2.62]; P < 0.001). The mean age at death was 48.5 years (SD, 16.2 years) for Indigenous patients and 75.1 years (SD, 18.7 years) for non-Indigenous patients (P < 0.001).Conclusion: Indigenous adults living in central Australia experience BSI rates that are among the highest reported in the world. These are associated with a high risk of death, and are a likely consequence of the poor socioeconomic circumstances of Indigenous people.

Lloyd J Einsiedel PhD, FRACP · Richard J Woodman PhD

Objective: To determine the burden of hospitalised, radiologically confirmed pneumonia (World Health Organization protocol) in Northern Territory Indigenous children.Design, setting and participants: Historical, observational study of all hospital admissions for any diagnosis of NT resident Indigenous children, aged between ≥ 29 days and < 5 years, 1 April 1997 to 31 March 2005.Intervention: All chest radiographs taken during these admissions, regardless of diagnosis, were assessed for pneumonia in accordance with the WHO protocol.Main outcome measure: The primary outcome was endpoint consolidation (dense fluffy consolidation [alveolar infiltrate] of a portion of a lobe or the entire lung) present on a chest radiograph within 3 days of hospitalisation.Results: We analysed data on 24 115 hospitalised episodes of care for 9492 children and 13 683 chest radiographs. The average annual cumulative incidence of endpoint consolidation was 26.6 per 1000 population per year (95% CI, 25.3–27.9); 57.5 per 1000 per year in infants aged 1–11 months, 38.3 per 1000 per year in those aged 12–23 months, and 13.3 per 1000 per year in those aged 24–59 months. In all age groups, rates of endpoint consolidation in children in the arid southern region of NT were about twice that of children in the tropical northern region.Conclusion: The rates of severe pneumonia in hospitalised NT Indigenous children are among the highest reported in the world. Reducing this unacceptable burden of disease should be a national health priority.

Kerry-Ann F O’Grady GDipPH, MAppEpid, PhD · Debbie M Taylor-Thomson BPharm · Anne B Chang FRACP, MPHTM, PhD · Paul J Torzillo AM, MB BS, FRACP, FJFICM · Peter S Morris MB BS, FRACP, PhD · Grant A Mackenzie MB BS, PhD · Gavin R Wheaton MB BS, FRACP, FCSANZ · Paul A Bauert MB BS, FRACP · Margaret P De Campo FRANZCR, MPH, GDipEpibiostats · John F De Campo FRANZCR, MHA, FRACMA · Alan R Ruben MB BS, MAppEpid

I was asked to review the article below, and found it a compelling read. Zimmet has clearly gone to central Australia with an open heart and mind, and has discovered an intriguing world previously not known to him. He ends his article with a gentle challenge to those of us who have the privilege to work in health care, to consider whether our current methods are best practice, and whether they are best suited to all who seek our help. Having read this article, I found myself with two unanswered questions. First, given that there have now been several generations of Aboriginal people advocating for improvement to the dire circumstances in Aboriginal health, how is it that our young colleagues are still so shocked when they come to our communities? What is it that we (older Aboriginal people) have failed to say to get the attention of our health care providers, and their teachers? Second, how can we see to it that we produce many more graduates of the quality of Zimmet, who see the world with fresh eyes, are not afraid to ask the obvious questions, and are bold enough to tell us all that the Emperor is indeed naked? I strongly recommend that Journal readers take the time to read this article, and spend a moment or two in reflection to examine their own souls, to see if they can rise to this young man’s challenge. Louis G Peachey, BMed, FACRRM, Foundation President, Australian Indigenous Doctors Association, Canberra, ACT. In the Alice Springs paediatric ward, the vast majority of the 20 or so children are Aboriginal. They often have unique first names with an African–American or biblical flavour and distinctive spellings. Some come from town, while others travel from hundreds of kilometres away. Parents often lie with their children on mattresses on the floor, watching Disney DVDs, drawing, and waiting for the sporadic visits of hospital staff. For families, a visit to the ward can mean a period of isolation from their community or time with relatives who live in Alice Springs or who also happen to be in the hospital. It may be an unwanted upheaval from relatively peaceful community life, or an urgent and welcome respite from upheavals at home. What distinguishes the Alice Springs ward most is the type and severity of paediatric health issues. There is a whole other spectrum of health and disease in central Australia — one that challenges the heart and the mind. Labels that don’t stickThe categorisations of disease as I knew them after several years working in Melbourne seemed to collapse when I arrived in Alice Springs. Trying to apply learnt diagnostic and management techniques proved futile in the face of the ostensibly distinct nature of “common” illnesses like gastroenteritis, pneumonia and ear infections in central Australian children, let alone their coexistence with nutritional, social, cultural and historical factors. It is not uncommon to see 4-month-old infants with perforated ear drums. In contrast to coastal city paediatrics, “pink” or “red” tympanic membranes suggesting otitis media do not show up as threats on the diagnostic radar. Ear examination in central Australia is focused on detecting the presence or absence of pus or perforation of the tympanic membrane. Anything less is considered “healthy”. A child presenting with “gastroenteritis” can mean anything from a prolonged cryptosporidium infection to multiple parasitic and worm infestations. Families often refer to these different ailments generically as “guts ache”. Treatment ranges from frequent correction of significant acidoses and hypokalaemia, to using nitazoxanide to treat cryptosporidium. This drug is only available on the special access scheme in Australia, not because it is unsafe, but because so few children need it. The evidence for its use, however, is limited to a few studies, mainly in settings somewhat different to Alice Springs. This is a recurring theme in paediatric medicine here — that evidence from either “first-world” metropolitan research centres or the “third-world” does not necessarily translate to what health workers see in central Australia, a “fourth-world” inside our country. Further, century-old pathological definitions that define disease rather than causation or environmental and social contributors often do not provide us with adequate solutions today. They help us to heal the surface of the skin or lungs, perhaps the lining of the gut, but not always the deeper tissues. The tragically prevalent conditions of chronic suppurative otitis media and chronic suppurative lung disease in children could perhaps be more accurately defined as “chronic exposure to over-crowding, tobacco smoke, inadequate nutrition and bacterial respiratory tract colonisation”. Similarly “failure to thrive” might often be described as “failures of family and community structures, supports and function”. Effects on causesAs paediatric doctors at the hospital, we work closely with families, Aboriginal liaison officers, community organisations and even traditional healers. However, I feel we see the causative cycles of the social determinants of Aboriginal child health, yet cannot always avert the outcomes. Just like someone watching the desert heat evaporate the land’s water over several days, I often feel incapable of doing more than merely waiting for the storm to arrive. Chronic ear infections cause endemic conductive hearing loss. The result for many children is developmental, learning and behavioural issues with profound ramifications for schooling, employment prospects, parenting capabilities, their own future children and their communities. We try to encourage and empower adults to mop their children’s suppurating ears regularly to facilitate healing and help antimicrobial ear drops reach the middle ear, but, often, we don’t properly explain why this is important, or there are no tissues available at home, no refrigerator to safely store the antibiotics, or more urgent daily issues arise. The daunting challenges of social disadvantage, disharmony, and physical distance can cause health practitioners to minimise our efforts. Sometimes optimum care is not provided on the basis of assumptions about what families will do when they leave. Rationalisations such as “they are not going to give the medication so why bother” or “they’ll be back with the same problem in a week” are sometimes heard. This can be a result of us not being able to see the children and families we look after in the foreground, with their own unique strengths and weaknesses, existing within and beyond these pervasive problems. Seeing difference, seeing ways through the gapsOur lack of flexibility and our inability to — accommodate difference can potentially perpetuate the health gaps. There are many situations in which the pressures of the ward have limited my time to be patient with a family, listen carefully, or negotiate a treatment plan meaningfully, in order to understand the family’s perspective better and expedite the child’s recovery. I have also found it extremely important always to look for differences between individual Aboriginal children and families to prevent comical gaffes, therapeutic disasters and the spectre of racism. Aboriginality is not homogenous. Alice Springs and central Australian people have a complexity that is at odds with the predictability of the desert heat. If we accept that a fundamental component of racism is generalisation, then we are all caught in its web more than we would like to admit. This can be as simple as me assuming that a very dark skinned Aboriginal mother could speak an Indigenous language, or that her English would be limited. Neither was true and she spent much time articulating her worries about breastfeeding. Language difficulties play a major role in paediatric health gaps in central Australia. So much still seems to be “lost in translation” in the gap between English and the multitude of local Aboriginal languages, and between differing understandings of symptom durations, rationales for treatment and discharge plans. Translators are not available after hours, when clarity is often critical. There are other dimensions. There are well known and beautiful places near and around Alice Springs called “gaps”, where the mountain ranges part to reveal waterholes and jagged red rock facades. These geographical gaps were given names like Heavitree Gap or Emily’s Gap by Anglo-European explorers. They are important dreaming sites for the local Arrernte people. Heavitree Gap is a place where the local traditional owners would formally welcome and accept visiting people onto their lands. For Arrernte people then, talk of closing “gaps”, may have very different meanings from our own. Dr Patricia Miller, a senior Arrernte woman, recalls another elder fearing that someone would literally close Heavitree Gap, thereby preventing people and transport from entering Alice Springs directly. She could not understand why there not been meetings to explain the closure of such a significant cultural place. “Closing the gap” can also have an array of ramifications for different families. For some, it may mean having to bring their children to clinics for a seemingly endless array of needles, whether for vaccinations, antibiotics or iron supplementation. For others, it is about not having to tell three or four different doctors in one day what has happened to their child after being transferred from a remote area, or not having to explain the same thing repeatedly because community and hospital information systems are in silos. For some Aboriginal people, “closing the gap” may mean doctors learning to “speak” to each other better. For one family, “closing the gap” is a hope for a larger home in which 20 people do not have to share two bedrooms, so their child can get some sleep away from noisy adults. For another family living in town, it may be that “closing the gap” means not having their child’s Aboriginal status questioned because of his or her lighter skin colour and mixed descent. Looking and listeningSome of the health gaps and misunderstandings in health care also relate to how, for many Aboriginal people, conceptions of space and time are significantly different to medical thought. The chain of cause and effect, and the ideas that illnesses have names, time courses and scientific reasons for appearing are often not the main paradigms for our patients in central Australia. A grandmother explained to me, with the assistance of an Aboriginal liaison officer, that the reason why her 18-month-old grand-daughter was not eating or growing properly was not because she was still breastfed by her mother and had trouble eating solids, but because the unborn baby her mother was carrying was playing tricks and interfering with its sibling’s eating habits. A few mothers on the ward told me about the changing winds and misplaced internal rocks that had ravaged their children’s bodies. They had taken their children to see the traditional healers before seeing a doctor. One mother, a painter and former Aboriginal liaison officer, told me she struggled with prioritising one form of healing over the other. This mother and her child are just one example of the astounding resilience of children and families in central Australia. Their ability to remain healthy, keep a sense of humour, stay positive and return to the hospital or clinic for a visit is remarkable. It is even more extraordinary considering the harsh environment and limited resources. This resilience needs to be supported and harnessed at all costs. It is critical that we strengthen Aboriginal families by using their unique structures, dynamics, hopes and needs. The challenge, then, is to balance a paediatric perspective with an Aboriginal one. The two are not mutually exclusive. We have to keep our paediatric medical gaze sharp and unprejudiced. An evidence base should be built for treating the unique conditions that are seen in central Australian children. Concurrently, ensuring that national standards of nutritional and child development health are implemented in the region is paramount, as a matter of health equity and human rights. We need to make sure that what we know as “truth” in paediatric medicine is applied equally to children living in remote areas and, at the same time, keep our eyes, ears and hearts open to the varying strengths and needs of each child, carer, family or community. We should listen to what they tell us and be comfortable with the silences. We need to find ways through the gaps from several vantage points, with Aboriginal people leading the way back to their own health.

Marcel D Zimmet MB BS/BA(Hons)

To the Editor: Aboriginal and Torres Strait Islander people were more at risk of hospitalisation, admission to intensive care units and death during the 2009 influenza A pandemic than non-Indigenous Australians.1 We conducted a descriptive analysis of our response to the pandemic at Winnunga Nimmityjah Aboriginal Health Service (Winnunga) — an Aboriginal community controlled health service in Canberra, Australian Capital Territory, which provides comprehensive primary health care to more than 3500 patients per year. Data were sourced from the Winnunga electronic patient record system, pathology laboratories and ACT Health. The Winnunga Board approved this analysis and report for publication. In May 2009, we implemented the pre-existing Winnunga influenza pandemic plan, working closely with ACT Health and the ACT Division of General Practice. We enhanced infection control, implemented influenza testing procedures, initiated electronic data collection and obtained oseltamivir from the ACT stockpile to dispense on site. We adapted ACT Health pandemic protocols to create a flow chart appropriate for Winnunga, with approval from the ACT Chief Health Officer. This involved using clinical discretion to decide whether to dispense oseltamivir to Aboriginal and Torres Strait Islander people with mild illness, and included the provision to supply prophylactic oseltamivir to high-risk household contacts, especially in overcrowded households. A plan was made to open an on-site influenza clinic, but this was not necessary. Increased testing for influenza commenced in late May. The first patient with pandemic (H1N1) 2009 influenza was identified on 1 July (Box). Of the 168 nasal swabs tested for influenza by polymerase chain reaction analysis, 52 (31%) were positive for pandemic (H1N1) 2009 influenza. In addition, six Winnunga patients tested positive at other locations. In late July, testing guidelines changed and laboratory testing was no longer recommended for most patients with influenza-like illness.2 Consequently, we did not identify test-positive cases past the beginning of August. The actual number of cases of pandemic influenza that occurred in Winnunga patients is unknown. Of the 58 patients who tested positive, 54 were Aboriginal and/or Torres Strait Islander, 28 were male, and 47 were ACT residents. The mean age was 22 years (range, 0–62 years), 31 patients were aged under 20 years and four patients were pregnant. There was one overnight hospitalisation. During July, Winnunga accounted for 8% (44/551) of all notified pandemic influenza cases in the ACT — more than expected based on patient numbers alone. However, more testing may have been done at Winnunga than at other organisations because of our high-risk population. In July and August, 13% (204/1604) of all presenting patients at Winnunga had an influenza-like illness. There were 229 recorded episodes of influenza-like illness between May and November with a sharp peak in July and a smaller peak in August (Box). Oseltamivir dispensing commenced 1 week before identification of the first patient who tested positive, and corresponded with episodes of influenza-like illness (Box). A total of 107 courses of oseltamivir were dispensed to 33 children and 74 adults. Clinical risk factors other than Aboriginal and Torres Strait Islander status were recorded for 47 of these patients. Oseltamivir dispensed to Winnunga patients at other locations was not included in our analysis. We do not know whether oseltamivir made a difference in reducing severity of disease or preventing hospitalisations in our patients. During July and August 2009, pandemic influenza created an increased workload at Winnunga. Although there were some staff absences due to pandemic influenza, these were short and did not significantly affect clinical functions. Pandemic influenza in patients was also not as severe as planned for. A more severe pandemic would place a significant burden on our already busy Aboriginal medical service. A pre-existing influenza pandemic plan, internal public health capacity, good working relationships with local health agencies, on-site dispensing and service-specific protocols were important features of our response to the 2009 pandemic. Vaccination for influenza is being strongly promoted at Winnunga in 2010. Influenza-like illness, influenza testing, tests positive for pandemic (H1N1) 2009 influenza, and courses of oseltamivir dispensed at Winnunga Nimmityjah Aboriginal Health Service, May to November 2009

Ana Herceg · Peter G Sharp · Christine G Arthur · Julie A Tongs

Doctors can best contribute to environmental sustainability by their example and by working actively to change social norms McDermott’s article in this issue of the Journal (The carbon footprints of obesity, chronic disease and population growth: four things doctors can do)1 calls doctors to arms, in the tradition of the famed 19th-century German pathologist Rudolf Virchow and today’s Medical Association for the Prevention of War, to contribute to a better world. Its writer draws attention to profound issues and is to be congratulated. However, her recommendations are not so straightforward. Taken neat, the cure might do more harm than good. Consider obesity. Indeed, a recent article found that an obese population requires substantially more food energy than one with a normal body mass index distribution,2 although it is unclear whether the authors fully considered the shorter life expectancy and lower class-related reduction in other aspects of the ecological footprint of the obese. Elite sportspeople and military recruits also consume disproportionate amounts of food and other resources, but these harder targets were not mentioned. Singling out the obese seems simplistic and discriminatory.3 McDermott also advocates enhanced rights-based family planning, in rich and poor nations, as a means to reduce climate change. She discusses a recent report that found a high climate return for a low cost (that of funding family planning).4 As she mentions,1 the methods used in this thesis can be challenged, as it is obvious that growth in size of wealthy populations fuels far more climate change than does growth in size of poor populations, a distinction that is not clearly made. Criticising the poor for their population growth rate risks becoming another form of victim blaming. However, in the long run, slower population growth everywhere (especially in countries like Australia and the United States) will slow greenhouse gas accumulation. It will also enhance population health in low-income countries. McDermott also correctly advocates social, health and rights-based strategies to complement the largely technical and economic approach to climate change that is now dominant.5 It is easy to list actions that will improve global public health. However, compilers of lists need not only to prioritise their lists’ components, but also to describe how we can realise them. It is true that doctors are powerful role models, and the recent tentative steps by doctors and medical associations to recognise and address the health and other risks of climate change6 are important. However, the virtual absence of health (and the global population) as agenda items for the recent climate change talks in Copenhagen underlines how far there is to go. It is also easy to call for “whole-of-government” approaches, whether to slow climate change, fix the obesogenic environment or to enhance equity. Easy to say, hard to achieve. A well known economic principle is the law of diminishing returns. A second ice-cream is not as tasty as the first. Less well known is the Matthew effect, or the law of increasing returns.7 This principle is a powerful impediment, not only to whole-of-government reforms, but to the transition to sustainability more broadly. Simply put, this principle describes how groups with influence are able to rig public opinion and legislate to benefit powerful minorities rather than the public good.8 The 18th-century philosopher Adam Smith warned against monopolies. The benefits to society and public health, including life expectancy, from reduced inequality are perennially rediscovered.9 Yet progress on reforming coal-fired electricity generation remains stalled both here and in Washington. Advancement of public goods such as public health and climate stability is thwarted by well funded and well organised lobbyists, who far outnumber public-good lobbyists.10 This illustrates an embedded Matthew effect, long operant in the US, and one about which Australia should not be complacent. Our long life expectancy might not always remain so.11 What is it, in this country, that prevents more extreme ideologies from taking root? The answer, in part, lies in our cultural norms and practices, such as our ostensibly “fair go” society, and in a reasonably free press. McDermott’s article1 and its receptive readers help counter the advantages of the powerful. On reflection, it is not hard to see how the attitudes and norms of readers sympathetic to this analysis evolved. We all received a publicly subsidised education. Some of us descend from people who struggled for the opportunities and wealth we may now take for granted. Before our birth, large social movements worked intensely for a fairer world, using organised tactics that reduced the advantages, often hereditary, of those more powerful. Some of this resolution was forged in the trauma of World War II and the preceding Great Depression, helping to deliver the National Health Service in the United Kingdom and diluted copies of it elsewhere. Then, largely in the same English-speaking world, a less vigilant generation was seduced by the “fool’s gold” of neoliberalism, the conceit that marketism would deliver more public goods than would regulation.12 This false remedy has not only generated a decline in equity, but now threatens the whole of civilization.11 What can doctors do? Reflect and act, not just on the four themes proposed by McDermott, but on four hundred more. They can green their clinics, reduce their own footprint and join like-minded groups. There is no single recipe, but the principles of environmental sustainability, justice and commonsense are integral, as are courage and collaboration. Such action may work as a social vaccine against despair. Doctors, with other groups, may long postpone the world’s admission to intensive care.

Colin D Butler BMed, MSc, PhD