Topics
Environmental health
Health in the green economy
Health reporter Ray Moynihan welcomes the side effects of prescriptions to fight climate change As one of the planet’s most polluting populations, it’s perhaps understandable that many Australians have a good deal of fear and loathing about cleaning up our act. What might lift our mood for change is the growing evidence that strategies to reduce greenhouse gas emissions can directly improve the length and quality of human life. The World Health Organization is currently assessing the health impacts of different climate change mitigation strategies, and it’s come to some compelling, though still tentative, conclusions. The project, called Health in the Green Economy, has found that although many policies will have benefits for both health and the environment, “some of those having the largest impact on mitigation may also deliver the largest health gains”.1 In housing design, for example, natural ventilation and better insulation are obvious energy-efficient measures, but they may also reduce allergies, asthma and, in some places, illnesses associated with cold and damp. In kitchens throughout the developing world, cleaner, more fuel-efficient stoves could cut rates of childhood pneumonia and adult lung cancer and chronic obstructive pulmonary disease, while also reducing greenhouse gas emissions in the residential sector. In the area of transport, the WHO has some strong words about the health benefits of shifting focus from the private car to public transport, pedal-power and pedestrians. Such a shift, it says, could reduce respiratory and heart disease from air pollution, cut injuries from road accidents, and help prevent obesity, diabetes and cancer by boosting physical activity, potentially saving millions of lives every year. “A shift to active transport (walking and cycling) and rapid transit/public transport”, says the WHO review of the evidence, “can yield much greater immediate health ‘co-benefits’ compared with improving fuel and vehicle efficiency, yet the latter has been the mitigation strategy most emphasized by the Intergovernmental Panel on Climate Change”.1 The health care sector itself has been identified as another key climate change culprit, with estimates that it contributes perhaps 8% of all greenhouse gas emissions in the United States.2 Energy-intensive activities, gaseous wastes and huge use of water and transportation all contribute to health’s unhealthy carbon footprint, which until now has failed to attract much attention from those seeking to slow global warming. The WHO review again suggests win–win strategies, including the “greening” of health care facilities, by using more renewable energy and procuring fewer medical products that ultimately remain unused. “[The health care] sector is worthy of special attention due to its size, its growth, and its direct impacts on health”, says the review.1 Other groups, such as the global non-government organisation Health Care Without Harm, are already working on more “ecologically sound” alternatives to existing health care practices. One of its current campaigns is promoting more sustainable management of toxic medical waste in a demonstration project across eight nations, designed to reduce polluting gases and improve the health and safety of health care workers.3 A futuristic vision of health care in the post-peak oil world appeared in the BMJ last year, complete with dreams of less energy-intensive therapies and non-petroleum-based pharmaceuticals, delivered via hospitals that are accessible to all by foot, bicycle and public transport.4 Whether that future appeals to you or not, it’s clear that as we finally face up to climate change, the business of health will increasingly be exposed to the glare of environmental scrutiny. In Australia, the newly formed Climate and Health Alliance is stressing the potential win–wins for health and the environment,5 and in December the world’s first Global Climate and Health Summit will meet in Durban, South Africa. For anyone simply interested in an evidence-informed approach to decision making, the WHO is putting some fascinating new facts on the table that are helping to show which climate change strategies might have the biggest health benefits, and which carry risks. At the launch of the Health in the Green Economy project earlier this year in Washington, DC, a leading WHO figure called for a “new alliance” of policymakers across the climate change, housing, transport and health sectors. Let’s hope the call was heard loud and clear down under.
Ray Moynihan BA
Adverse events associated with 2010 CSL and other inactivated influenza vaccines
The 2010 trivalent influenza vaccine (TIV) manufactured by CSL Biotherapies (CSL) was associated with increased febrile reactions, including febrile convulsions, among Australian children. CSL is one of the few manufacturers that use deoxycholate as the virus-splitting agent in the manufacture of TIV. Clusters of adverse events following immunisation (AEFI) have been previously linked to other deoxycholate-split TIV formulations in Europe and Canada. We hypothesise that suboptimal virus splitting or other mechanisms related to the use of deoxycholate may have played a role in adverse events linked to the 2010 CSL TIV. This hypothesis garners support from a recent United States Food and Drug Administration warning letter indicating that CSL failed to determine optimal splitting conditions for new virus strains and that assays to assess virus splitting had not been validated. While there may be other causes, the use of deoxycholate should be further explored. Comprehensive and timely investigations of AEFI, especially those involving children, are necessary to prevent their recurrence and to maintain public confidence in vaccination programs.
Heath A Kelly BSc, MB BS, MPH · Danuta M Skowronski MD, FRCPC · Gaston De Serres MD, PhD · Paul V Effler MD, MPH
Challenges in postexposure prophylaxis of a vaccinated bat carer
To the Editor: Australian bat lyssavirus (ABL) has the potential to cause fatal encephalitis in humans exposed to infection through bat bites or scratches. There is no cure for rabies currently available, so postexposure prophylaxis with rabies vaccine and rabies immune globulin is recommended following potential human exposure, such as after bites or scratches. People who work with or handle bats should be vaccinated, should regularly monitor their rabies antibody levels to ensure maximum protection, and should seek immediate medical attention for all potential ABL exposures.1 We report the case of a 42-year-old man bitten by a black flying fox (Pteropus alecto) during the retrieval of the bat from a suburban Brisbane, Queensland, backyard. The bat had been found on the ground in the daytime, vocalising and acting aggressively. The patient was a member of a local organisation which cares for injured bats. The Logan and West Moreton Public Health Unit was notified the day after the incident. The patient reported that he had been vaccinated against rabies previously, and that his rabies virus-neutralising antibody titres were adequate. However, the patient’s available titres were below 0.50 IU/mL in 2002 and 0.43 IU/mL in 2008 (no boosters were given), both of which were below the World Health Organization recommended level that confers protection against rabies virus.2 The bat was euthanased for testing (because it had bitten a person, as per Qld Health protocol), and tests on the brain tissue showed it to be reactive for lyssavirus antigen (using an immuno-fluorescence antibody test) and lyssavirus RNA (using a TaqMan assay). In view of the patient’s recent serological tests indicating subprotective antibody levels and definite exposure to an ABL-positive bat, he was given postexposure prophylaxis comprising rabies immune globulin into the wound and five doses of rabies vaccine. He is currently well. The Public Health Unit determined that others were not potentially exposed to the bat. The prompt reporting of all potential ABL exposures to public health units is especially important because bat carers may underreport potential ABL exposures.3 Current guidelines recommend that bat carers with ongoing potential exposure to ABL should check their rabies virus-neutralising antibody titres every 2 years and have a booster if the titre is reported as inadequate (< 0.5 IU/mL). Alternatively, booster doses may be offered every 2 years without determining antibody levels.1 Further education of the bat-handling community and their doctors is necessary to maintain awareness and best practice to protect the people who do this potentially dangerous work.
Heidi J Carroll · Bradley J McCall · David Looke · Bruce Fraser
Surgical implications of global warming
To the Editor: There is international recognition of the substantial threat that global warming presents to human health and of the challenges that it poses to health service delivery. The World Health Organization has estimated that global warming and climate change-related natural disasters account for over 60 000 deaths globally per year.1 Global warming will also have implications for surgery and surgical practice. The Victorian “Black Saturday” bushfires of February 2009 saw 414 people presenting to hospital emergency departments, stretching hospital resources,2 and 173 deaths were attributed to the bushfires. Nineteen patients were admitted to the Alfred Hospital (Melbourne’s burns service) with burns to more than 30% of their bodies. The care of severe burns victims is complex and highly labour-intensive, often with a patient–nurse ratio of 1 : 1. There would have been even more burns victims if the fire had been less ferocious and had not resulted in such a high loss of life.3 In other words, there were fewer injuries because this intense fire killed people outright; a less intense fire may kill fewer people but leave more injured. The extreme weather that led to the fires is an example of the type of event that may become more frequent as global warming increases. The Garnaut climate change review predicts more frequent extreme wind, rain and intense tropical cyclones, and predicts that category 3–5 storms are likely to increase in intensity by 60% by 2030, and by 140% by 2070.4 Increasing population densities along the northern Queensland coast will also expose more people to the risks of floods, storms and cyclones. These natural disasters often produce wounds which are highly contaminated, and primary wound care services may face increased demand. One of the practical implications of research in the field of surgery and climate change will be the need for modelling of future demands for surgical intervention in Australia. The range of trauma impact due to climate change needs to be defined, and the incidence with which this is likely to occur needs to be determined, based on climate change modelling. With this information, models of future demand for surgical interventions can be determined.
Joseph W Smith · Guy J Maddern
The German Escherichia coli outbreak — could it happen here?
To the Editor: Recent media reports queried whether Australia could experience a serious outbreak of foodborne disease, such as the massive outbreak in May this year of Shiga toxin-producing Escherichia coli (STEC) serotype O104:H4 in Germany.1 Australia is potentially vulnerable to foodborne disease outbreaks from contaminated fresh produce, and health and food safety authorities need to plan for these events and assess our capacity to respond. Australian health agencies investigate 100–150 outbreaks of foodborne illness each year, although < 10% are associated with fresh produce.2 Australia has a very high-quality food supply, but we are still vulnerable to outbreaks. In 1991, norovirus-contaminated orange juice served by airlines infected 25 000 people, despite the juice being sourced from a single small factory.2 Foodborne outbreaks can become very large and spread internationally before health agencies identify a vehicle of transmission. In 2009–2010, an outbreak of hepatitis A infection in more than 400 people in multiple Australian states, France and the Netherlands was associated with consumption of semidried tomatoes from Turkey.3 The recent outbreak of STEC O104:H4 also occurred in other European countries and was associated with a common source of fenugreek seeds used for growing sprouts.4 Seed sprouts have caused many outbreaks of foodborne illness, including two outbreaks of Salmonella Oranienburg in Western Australia and Victoria in 2005–2006 where alfalfa sprouts were implicated.2 STEC outbreaks overseas have implicated seeds originating from Australia.5 Seeds may become contaminated during plant growth, particularly due to livestock and feral animal grazing, or during storage, neither of which can be effectively controlled by disinfection at sprouting facilities.5 In light of the recent European STEC outbreak, Australian food safety agencies should urgently assess the risks posed to the food supply by sprouted seeds. Australia does have well functioning plans to respond to multijurisdictional outbreaks and national food safety incidents,2 but has not had to respond to a massive outbreak. German investigators reported 3222 outbreak cases of STEC, including 810 cases of haemolytic–uraemic syndrome, in less than 2 months.1 The health system resources required to manage such an outbreak would be immense and costly. In Australia, treatment and other costs for two cases of haemolytic–uraemic syndrome totalled an estimated $14 000 each, despite neither patient requiring dialysis, developing end-stage renal disease or requiring a transplant.6 As with other national plans for responding to epidemics, government agencies need to ensure that possible impacts on the health system and industry are taken into account.
Martyn D Kirk
Medicine use, heat and thermoregulation in Australian patients
To the Editor: Australia is already a hot country and the frequency of hot spells looks set to increase over coming decades.1 Health care professionals will therefore need to consider the effect that medications can have on people’s capacity to respond to hot conditions. Medications can directly increase body temperature by altering thermoregulatory mechanisms, pharmacological action, idiosyncratic reactions, or hypersensitivity reactions.2-4 Uncommon side effects — including toxic states, anticholinergic poisoning syndrome, serotonin syndrome and neuroleptic malignant syndrome — can also generate heat. Indirect impairment of physiological response to thermal stress may occur by preventing adjustment to hypotension, or by interfering with behavioural responses. Despite these risks, hyperthermia and reduced sweating each rate only one mention in the 2010 Australian medicines handbook (in relation to anticholinergics).5 The handbook does not list heat stress as an adverse reaction to dexamphetamine,5 which can impair thermoregulation by increasing metabolic rate. Medications can affect thermoregulation by:2-5 impairing sweating triggered by the parasympathetic nervous system — eg, anticholinergics, phenothiazines; impairing sweating by carbonic anhydrase inhibition — eg, topiramate, zonisamide; impairing cardiac output or causing hypovolaemia — eg, antihypertensives, alpha-blockers, diuretics; impairing behavioural responses to heat (such as drinking or taking cooling action) — eg, sedatives and hypnotics, anxiolytics, phenothiazines, illicit drugs; or rarer effects, such as increasing metabolic rate — eg, monoamine oxidase inhibitors, thyroxine, amphetamines, cimetidine. Elderly people with impaired thermoregulation, the socially disadvantaged and people with mental illness have been identified as being most at risk from heat stress.6 Although the risk of medications directly impairing physiological responses to heat is low, thermoregulatory effects can be cumulative. People in certain occupations (eg, outdoor labourers and tradespeople, indoor workers in hot industries such as metal manufacturing) may be at increased risk of heat exposure, and there are anecdotal reports of tourists suffering heat stress in climates that are hotter than those to which they are accustomed. There is a need to educate workers, the public and health practitioners about the relationship between certain medications and heat. Professional associations and trade unions have a responsibility to warn and educate their members. It may be helpful for the Therapeutic Drugs Administration to actively solicit reports of adverse events related to medicine use, heat and thermoregulation via the Australian Adverse Drug Reaction Reporting System. Carers of elderly and chronically ill people might flag patients on certain medications for extra care during hot spells. Additionally, health practitioners can ensure that these people are on appropriate heatwave notification and emergency support lists, which are being developed by Australian state and territory health departments and emergency service agencies.
Peter W Tait
The mining and burning of coal: effects on health and the environment
Australia’s coal conundrum is that all political parties say they are concerned about climate change while sanctioning an unprecedented expansion of coalmining and coal seam gas extraction in Australia. Australia’s coal contributes to climate change and its global health impacts. Each phase of coal’s lifecycle (mining, disposal of contaminated water and tailings, transportation, washing, combustion, and disposing of postcombustion wastes) produces pollutants that affect human health. Communities in which coalmining or burning occurs have been shown to suffer significant health impacts. The health and climate costs of coal are unseen, and when costs to health systems are included, coal is an expensive fuel. Coalmining and healthConcerns about the expansion of coalmining are growing and, as a result, medical practitioners and other health experts are being asked about coal and its effects on health. While there has been no Australian overview of the health effects of coalmining on inhabitants of coalmining areas, evidence from the United States indicates that coalmining communities in West Virginia had an increased risk for developing cardiopulmonary disease, chronic obstructive pulmonary disease (COPD), hypertension, other lung diseases and kidney disease.1 Mortality rates for these diseases were higher in coalmining areas compared with non-mining areas of the region.2 Potentially confounding risk factors, such as smoking rates, were not reported. Coal-processing chemicals, fumes from diesel powered equipment, explosives, toxic impurities in coal and dust from uncovered coal trucks could all have affected the health of respondents. Deaths and injuriesMining is a dangerous occupation. Coalminers die and suffer more lost time from injuries than all other miners,3 most often from fires and structural instability of underground mines. Hazards arise from collapse of parts of a mine, explosions and gaseous asphyxiation, as well as machinery malfunction and misuse. The risks to coalminers from suffocation or explosion from release of methane and other toxic gases were demonstrated at the Pike Hill coalmine near Greymouth in New Zealand on 19 November 2010 when 29 miners died. Despite some evidence that fatalities and injuries are decreasing in Australia with tighter legislation, there are still significant health and safety concerns.4 Pneumoconiosis, dust and contaminationHowever careful the operator, miners’ lungs can be damaged by coal dust. According to the National Institute for Occupational Safety and Health, pneumoconiosis was responsible for about 10 000 deaths in the US in the 10 years to November 2009.5 In Australia, the incidence of coal workers’ pneumoconiosis has fallen with diligent monitoring of dust levels and better occupational health measures.6 Dust exposure in 33 longwall coalmines in New South Wales exceeded the Australian National Standard of 3 mg/m3 in 6.9% of measurements, and the risk of pneumoconiosis and lung fibrosis was estimated to be about 2% after a 40-year working life.7 Road traumaCoal is transported from mine to railhead, or mine to port, by road, increasing the risk of accidents and traffic fatalities and releasing greenhouse gases. Data on coal-related road trauma for Australia are unavailable; however, in Kentucky, between 2000 and 2004, 53 people were killed and 536 injured as a result of accidents with vehicles licensed to transport coal.8 Environmental damage, water and healthCoalmining poses a significant threat to the integrity of aquifers, which may be hydrologically connected to other groundwater-dependent ecosystems including farm dams, bores and rivers. Water from coalmines must be disposed of and waste material is often held within the surface lease of a mine, introducing a risk of contamination of human food sources. Pollution of the environment can also occur through windblown dust during transportation, where coal is washed and at export ports. In 2010, coal seam gas operations in Queensland were held up at two sites because groundwater had become contaminated with a potentially dangerous combination of benzene, toluene, ethylbenzene and xylene (BTEX).9 Similar contamination occurred after an underground coal gasification trial near Kingaroy.10 The Queensland government has recently banned BTEX chemicals from coal-bed fracturing fluids. Social and mental health impactsCoalmining can change the lifestyle and character of a community. Higginbotham and colleagues detailed the social and political consequences that result.11 Medical practitioners in coalmining areas have reported that increases in asthma, stress and mental ill health have become more common.12 As more coalmines are opened, as has occurred in parts of the Hunter Valley in New South Wales, the social fabric of a region changes, the role and function of a township alters, and many inhabitants of these regions have developed depression, anxiety and ill health.13 Coal combustion: coal-fired power generationOnce coal is mined, it is burned, usually to generate electricity or to make steel. Burning coal emits many pollutants that harm human health and increase the major public health problems facing the industrialised world. An Australian review of air pollution by Kjellstrom and colleagues, while not specifically focusing on the effects of coal combustion, summarises the effects of particle exposure on health.14 These include respiratory symptoms such as cough, aggravated asthma, the development of chronic bronchitis and decreased lung function; arrhythmias, non-fatal heart attacks and premature death in people with heart or lung disease; the effects of absorption of toxic material; and allergic or hypersensitivity effects. The smallest particles, particulate matter (PM) 2.5, are the most damaging.15 Many PM 2.5 particles are produced during coal-fired power generation. Specific data in Australia are lacking; however, in the US, the Physicians for Social Responsibility examined the evidence for health damage caused by coal.5 The risk of premature death for people living within 30 miles of coal-burning power plants has been quoted to be three to four times that of people living at a distance.8 Fifty thousand deaths each year have been attributed to air pollution,5 and in Canada, it is estimated to cause more than 5000 deaths each year.16,17 In the US, air pollution from combustion of coal, diesel fuel and wood was estimated to account for 5% of male and 3% of female cancer deaths between 1970 and 1994.18 Other toxic elements released with coal combustion include arsenic, mercury, fluorine, cadmium, lead, selenium and zinc. Mercury is of greatest concern. Over a third of all mercury emissions attributable to human activity come from coal-fired power stations.5 It enters the environment and accumulates in the food chain, particularly in fish. In 1999–2000, 15.7% of American women of childbearing age had blood mercury levels that could have affected the brain development of an unborn child.5,19 Australian dataThe limited evidence on the impacts of air pollution from burning coal in Australia suggests that the health impacts are similar to those reported from other developed countries.20 A 1993 study reported an increase in symptoms of childhood wheeze and asthma-like breathing difficulties from a community near a coal-fired power station.21 Climate change, health and the environmentThe World Health Organization states that climate change is the greatest emerging threat to public health and to the environment. Coal-fired power stations are potent emitters of greenhouse gases and are important contributors to climate change. Climate change will profoundly affect some of the most fundamental prerequisites for good health: clean air and water, sufficient food, adequate shelter and freedom from disease.22 These health impacts are beginning to be felt in Australia. The elderly, the very young and those with existing heart and respiratory disease are vulnerable to the increase in heat waves due to climate change. Drought has affected farming communities who have suffered from stress, social disruption and depression. More extreme weather events can be expected with threats to food and water security; rising sea levels; changes in vector-, food- and water-borne diseases; exacerbation of air pollution; increases in aeroallergens and impacts on mental health. An increase in the number of climate refugees is likely.23 Costs of burning coal in AustraliaThe most recent and comprehensive study on the negative effects of power generation was released by the Australian Academy of Technological Sciences and Engineering (ATSE) in March 2009.24 ATSE calculated the greenhouse impacts and health damage costs of different power generation technologies including coal, gas, wind, solar photovoltaic, solar thermal, geothermal, carbon capture and storage, and nuclear energy. The health costs of burning coal are equivalent to a national health burden of around $A2.6 billion per annum. Coal-fired power stations also produce more greenhouse gases (such as CO2) per unit of energy than any other type of power station. Combining greenhouse and health damage costs for Australia gives representative total external costs of $A52/MWh for brown coal, $A42/MWh for black coal and $A19/MWh for natural gas.24 By the ATSE analysis, carried out before the costs of the 2011 Fukushima nuclear meltdown could begin to be calculated (ATSE specifically excluded nuclear disaster costs), the external costs of nuclear power would have been around $A7/MWh. The external costs of genuinely renewable sources of power generation, such as wind and solar power, are even less. If the external costs of burning coal were recovered by a coal tax, coal would be the most expensive of all energy-generating fuels. Epstein and colleagues recently reported an analysis of the health and environmental costs of coal in the US and concluded that the damage caused by coal should double or triple the costs of coal-generated electricity.25 DiscussionElectricity contributes to economic growth and a higher standard of living. It produces opportunities for better health and gains in longevity, but in Australia, coal produces 84% of the nation’s power, and its combustion is responsible for a significant proportion of the country’s greenhouse emissions. Australia is the world’s largest exporter of coal. Although it may well produce economic benefit, it will also have injurious effects on the health of the populations of recipient countries, and contribute to global greenhouse gas emissions. Under our present accounting system, these external negative factors are excluded; coal-generated power is falsely represented as the cheapest source of electrical power. Although burning coal no longer causes London’s smogs or cancer of the scrotum in young chimney sweeps, and acid rain from uncontrolled sulfur dioxide emissions has abated (proof that an emissions trading scheme can work), there is overwhelming evidence that coalmining and the burning of coal is harmful to physical and environmental health, and can have a significant impact on local communities. Regrettably, peer-reviewed environmental health studies from Australian coal towns are sparse. When a new mine is proposed for a particular area, Australian mining Acts (designed for protection and certainty in the mining industry) do not protect communities who can suffer years of frozen assets, apprehension and future risks to health when a new mine is proposed in their locality. State environmental protection authorities (EPAs) are the statutory independent bodies charged with assessing the environmental safety of proposed mines. Australia’s international obligations under the agreement reached at the United Nations Conference on Environment and Development (UNCED June 1992) give EPAs permission to use the precautionary principle — that an action should not be taken if the consequences are uncertain and likely to be dangerous to the public or the environment — in their assessments. This is rarely, if ever, invoked in the case of approving new coalmines. Health impact statements for proposed mines are not requested by state governments, so the EPAs have, unwittingly, become responsible for the protection of significant aspects of public health. The time has come for EPAs to take the precautionary principle into account during their deliberations on new coalmining applications. To persist in mining and burning coal will condemn future generations to catastrophic climate change, which is clearly the biggest health problem of the future. Australia is a rich and technologically sophisticated country with the second-highest human development index in the world.26 It should have the ability to gradually phase out the use of coal and to expand the generation of electricity from renewable energy sources. Such a change will have the greatest benefit for Australian and global health and for protection of the environment. Recently, the Australian government has announced it will introduce a carbon tax to mesh seamlessly into an emissions trading scheme. This initiative to put a price on carbon is an important public health measure.
William M Castleden MS, FRCS, FRACS · David Shearman PhD, FRACP · George Crisp MB BS, MRCGP · Philip Finch MB BS, FFARCS
Changes in the sodium content of bread in Australia and New Zealand between 2007 and 2010: implications for policy
Objective: To define the effectiveness of recent efforts by the Australian Division of World Action on Salt and Health, and the Heart Foundation in New Zealand to reduce sodium levels in breads in Australia and New Zealand.Design and setting: Data on the sodium contents of packaged sliced bread products sold in Australian and New Zealand supermarkets were collected from the product labels of 157 breads in 2007 and 167 breads in 2010, and were compared overall, by bread type, by manufacturer, and between nations.Main outcome measures: Mean sodium values in bread and proportions of breads meeting the targets of 400 mg/100 g in Australia and 450 mg/100 g in New Zealand.Results: Overall mean sodium content in bread in Australia was 434 mg/100 g in 2007 and 435 mg/100 g in 2010; corresponding values for New Zealand were 469 mg/100 g and 439 mg/100 g. The proportion of Australian breads meeting the national target increased from 29% in 2007 to 50% in 2010; the proportion of New Zealand breads meeting the national target increased from 49% in 2007 to 90% in 2010. There were clear differences between the results achieved by different companies.Conclusions: Voluntary efforts by non-governmental organisations have had some impact on sodium levels in bread, particularly in New Zealand. However, substantial room for further improvement remains. If additional reductions are not achieved under the current voluntary arrangements, legislated approaches may be required.
Elizabeth K Dunford MPH · Helen Eyles MSc, PhD · Cliona Ni Mhurchu BSc(Hons), PhD · Jacqui L Webster MA, PhD · Bruce C Neal MB ChB, PhD
An unusual cause of caustic burns
Two children in far northern Western Australia tattooed their arms with maangga berries (Grevillea pyramidalis ssp. leucadendron), which resulted in unintentional, caustic, partial thickness skin burns requiring specialist burn care. An understanding of the chemistry of the burn agent (5-n-alkyl resorcinol), appropriate first aid management and referral, and possible physiological sequelae are essential for optimal medical management and preventive community education. Clinical recordsPatient 1A 10-year-old Aboriginal girl with burns was referred to the Princess Margaret Hospital burns unit by a local general practitioner in far northern Western Australia. Relatively little was known about the nature of her burns or the potential toxic chemical sequelae and, because of the distances involved, it was decided to bring her to Perth. The patient had used local berries to “tattoo” both her forearms, causing bilateral caustic burns to 1% of her body surface area (Box 1, A). After consultation with the burns unit, the area was washed thoroughly with water to remove any remaining traces of caustic substance and the pH of the area was repeatedly tested. The berries had induced a partial thickness burn with blistering of the skin. The blisters were deroofed and washed and the pH checked again. The child was observed overnight for systemic and metabolic effects. The burns were initially treated with nanocrystalline silver dressing and hydrocolloid dressing, which were changed every 2 days (Box 1, B and C). These were later replaced with calcium alginate dressing and hypoallergenic polyacrylate adhesive, which were changed every 2 days until complete resolution 3 weeks later. The patient was advised to massage and moisturise the area and to use sunscreen protection. Patient 2Almost exactly 1 year later, a 14-year-old Aboriginal girl with burns was referred to the burns unit from the same area as Patient 1. The maangga berry was confirmed as the seed pod she had used. She had burns on her right forearm, cubital fossa and distal arm. The area was washed with soap and water and irrigated while determining the pH of the wound area. She was admitted for wound dressing, observation and treatment for metabolic derangement. She sustained partial thickness burns to 3% of her body surface area. Her forearm was treated with nanocrystalline silver dressing and hydrocolloid dressing, which were changed every 2 days, then replaced with calcium alginate dressing and hypoallergenic polyacrylate adhesive, which were changed every 3 days until complete resolution after 3 weeks. She was advised to massage and moisturise the affected area and protect it from direct sunlight. DiscussionMost caustic burns are secondary to accidental ingestion of a corrosive substance, causing significant oesophageal stricture or perforation, or from topical exposure to agricultural or building chemicals.1,2 According to some studies, almost half the burns described are in children (despite them comprising less than 3% of all burns), and burns have significant cultural and psychological sequelae.3,4 Excluding a few case series of self-inflicted garlic burns and fruit juice mouthwash gingivitis, as far as we are aware, no described cases exist of caustic burns from plant matter, especially plants that have cultural significance for the Aboriginal people of Australia.5 Of further interest is that the topical chemical burn also may have significant systemic consequences related to the burn chemical. Regional and national poisons centres were contacted for advice, but staff were unable to advise on the management of the patients because little is known about this berry internationally. The patients were from an area that is a natural habitat for Grevillea pyramidalis ssp. leucadendron. The tree is also known as the konkerberry, maangga berry or caustic tree, which are generic terms for many different species of berry shrubs. These berries have traditionally been used by local Aboriginal people for tattooing; the berry is used to puncture the skin, and the fluid released from the berry causes a greenish discoloration of the skin followed by permanent black tattooing. The elders of the various tribes within the relevant region have been made aware (after liaising with the burns unit) of the potential harmful effects of the berries when used incorrectly by inexperienced users. High-performance liquid chromatography has been used to isolate the corrosive substance, identified as 5-n-alkyl resorcinol, a phenol derivative, which is also a precursor for tetrahydrocannabinoid (the psychoactive chemical in marijuana). There has been a resurgence of interest in 5-n-alkyl resorcinol because of its antioxidant, antigenotoxic and cytostatic characteristics. It is a phenolic lipid metabolite of plants, animals, fungi and bacteria during normal development, as well as during times of stress, such as when infection or wounds are present or when the organism is affected by ultraviolet radiation. It has also been found to inhibit bacterial, fungal, parasitic and protozoal growth, and to reduce the efficacy of viral transfection.6 Chemical burning seems to occur when 5-n-alkyl resorcinol binds with proteins to form esters that irreversibly bind calcium. This interferes with cellular mitochondrial performance, leading to cellular anoxia and energy deprivation, causing protoplasmic poisoning and necrosis. This organic compound also binds and dissolves the lipid membrane of the skin cells, leading to proteinaceous structural disruption. In a medical setting, naturally derived 5-n-alkyl resorcinol could be used as a potent heat shock protein-90 (Hsp-90) inhibitor. Hsp-90 is instrumental in the regulation of oncoproteins Her2, Akt, Bcr-Abl, c-Kit, EGFR and mutant BRAF, and when these oncoproteins are dysregulated, they lead to solid and haematological cancers.7 Clinically, Hsp-90 is the active compound in endodontic fillings and vascular glue and has been used extensively as a peeling agent.8 5-n-alkyl resorcinol has many side effects, including theoretical goitrogenic consequences, and G. pyramidalis is listed as poisonous in the United States Food and Drug Administration Poisonous Plant Database (http://www.accessdata.fda.gov/scripts/plantox/index.cfm). The fact that G. pyramidalis berry juice causes haemolysis is of concern, but the cardiac glycosides it contains may be of more concern, even though ingestion (not skin penetration) is required for a lethal dose. Other effects of cardiac glycosides include blurred vision, nausea, vomiting, bradycardia, confusion and lethargy, and people showing these signs after contact with G. pyramidalis should be referred to an emergency department immediately. We hope this article may be educational for doctors in far northern Western Australia and anyone coming into contact with the Grevillea species, some of which (eg, G. banksii and G. robusta) contain trace cyanide and grow in residential Australian gardens. We believe these two cases offer a unique insight into a region-specific phenomenon. 1 Partial thickness burns to the left arm of a 10-year-old Aboriginal girl (Patient 1), secondary to self-tattoo with berries from Grevillea pyramidalis ssp. leucadendron A. Day 1. B. Day 3 (after 2 days’ dressings). C. Day 6 (after 5 days’ dressings). 2 Grevillea pyramidalis ssp. leucadendron Photography by Lynley Wallis. Used with permission (http://florabase.dec.wa.gov.au/help/copyright). 3 Geographic distribution of Grevillea pyramidalis ssp. leucodendron Map data by Paul Gioia and the Western Australian Herbarium. Used with permission (http://florabase.dec.wa.gov.au/help/copyright).
Robert J Knight MB BCh, MRCS · Tania McWilliams BScNurs · Dawn Reeler MB ChB, DA · Liz Whan FRACS · Fiona Wood FRACS, AM
Minimising the misuse of oxycodone and other pharmaceutical opioids in Australia
Simple strategies can reduce harms from misuse of pharmaceutical opioids Sustained-release opioid drugs have been used increasingly over the past two decades to treat all types of chronic pain, including chronic non-cancer pain.1 Rates of prescribing have increased in developed countries such as Australia, Canada, the United Kingdom and the United States since the beginning of the 21st century.2-4 In the US, aggressive marketing of sustained-release formulations of oxycodone to primary care physicians and directly to patients between 1996 and 20075,6 resulted in a 10-fold increase in their per-capita use, and an alarming increase in the number of deaths from overdose with prescription opioids. In 2007, the number of deaths from oxycodone and other pharmaceutical opioids (11 499) outnumbered overdose deaths from illicit heroin and cocaine combined (around 8000).7 The article by Roxburgh and colleagues in this issue of the Journal8 provides an assessment of harms arising from recent increases in opioid prescribing in Australia.1 Roxburgh and colleagues show that pharmaceutical opioid prescribing has increased, with those for sustained-release forms of oxycodone supplanting those for morphine.8 Most oxycodone prescriptions have been to adults over the age of 50, with the steepest increases in rates of prescribing to patients aged over 70 years.8 These patterns suggest that most prescribing has been for chronic non-malignant pain, the prevalence of which increases steeply with age.1 Increased opioid prescribing has been accompanied by increases in the number of people seeking treatment for dependence on prescribed opioids in Australia. The number of fatal overdoses involving oxycodone has also increased, but, unlike in the US, the number of deaths in Australia from oxycodone reported by Roxburgh and colleagues was much lower (59) than the number of deaths from all other opioids (including heroin; 315) in 2005 (this was the most recent year in which the two could be directly compared). Roxburgh and colleagues report that in 90% of cases, deaths from oxycodone overdose involved either the use of the drug in combination with other opioids, benzodiazepines and alcohol, or the contribution of concomitant medical conditions. Just over half of the deaths (53%) occurred in people who were prescribed oxycodone, probably for the relief of chronic pain. A quarter of all these deaths, and those of a third of people with no history of illicit injecting drug use, were found to be suicides. Fatal overdoses among those with a history of injecting drug use were more likely to involve males, as is true of overdose deaths in this population more generally.9 Injecting drug users were more likely to be using diverted opioids at the time of their death, although a third were prescribed these drugs. There are a number of strategies available to governments to reduce pharmaceutical opioid misuse and the harms arising from it.1 Clinical recommendations are as follows: First, doctors and patients need to be educated about the risks of dependence on, and overdose of, these drugs, especially when higher doses are prescribed. Patients need to be informed by prescribers and pharmacists about the risk of fatal overdose if they use these drugs in combination with other drugs that depress the central nervous system, whether prescribed ones like benzodiazepines, or the more readily available alcohol. Second, clinical guidelines are needed on the place of opioids in the treatment of chronic pain, especially non-cancer pain. There is a need for clearer clinical guidelines for primary health practitioners to ensure that opioids are not used as first-line drugs for chronic pain, but are reserved for use when other forms of treatment have been tried.1,5,10 Third, clinical priority should be given to reducing suicides in patients who experience chronic pain and who are prescribed opioids. Prescribers need to be cautious in prescribing opioids to depressed patients. They should also enquire about suicidal ideation in patients who have chronic pain and who have been prescribed these drugs long term but have incomplete pain relief. Fourth, smaller quantities of these drugs should be prescribed to allow for more regular review of their effectiveness in relieving pain. Compliance with the prescribed medication regimen should be carefully recorded and a clear plan of action should be documented when significant non-compliance is identified. Referral to pain specialists should be considered if pain control is incomplete, and referral to addiction specialists should be considered if dependence on opioids is suspected. Policy recommendations are as follows: Enhanced prescription monitoring systems are needed to reduce both doctor-shopping by patients and imprudent prescribing by doctors. These systems should be computerised, nationally consistent and, ideally, real-time.1,5 It is also critical for doctors and pharmacists to monitor patterns of chronic opioid use in patients whom they see. The pharmaceutical industry needs to ensure that these drugs are marketed to prescribers in responsible ways, and that clinical information for patients advises about the risks of using these drugs in combination with other central nervous system depressants. Governments need to examine ways of increasing access to buprenorphine and methadone treatment for people who use opioids illicitly, and who may be using pharmaceutical opioids to self-treat.1 If Australian policymakers and doctors want to avoid the disastrous US experience with pharmaceutical opioids, these steps should be taken now while the misuse of these drugs is still a manageable problem. Whatever policies are implemented, it is essential that we assess rigorously their impacts on both the quality use of these medicines in relieving chronic pain and on the harms arising from their inappropriate use.
Wayne D Hall PhD · Michael P Farrell MB, FRCP, FRCPsych
Hendra virus
Low infectivity but high mortality: strategies to minimise spread until the vaccine arrives are the key Hendra virus (HeV) infection in humans is an emerging zoonotic disease that has a high mortality rate, but low infectivity. In all cases to date, the infection has been transmitted to humans from bats of the genus Pteropus (flying foxes) via an intermediate equine host. HeV and Nipah virus are the only known members of a new genus, Henipavirus, within the family Paramyxoviridae. HeV was first described after an outbreak of severe respiratory disease in horses that led to the deaths of 14 of 20 infected horses and the death of a horse trainer — one of two humans infected — in Brisbane in 1994.2 There have been seven cases of HeV infection producing pneumonic or encephalitic illnesses in humans. Four of these people died, three soon after exposure and the fourth from fatal encephalitis caused by HeV, which developed 13 months after full recovery from an initial aseptic meningitis.3 Of the three survivors, two made complete recoveries while the third experienced ongoing complications of the initial encephalitis.4,5 Subsequent serological testing for HeV in a large number of human contacts of the first three cases of HeV infection was completely negative.6 Before 2011, there had been 14 events of spillover of HeV infection from flying foxes to horses, and subsequent transmission to humans in five of these events. All events occurred in coastal Queensland except for one in northern New South Wales. Forty-four horses were infected; 34 of these (75%) died and the remaining 10 survived but were later euthanased. Seroepidemiological studies of more than 2000 horses and more than 5000 samples from 46 other animal species in Queensland did not identify HeV infection.7 Spillover events have occurred through most months of the year, but with increased frequency from June to September. The virus can survive under ideal cool and moist environmental conditions (eg, in bat urine at 22°C in the laboratory) for up to 4 days, but is generally thought to survive for only hours. Horses are thought to be infected by ingesting food or water contaminated by urine, saliva or birthing products of infected flying foxes. The virus amplifies within the horse, and humans who are exposed to a large amount of the secretions or blood from an infected horse can become infected. Laboratory studies have shown that horses may excrete virus for up to 72 hours before showing clinical signs.8 All seven humans infected with HeV to date had high levels of exposure to body fluids of infected horses, such as during unprotected autopsy or by direct contact with respiratory secretions or aerosols. Not all people with high-level exposure have contracted the disease or seroconverted. There is no evidence that prolonged close contact with flying foxes engenders a risk of HeV infection in humans.9 A wide range of mammals carry the appropriate receptor enabling them to be infected with HeV experimentally.10 Yet, although HeV infects the endothelium of blood vessels in many species in the laboratory, resulting in systemic vasculitis, outside the laboratory setting, only flying foxes, horses and humans are known to have been infected. One dog is known to have seroconverted without any clinical illness or detection of virus. Flying foxes were identified as the natural host in 1996, and antibodies to HeV have been found in archived samples of flying fox serum dating back to 1982.11 Flying foxes do not develop overt disease. All four species of flying fox in Australia, from as far north as Madang in Papua New Guinea to as far south as Melbourne, have been found to carry the virus.12 HeV is genetically stable, and there is no evidence that the virus has changed significantly since it was first isolated in 1994.8 This year has been a major year for the detection of spillovers of HeV into horses, with 14 events being notified by 17 August. Eight of these occurred in Queensland, with one being the first event notified west of the Great Dividing Range, in Chinchilla. Ten horses had been infected in Queensland and, for the first time, a dog has seroconverted, probably through contact with an infected horse. Six spillover events had occurred in northern NSW, with seven horses becoming infected. No humans have been infected this year to date, although not all of those potentially exposed have reached the end of their incubation periods; no one had a high degree of exposure to infected secretions. The incubation period in humans is 5 to 21 days. The clinical presentation has been variable, with both respiratory and encephalitic symptoms. There has been no transmission of HeV between people, but routine droplet precautions are advised. There is no known effective treatment for Hendra virus infection, and clinical management is based on treating symptoms as they arise. When a person has had high-level exposure to body fluids of infected horses, an experimental human monoclonal antibody (mAb) can be made available for postexposure prophylaxis. Henipavirus mAb has been shown to be effective in preventing infection in ferrets if administered within 12 hours of intrathecal injection of a high dose of HeV.13 However, this product has not yet been trialled for safety or efficacy in humans. It has been administered to three humans. The first person was late into the progression of severe encephalitis and subsequently died. The second two had moderately high-risk exposure, but no evidence of infection, and they did not develop illness or seroconvert. Currently, despite its unknown safety or efficacy, mAb is offered to people who have had high-level exposure to infected horse blood or secretions, after obtaining ethics approval and appropriate consent for each individual. Preventive measures are essential. Horse owners are advised to keep horses away from flowering and fruiting trees, and to remove feed and water troughs from under trees. Vets are advised to wear appropriate personal protective equipment when attending a sick horse or when performing invasive or aerosol-generating procedures on any horse. Horse owners and the public are advised to isolate sick horses from people, horses and other animals. The most promising prospect for controlling HeV outbreaks in humans is the vaccine for horses that is expected to be marketed in 2013.14
Jeannette R Young MB BS, FRACMA, FFPH · Christine E Selvey MB BS, MSc · Rick Symons DSC, PhD, MACVS
Why the tobacco industry fears plain packaging
Tobacco control advocate Simon Chapman explains how this public health reform will work In past months, Australian news audiences have been exposed to some exotic, presumed-extinct species on their screens and radios. After more than 15 years, the tobacco industry dodo is back and walking among us, attempting to fly. Australia’s pioneering plain packaging legislation has brought it out into public, in a desperate effort to prevent the fall of a domino that promises to cascade globally, ending the industry’s centrepiece of tobacco promotion: the lure of the pack. The University of California’s Stan Glantz once remarked that those who lead the tobacco industry are like cockroaches: “They love the dark and they spread disease.”1 Ever since the magnesium glare unleashed by the public release of its internal documents via the 1998 Tobacco Master Settlement Agreement in the United States, the industry has kept well out of public view, working behind the scenes to shore up its ebbing credibility. The court of public opinion told tobacco companies they were regarded as the most untrustworthy of all industries.2 Media appearances had become progressively humiliating as their spin was rejected. But the truth serum contained in the millions of now-public pages of court-ordered internal documents sealed their public fate. The industry had known tobacco killed, but had lied about it for decades. Their marketing divisions had underlined the vital importance of recruiting youth, and their chemists had been busy working to enhance the addictiveness of nicotine. Australia’s historic plain cigarette packaging legislation is a weapons-grade public health policy that is causing apoplexy in the international industry. It is likely to have little effect on heavily dependent smokers, who tend to be brand-loyal and less image-conscious, but without branding, future generations will grow up never having seen category A carcinogens packaged in attractive packs. Today’s 19-year-olds have never seen local tobacco advertising and youth smoking rates are at an all-time low. Plain packs will turbocharge this trend, making smoking history. Tobacco is a dying market in nations like Australia, which leads the world in comprehensive tobacco control. Australian Institute of Health and Welfare data released in July of this year show only 15.1% of Australians are now smoking daily3 — the lowest percentage ever recorded. From the beginning of the 20th century, when machine-manufactured cigarettes were first marketed, the advertising and packaging industries did all they could to portray cigarettes as a means of signalling personal identity to the young as they took up smoking. A callow youth who wouldn’t be seen dead with an Alpine felt assured by the promise of masculinity in pulling out a packet of Marlboros. Those not wanting the social opprobrium that can come with being showy had the iconic ordinariness of Winfield to clutch as their totem. Those wanting to affect retro stylishness have Peter Stuyvesant or Lucky Strike, and wannabes, any number of haute couture brands — designer carcinogens. But from next year, all cigarette packages will look the same, distinguished only by the brand name in standard typeface. The industry’s re-entry into policy debate has produced some high comedy. In advising government that plain packs will “not work”, it sought a role as a wise public health authority, when of course its fiduciary duty to its shareholders demands that it support policies that maximise use. It has commissioned reports that purport to show that 15.9% (1 in 6) of cigarettes being smoked now are illicit, when the latest Australian Institute of Health and Welfare national survey reports that a mere 1.5% of smokers use illegal tobacco more than half the time.3 Most of all though, its blank-cheque advertising campaigns, imploring the government to desist, say to anyone with half a brain that the industry knows plain packs will “kill their business”, as the cover story of a tobacco trade magazine put it in 2008. That’s precisely the plan. Tobacco kills one in two of its long-term users. The tobacco industry’s current undisguised panic shows that plain packs will hit them very hard. If she were to do nothing else, Minister for Health and Ageing Nicola Roxon has marked her tenure with this legislation, which has just been passed, unopposed, in the lower house of Parliament. It will stand in public health history as a major chapter of how governments put the health of the population before the corporate interests of a pariah industry. Just one disease caused by smoking — lung cancer — was rare before 1930. Over the next 50 years, it rose to become the world’s leading cause of cancer death. In countries like Australia, it is now on the wane. Plain packaging will accelerate its eventual demise as a major cause of death.
Simon Chapman PhD, FASSA
Increasing incidence of malignant mesothelioma after exposure to asbestos during home maintenance and renovation
Objective: To determine trends in incidence of malignant mesothelioma (MM) caused by exposure to asbestos during home maintenance and renovation.Design, setting and participants: Using the Western Australian Mesothelioma Register, we reviewed all cases of MM diagnosed in WA from 1960 to the end of 2008, and determined the primary source of exposure to asbestos. Categories of exposure were collapsed into seven groups: asbestos miners and millers from Wittenoom; all other asbestos workers; residents from Wittenoom; home maintenance/renovators; other people exposed but not through their occupation; and people with unknown asbestos exposure; or no known asbestos exposure. Latency periods and age at diagnosis for each group were calculated and compared.Results: In WA, 1631 people (1408 men, 223 women) were diagnosed with MM between 1960 and 2008. Since 1981, there have been 87 cases (55 in men) of MM attributed to asbestos exposure during home maintenance and renovation, and an increasing trend in such cases, in both men and women. In the last 4 years of the study (2005–2008), home renovators accounted for 8.4% of all men and 35.7% of all women diagnosed with MM. After controlling for sex and both year and age at diagnosis, the latency period for people exposed to asbestos during home renovation was significantly shorter than that for all other exposure groups, but the shorter follow-up and difficulty recalling when exposure first occurred in this group may partly explain this.Conclusions: MM after exposure to asbestos during home renovation is an increasing problem in WA, and these cases seem to have a shorter latency period than other types of exposure. MM cases related to renovation will probably continue to increase because of the many homes that have contained, and still contain, asbestos building products.
Nola J Olsen BAppSc, RGN · Peter J Franklin BSc(Hons), PostGradDipEnvSci, PhD · Alison Reid RGN, MSc, PhD · Nicholas H de Klerk BSc, MSc, PhD · Timothy J Threlfall MB BS, MPH, PhD · Keith Shilkin FRCPA, FCRPath, FHKCPath · Bill Musk FRACP, MSc, MD
Beyond builders and miners: mesothelioma hits home
Desley and Les Carbon are preparing for a much-anticipated road trip from their home in Perth up the Western Australian coast to Exmouth. “I’ve just purchased a couple of large fishing rods”, says Mr Carbon. “My wife loves fishing but she’s allergic to fish — so if she catches any I’ll eat them!” The couple in their 60s are looking forward to a few weeks of relaxation after what’s been a difficult 18 months. Early last year, Mrs Carbon began experiencing recurrent flu-like symptoms, with a hacking cough and difficulty breathing. Multiple courses of antibiotics did little to relieve the symptoms. Her asthma worsened, and she was diagnosed with pneumonia. She had a litre of fluid drained from her lungs, but continued to experience chest pain. “I saw a specialist and said ‘why do I still have pain, when all the fluid’s gone?’” She had various chest x-rays and a CT scan, but nothing showed up. In April, after a PET scan followed by a biopsy, Mrs Carbon was diagnosed with pleural mesothelioma. “The first question I asked was, ‘How long have I got?’ The doctor said 12 months. But I hope I will get a bit longer than that.” **** Mesothelioma is a rare and fatal cancer of the pleura or peritoneum, almost always caused by exposure to asbestos. As Nola Olsen and colleagues write in this issue of the Journal, asbestos was mined and used widely as a building material for decades in Australia. Until the 1960s, 25% of all new homes used asbestos cement cladding. The legacy of this era is that Australia now has the highest mesothelioma rate in the world.1 Historically, mesothelioma was mainly an occupational cancer, but Mrs Carbon is one of a growing number of people with the disease who were exposed to asbestos at home, particularly during renovations or home maintenance. Olsen and coauthors find that although the number of cases associated with occupational asbestos exposure has plateaued, those related to domestic exposure continue to rise. “Malignant mesothelioma cases associated with home maintenance and renovation have increased markedly over the past 10 years and remain on an upward trend”, they write. This group of mesothelioma cases has been called the “third wave”, and it is not known when this wave will peak. The first wave affected workers involved in mining, milling and manufacturing asbestos products, while the second wave comprised workers who used asbestos products in industry, such as builders and plumbers. Margaret Kent, practice group leader in asbestos litigation at Slater & Gordon lawyers, has been obtaining compensation for people with asbestos diseases for the past 15 years. Like Olsen and colleagues, she has noted a “gradual and very discernible” trend in the nature of asbestos exposure among people seeking compensation for mesothelioma. “The decrease in occupationally exposed people and the increase in non-occupationally exposed people have been very obvious. Once upon a time most people who called us would be occupationally exposed but that’s not the case any more.” Clients have included people who developed mesothelioma after washing the clothes of their husband or father who worked in the asbestos industry, people living near a business that used asbestos, or painters who’ve sanded back asbestos-laced walls. Although most of Slater & Gordon’s clients are over 60 years of age, some are in their 30s and 40s. The youngest that Ms Kent has worked with was only 22 years old and may have been exposed as a toddler. **** As an indication of how ubiquitous asbestos is in Australia, Mrs Carbon has identified six occasions when she may have inhaled asbestos fibres, starting from when she was a young girl watching her uncle build extra bedrooms on to their farmhouse. “I used to help my uncle hold the big asbestos sheets while he was cutting them. We would play with the bits that fell off.” At age 25, and newly married, she lived in a house in Albany, WA. When Cyclone Alby tore the asbestos-laden roof off the house in April 1978, she and her husband lifted the pieces of broken roof to be cleared away. The newlyweds renovated their house, including sanding down the eaves, which also contained asbestos. “We used a steel wire brush, and sometimes we used sandpaper. There was lots of dust going everywhere.” Mrs Carbon knew other people with mesothelioma at the time of her diagnosis, but she was shocked to be diagnosed herself. “I had thought it could be cancer, but I never for one minute thought that it was mesothelioma.” **** Ms Kent from Slater & Gordon says there is still a public perception that mesothelioma is an occupational disease. She says most people exposed to asbestos during home renovation had no idea of the dangers and receive a “particularly bad and huge shock when they discover they have an asbestos-related illness”. She is concerned that there is a lot of misinformation in the community about the nature of asbestos and the potential risks of home renovation. “It worries me. We’re a great renovating country and the estimate is that one in three houses has some asbestos in it. Increasingly, people don’t know what it looks like, and they don’t understand that it’s very hazardous, potentially even in small quantities.” She adds that do-it-yourself TV shows have a role to play in increasing awareness of the risks of home renovation. “If they show pictures of people hacking with sledgehammers into asbestos sheeting, then it’s incredibly irresponsible, but if an explanation of the hazards is given, and some attempt to demonstrate doing it properly — then that could be a good thing.” Ms Kent’s concerns are shared by Unions NSW, which passed a unanimous resolution last month, calling on home renovation TV shows to include on-air warnings about the dangers of asbestos. Network Ten’s TV program The Renovators did not respond to the Journal’s request for a comment. Mrs Carbon agrees that there needs to be greater awareness of the risks of home renovation. “You have to be very careful; it only takes one fibre. You really have to wear masks, but we didn’t. We didn’t know anything about it.” **** Mrs Gladys (Joyce) Hyde, aged 78, was similarly surprised when she was diagnosed with mesothelioma 18 months ago, particularly given that she had never worked with asbestos or handled it during home renovation. Her asbestos exposure was indirect and probably occurred when she was living with her family in south-west Melbourne. They were next door to an agricultural company that conducted substantial building work in the late 1970s and early 80s. No one warned the family of possible risks and she had no idea her health was potentially in danger. “We didn’t think about it at all.” She was admitted to hospital 18 months ago because she was having difficulty breathing. “I could barely get to the bathroom to have a shower, it was that bad.” She ended up having five litres of fluid drained. “When they found the mesothelioma, it was a shock.” Professor Bill Musk, a Perth-based respiratory physician, says patients with mesothelioma typically present to their GP with chest pain or breathlessness. “The GP then does a chest x-ray and finds something on it, particularly pleural effusion.” A cell sample to confirm the diagnosis is usually obtained by aspirating the pleural effusion, but false negative results are common. A closed biopsy, a video-assisted thoracoscopic biopsy, or occasionally an open biopsy, can also confirm the diagnosis of mesothelioma. **** Mesothelioma is an unpredictable disease. Once diagnosed, the median survival is 9 to 12 months, but it is difficult to give an accurate prognosis. “Occasionally, a patient survives 10 to 15 years”, says Professor Musk. And although the cancer is almost always linked to asbestos exposure, it’s impossible to predict who, of those exposed, will develop the cancer. Mr Carbon has luckily not developed the disease, despite having sanded back the same eaves with his wife in Albany in the late 1970s. He also had a career as a ship’s master, which involved putting asbestos lagging on exhaust pipes, and later breaking it off when it became hard and brittle. “It was the most dangerous thing we could do to it, but I’ve never experienced any problems”, he said. Mrs Hyde is also acutely aware of the unpredictability of mesothelioma. “My oncologist said that a man could work with asbestos all of his life and never get it, but his wife could wash his clothes and get it. His view was it’s just the luck of the draw.” **** At the urging of her grandson, Mrs Hyde approached the law firm Slater & Gordon to seek compensation. Slater & Gordon’s defendants have included everyone from asbestos manufacturers, James Hardie and Wunderlich (a subsidiary of CSR), to state and federal government bodies. Legal claims focus on proving that there was a failure to warn of the dangers or of the need to take precautions, or to provide ways of minimising the asbestos dust. “It ranges from failure to put a warning on the product to failing to inform the public of the known dangers”, says Ms Kent. As lawyer John Gordon writes in this issue of the Journal , neither James Hardie nor CSR have ever taken any steps to systematically warn people of the dangers of asbestos products in their homes, or “of the potential for fatal consequences in 20 to 40 years if they demolish those products today”. **** Both Mrs Hyde and Mrs Carbon have had chemotherapy. “I’m waiting for 4 weeks to see if the cancer has shrunk. I’m a bit in limbo at the present”, says Mrs Hyde. A grandmother of 10, she is enjoying time with her family. Twice a week she helps with reading lessons at the school where her daughter works. “That’s been fabulous”, she says. She used to be a keen lawn and tenpin bowler, but the cancer and treatment have tired her out. “I was always reasonably active, and then to get something like this and it mucks everything up. It is hard but I’ve got a good family. You just have to keep on going.” Mr and Mrs Carbon are also pushing on. With the oversized fishing rods packed in their motorhome, they’re taking their minds off the diagnosis for a few weeks. “When I was first told it was mesothelioma I thought, ‘how am I going to get this out of my mind? I was thinking about it all day’”, Mrs Carbon says. Mr Carbon says the couple are only now coming to realise the full impact of the diagnosis. “But we’re boxing on and trying to enjoy life, making the most of every minute.”
Sophie McNamara
Unintended pregnancy in Australia: what more can we do?
Emergency contraception and medical abortion are options, but education about them is vital Prevention is better than cure — especially in the field of sexual and reproductive health. Australia’s teenage pregnancy rates (17.3 per 1000 women in 2003)1 and abortion rates (19.7 per 1000 women in 2008)2 are high compared with other Western countries. Such rates are not inevitable, and recent contraceptive strategies were developed to help in reducing them. One such strategy was the rescheduling in Australia of the emergency contraceptive pill (ECP) containing levonorgestrel to Schedule 3 (over-the-counter) status, making it available from pharmacists without a prescription. Improved access to the ECP is a crucial issue, given that the sooner it is taken after unprotected intercourse, the more effective it is. By rescheduling the ECP, it was hoped that women would be able to obtain it more easily within the narrow time frame recommended, especially after hours and on weekends, when it is more difficult to access a general practitioner. A second-generation antiprogestin ECP, ulipristal acetate (30 mg), has now been released and is thought to be a more effective option up to 120 hours after unprotected intercourse.3 Our recently published Australian population study of over 600 women aged 16 to 35 years found that although 95% had heard of the ECP and 26% had used it, just under half (48%) were aware that the ECP was available over the counter.4 In addition, under half (45%) thought it was safe for the health of women, most (61%) erroneously believed that it would damage a pre-existing pregnancy, and 32% that it was an abortifacient, similar to mifepristone — all findings consistent with overseas studies.5,6 Women’s attitudes towards the ECP revealed various views and beliefs influencing their use, including moral and religious reasons, fear of side effects, and unrealistically low perceptions of pregnancy risk.4 Unsurprisingly, women with good knowledge of the ECP were more likely to report having used it. Some women (12%) thought they were unlikely to become pregnant, even when having unprotected intercourse at the most fertile time of the menstrual cycle.4 Although our linked study found that pharmacists believe further information provision following ECP dispensing is their responsibility,7 most women (84%) prefer to receive information from a doctor rather than a pharmacist.4 This offers an important opportunity for GPs to help patients prevent unintended pregnancy and abortion. GPs could include discussion of the ECP in all general consultations with women of reproductive age regarding contraception or reproductive issues, such as cervical cancer screening. Ideally, GPs should seek opportunities to discuss the ECP within an overall contraceptive strategy and with all female adolescents during routine health care visits. GPs can play a critical role in informing and educating women about their risks of becoming pregnant, the use of contraceptives generally and how to use them correctly and consistently. They can also counsel about risky sexual behaviour and the higher risk of an unplanned pregnancy resulting from such behaviour. They could encourage women to keep an advance supply of the ECP at home, if appropriate. Access to such ECP options would be more widely available if it were to be subsidised or free for women who are socioeconomically disadvantaged (eg, health care card holders). As well as the prevention of unplanned pregnancy, assistance with pregnancy termination may be necessary and should always be available if women are unable to continue with a pregnancy. There are parts of Australia where sex education is inadequate, access to contraceptive advice or support is lacking, and hospitals do not provide pregnancy termination services. This can lead to problematically late presentations for abortion.8 In Australia, the removal of the requirement for ministerial approval for the importation and supply of mifepristone means that doctors can now apply to the Therapeutic Goods Administration for approval to provide this drug to their patients for medical termination of pregnancy. Mifepristone is widely used in many countries, including the United Kingdom, the United States, France, New Zealand, Sweden and China and has been shown to be a safe, effective and highly successful treatment for the termination of early pregnancy.9,10 Already, women are being offered greater options when making the decision about an unintended pregnancy — they can choose to continue with the pregnancy, to place the baby for adoption, or if they opt for termination, a limited number of clinics, such as Marie Stopes International Australia,11 are now able to provide medical termination with mifepristone as an alternative to referral for surgical abortion. This option could, and probably should, be more widely available, but a greater emphasis on prevention is clearly needed. At the very least, a sustained public information campaign should address the misconceptions we have uncovered, and publicise the availability of effective contraceptive options. At most, a more comprehensive national sexual and reproductive health strategy should be implemented.
Angela J Taft MPH, PhD · Melissa K Hobbs MPH, PhD · Safeera Y Hussainy BPharmSci, PhD · Lisa H Amir MB BS, PhD · Kay Stewart BPharmSci, PhD · Anthony M A Smith BA(Hons), PhD · Julia M Shelley MPH, PhD · Colin B Chapman BPharmSci, BVSci, PhD
General practice and preventive health care: a view through the eyes of community members
Objective: To identify barriers to, and enablers of, the uptake of preventive care in general practice from the perspective of community members, and to explore their sense of the effectiveness of that care.Design, participants and setting: Qualitative study involving 18 focus groups comprising 85 community members aged over 25 years, from two areas of metropolitan Melbourne that were identified as being of high and low socioeconomic status (SES). The study was performed between 25 May and 9 December 2010. Groups were stratified by age, sex and location (high or low SES).Main outcome measures: Factors related to practitioners, patients and structure and organisation that may act as barriers to and/or enablers of preventive care in general practice.Results: Participants saw preventive care as legitimate in general practice when it was associated with concrete action or a test, but rated their general practitioners as poor at delivering prevention. Trust, rapport and continuity of care were viewed as enablers for participants to engage in prevention with their GP. Barriers to participants seeking preventive care through their GPs included lack of knowledge about what preventive care was relevant to them, consultations focused exclusively on acute-care concerns, time pressures and the cost of consultations.Conclusions: A disconnect exists between patient perceptions of prevention in general practice and government expectations of this sector at a time when general practice is being asked to increase its focus and effectiveness in this field.
Danielle Mazza MD, FRACGP · Lyndel K Shand BA(Hons) · Narelle Warren BA(Hons)/BSc, PhD · Helen Keleher PhD, FPHAA · Colette J Browning MSc, PhD, FAPS · Emma J Bruce BAppSc(Hons), PhD
Association of adolescent symptoms of depression and anxiety with alcohol use disorders in young adulthood: findings from the Victorian Adolescent Health Cohort Study
Objective: To examine the association of adolescent depression and anxiety symptoms with alcohol abuse or dependence in young adulthood.Design, setting and participants: Cohort study of the health and wellbeing of adolescents and young adults in Victoria, assessed at 8 waves (periods) of data collection, from age 14 to 24 years, between 1992 and 2003. Young people who participated in the cohort study at least once during the six adolescent assessment points (conducted 6 months apart, from age 14 to 17 years), at least once during young adulthood and who were alive at Wave 8 (n = 1758).Main outcome measure: Alcohol abuse or dependence assessed using the alcohol and substance abuse modules of the Composite International Diagnostic Interview at age 24 years.Results: Adolescents with moderate to high levels of depression and anxiety symptoms (measured by the revised Clinical Interview Schedule) had an increased risk of alcohol abuse or dependence in young adulthood, compared with young adults with low levels of adolescent depression and anxiety symptoms, after adjusting for potential confounding factors. Risk was higher for those with symptoms at more than two adolescent assessment points (odds ratio [OR] 1.9; 95% CI, 1.7–2.0) and for those with symptoms at one or two assessment points (OR 1.3; 95% CI, 1.2–1.4), compared with those with no above-threshold symptoms in adolescence.Conclusions: Adolescents with depression and anxiety symptoms are at increased risk for alcohol use disorders into young adulthood. They warrant vigilance from primary care providers in relation to alcohol use well into adulthood.
Maria McKenzie BBSc(Hons) · Anthony F Jorm PhD, DSc · Helena Romaniuk BSc, MSc, PhD · Craig A Olsson PhD · George C Patton MB BS, MD
Why is treating obesity so difficult? Justification for the role of bariatric surgery
There is little evidence that public health measures adopted so far have had any impact on the rise in the prevalence of obesity. Weight-loss programs have a very high long-term failure rate. There is emerging evidence that weight is regulated by the hypothalamus and is physiologically defended. There is also a strong genetic predisposition to the development of obesity. The availability and promotion of high-energy foods and the absence of any obligatory need for physical activity compound the problem, but this social change is not easily reversible. One way forward is to focus public health measures on preventing obesity in children while making resources available to treat people who are already obese, including providing funding for bariatric surgery in public hospitals.
Joseph Proietto MB BS, FRACP, PhD
Lack of caregiver supervision: a contributing factor in Australian unintentional child drowning deaths, 2000–2009
To the Editor: In their recent article on unintentional child drowning deaths, Petrass, Blivitch and Finch refer to the “limited detail within both police reports and findings” for South Australian cases of drowning.1 Since 2005, South Australia’s Child Death and Serious Injury Review Committee (CDSIRC), which I chair, has considered the circumstances and causes of all child deaths in SA. The legislation governing the CDSIRC’s work quite rightly precludes the publication of individual details of children’s deaths, but, since 2005, the CDSIRC’s annual report has given a summary of the circumstances and causes of drowning deaths for children in each year. Children drown in a variety of circumstances — in fish ponds, rivers, lakes, dams, buckets of water and in boating accidents — but the greatest number, especially among those under 4 years of age, drown in backyard swimming pools.2 In these incidents, time and again I read about failures of supervision, gate closure and adherence to pool fencing regulations and the maintenance of this fencing. Although the extent and nature of supervision may be of academic interest, the prevention of childhood drowning would best be served by the ongoing promulgation of well researched public health campaigns, such as those delivered by the Royal Life Saving Society — Australia and Kidsafe Australia, and attention to legislative changes that will ensure the regular inspection and maintenance of swimming pool fencing. The CDSIRC’s review of child drownings in SA is based on the detailed information obtained by SA police from witnesses present at the time of the event. This almost always provides a great depth of detail that enables the identification of the key risk factors present in the circumstances of the death. It is unfortunate if this information was not available to Petrass and colleagues, but it is incorrect to infer that such information is not collected in SA. The CDSIRC’s annual reports are available from its website.3 Similar reports are produced by child death review committees or teams in Queensland, New South Wales and Victoria.
Dymphna Eszenyi
Lack of caregiver supervision: a contributing factor in Australian unintentional child drowning deaths, 2000–2009
In reply: Information made available by South Australia’s Child Death and Serious Injury Review Committee is similar to that in other Australian states that have a Child Death Review Committee; all produce an annual report of circumstances related to child deaths, including child drowning. While we are aware of these reports, for our study of child drowning, individual case details were required that cannot be extracted from compiled summaries in annual reports. By contrast, the National Coroners Information System (NCIS) provides access to original documents for individual drowning cases. Details for South Australian child drownings in the NCIS database were very limited, although at no point in our article did we infer that this information is not collected in SA; rather we stated that that coroners findings were only available for 38.1% of cases in the NCIS, and that autopsy and toxicology reports are not routinely uploaded.1 Further, the recently revised position paper of the National Drowning Prevention Alliance (NDPA) states that neither a single device nor a single solution can prevent child drownings, and recommended that caregivers, aquatic facility owners, managers and operators use “layers of protection” to aid in child drowning prevention.2 We certainly agree that the ongoing promulgation of well researched public health campaigns is an important layer in the prevention of child drowning, although, to date, no published studies have investigated the effectiveness or rigorously evaluated Australian aquatic death prevention campaigns (such as Keep Watch, Kids Alive — Do The Five, SafeWaters and Play it Safe by the Water). However, the NDPA did identify that supervision is the one layer that should be ever-present, regardless of what other layers are used.2
Lauren A Petrass · Jennifer D Blitvich · Caroline F Finch
Improving Aboriginal and Torres Strait Islander people’s access to medicines — the QUMAX program
Building on a successful program to extend PBS copayment relief to more patients Cost is a well established influence on both access to medicines and medication adherence rates. Prescription fees can lead to patients forgoing essential medications and to a decline in health care status among needy populations,1,2 an observation that is very familiar to Aboriginal community-controlled health services (ACCHSs). While capped patient copayments and the Pharmaceutical Benefits Scheme (PBS) Safety Net minimise the medication cost burden on all Australians, these mechanisms are ineffective for many Aboriginal and Torres Strait Islander peoples. The reasons for this include high rates of unrecorded concession and Safety Net status, disproportionately higher rates of chronic disease and comorbidity, extended social and family obligations, “shame” in accessing prescriptions in culturally alienating settings, high patient mobility, and poor health literacy. PBS utilisation is further reduced in this population by factors that preclude medicines storage and adherence, such as overcrowding, and disease profiles that are inconsistent with medicines listed on the PBS. The Council of Australian Governments (COAG) National Indigenous Reform Agreement of November 2008 led to strategies designed to close the gap in Aboriginal and Torres Strait Islander people’s life expectancy.3 One of these strategies is the $88.7 million “Subsidising PBS Medicine Co-payments” measure,4 which commenced in July 2010 and is predicted to provide financial assistance to “over 70 000 Indigenous people”, to improve their access to PBS medicines.3 This measure was, in fact, built on an existing program — Quality Use of Medicines Maximised for Aboriginal and Torres Strait Islander Peoples (QUMAX)5 — the details and outcomes of which have been kept under wraps until the recent release of the findings of an independent evaluation.6 The QUMAX program, which commenced in November 2008, aimed to overcome a range of known barriers to Aboriginal and Torres Strait Islander peoples’ access to medicines, and was jointly developed and managed by the National Aboriginal Community Controlled Health Organisation and the Pharmacy Guild of Australia, and funded by the Australian Government under the Fourth Community Pharmacy Agreement (2005–2010). Aboriginal and Torres Strait Islander patients could access the QUMAX program through ACCHSs in rural, regional and urban (ie, non-remote) areas. The cost of medicines for eligible needy and disadvantaged patients (as defined in the business rules for the program6) was subsidised through an online system of coordinated, secure and accountable copayment relief arrangements between ACCHSs and participating community pharmacies. The program also supported local quality use of medicines (QUM) initiatives through support pharmacists assigned to each ACCHS, provided QUM education for ACCHS staff, provided dose-administration aids and transport for the delivery of medicines, focused attention on patients’ PBS Safety Net entitlements, and fostered collaboration with community pharmacies — all within the context of culturally appropriate primary health care. Administration of QUMAX was lean, with the majority of the funds appropriately devolved to supplying medicines. The independent evaluation showed almost universal participation by ACCHSs (69 of 70) and involvement of 541 community pharmacies. The capped nature of QUMAX funding to each ACCHS meant that only 20% of the services’ Aboriginal and Torres Strait Islander clients (nearly 34 000 of the 171 094 patients who attended the participating services annually) could receive support for medicines and medication aids. Over 271 000 medicines were dispensed to these patients with the PBS copayment waived.6 Between November 2009 and April 2010, the proportionate increase in the number of PBS medicines dispensed to patients of non-remote ACCHSs was nearly five times greater than the increase in medicines dispensed to all Australians, and exceeded the increase seen in remote areas by a factor of seven. Greater access to medicines for chronic disease (lipid-lowering, antihypertensive and asthma medications) accounted for most of the increase. This increase occurred on a background of substantial inequities in access to medicines. In the 2006–07 financial year, for every dollar per person spent on PBS medicines for non-Indigenous Australians, only 60 cents was spent on Indigenous Australians.7 Among Aboriginal and Torres Strait Islander peoples, geographical disparities in access to medicines had been the reverse of those expected — Aboriginal peoples in non-remote parts of Australia had lower PBS expenditure per person than those in remote locations ($159 in major cities versus $223 in remote and very remote areas).7 This is probably due to the enduring success of another scheme — the special PBS arrangements under section 100 of the National Health Act 1953 for the supply of medicines to remote-area Indigenous health services.8 It is unclear if QUMAX has alleviated the PBS expenditure inequities, but the evaluation report states that, for Aboriginal and Torres Strait Islander peoples, there is “strong evidence that the QUMAX program has helped to overcome the financial barrier to accessing PBS medicines in non-remote areas”.6 In addition to patients of non-remote ACCHSs, the new PBS medicine copayment measure now extends copayment relief to eligible Aboriginal and Torres Strait Islander people who have, or are at risk of, chronic disease and are patients of any private general practice. Although the QUMAX program no longer includes the copayment relief element, it has been extended until 2015 under the Fifth Community Pharmacy Agreement to continue to augment QUM within ACCHSs. PBS listings have also improved, with more medicines now available for conditions that predominate in the Aboriginal and Torres Strait Islander population.9 There is no doubt that ACCHSs have substantially improved access to medicines for their disadvantaged Aboriginal and Torres Strait Islander patients and will continue to do so — to a level likely to eliminate disparity. They are able to do this through multifaceted strategies built on their intense community knowledge and involvement. When gauging the impact of the Subsidising PBS Medicine Co-payments scheme, it will be crucial for data on PBS utilisation by Aboriginal and Torres Strait Islander peoples to be disaggregated by “service type”. While ACCHSs participating in QUMAX have transitioned readily to the new copayment measure, its effectiveness in the private general practice sector now needs to be explicitly understood.10
Sophie Couzos FRACGP, FACRRM, FAFPHM · Vicki Sheedy BA, BEd · Dea Delaney Thiele PGDipHlthMgt
Is the “alcopops” tax working? Probably yes but there is a bigger picture
The Australian Government’s decision to raise taxes on ready-to-drink spirit-based beverages (RTDs; “alcopops”) in 2008 caused great controversy. Interest groups have selectively cited evidence to support their points of view. The alcohol industry cited Victorian data from the Australian Secondary Students’ Alcohol and Drug Survey (ASSADS) as evidence that the tax had failed, but closer examination of the data suggests that fewer students are drinking, and fewer are drinking at risky or high-risk levels. Excise data from the first full year after the tax came into effect showed a more than 30% reduction in RTD sales and a 1.5% reduction in total pure alcohol sold in Australia. Although understanding the impact of the alcopops tax will require critical analysis of a range of evidence, sales and ASSADS data suggest that the tax has resulted in reduced consumption of RTDs and total alcohol. The most effective and cost-effective measures for reducing consumption and harm are a comprehensive graduated volumetric alcohol taxation system, a minimum price per standard drink, and special measures for particular products that may cause disproportionate harm. While welcoming the alcopops tax, public health advocates have consistently argued for a comprehensive package of reform that covers pricing, availability and promotion of alcohol, as well as education and treatment services.
Steven J Skov MB BS, MPH, FAFPHM · Tanya N Chikritzhs BA(Hons), GradDipEpidBioStats, PhD · Kypros Kypri BA(Hons), PhD · Peter G Miller PhD · Wayne D Hall BSc, PhD · Michael M Daube BA(Hons), HonDSci · A Rob Moodie MB BS, MPH, FAFPHM
Skin cancer screening of outdoor workers in Queensland
To the Editor: The Australian state of Queensland has one of the highest rates of melanoma and non-melanoma skin cancer in the world.1,2 Solar ultraviolet (UV) radiation is the most important environmental risk factor,3 highlighting the need for sun safety education and skin cancer screening among outdoor workers in Queensland. Many such programs are currently in place, including the Sunsafe Workplace Program developed by the University of Queensland in collaboration with the Queensland Skin and Cancer Foundation in 2007. In August 2010, we attended an outdoor workplace in Brisbane, with extensive sun safety policies already in place, to perform free voluntary skin checks on employees. Of 55 people invited to participate, 39 accepted. Of these, 36 were male, the median age was 35 years (range, 19–62 years), and 28 were of British and/or Irish ancestry. Eighteen participants reported spending 5–8 hours a day outdoors mid week and 20 reported the same at weekends. Six reported that at the start of summer, they never tanned and always burned, and 31 reported burning first, then tanning. Nearly half reported having had more than five painful sunburns in their lifetime. Despite these results, only a third of participants (13) reported wearing sunscreen, less than half (17) reported wearing a hat, and two-thirds (26) reported wearing sunglasses more than 50% of the time. Of the 39 participants, we referred one to his general practitioner for management of two non-melanoma skin cancers. About half of the participants reported having had formal skin checks before. Of these, one had previously had melanoma and five had non-melanoma skin cancers, and 10 had one or more suspicious naevi removed in their lifetimes. The main reasons given for not having had a previous skin examination were fear of skin cancer diagnosis and difficulty attending appointments during working hours. We found that providing easy access to free on-site skin examinations reduced interference to the work day, made appointments more accessible (both physically and financially), and enabled us to provide personalised information about participants’ skin and skin cancer risks and reassure those who had been anxious about receiving skin cancer diagnoses. We found that workers were relieved when told they had nothing suspicious presenting on the day, and that they seemed less anxious about seeking skin checks in the future. Despite many public awareness campaigns on skin cancer and the establishment of sun safety programs in the workplace, we found there is still room for improvement. Although clinical guidelines do not currently recommend routine skin cancer screening for the general population,4 the success of our visit leads us to encourage workplaces that are exposed to solar UV radiation to consider providing on-site skin examinations for employees, as well as ongoing sun safety education. We believe such services can help to break down barriers that prevent people from seeking medical assessment and management, and can help to spread the safety-in-the-sun message.
Nicola C Douglas · Laura Baillie · H Peter Soyer
A no-fault compensation scheme for serious adverse events attributed to vaccination
No-fault compensation, based on the ethical principle of redistributive justice, should form a cornerstone of Australia’s immunisation strategy Australia has an enviable reputation for its publicly funded vaccine program — a program that has benefited Australian children and adults over many years. In 2010, the National Immunisation Program funded 12 vaccines, twice as many as a decade previously. To monitor outcomes from this program, the Australian Childhood Immunisation Register, which commenced data collection in 1996, provides a detailed record of vaccine uptake by children.1 Funding for the register and for incentives to general practitioners to improve vaccine uptake are part of the total budget for Australia’s vaccine program, estimated to exceed $400 million annually.2,3 One area for improvement in the vaccine program is monitoring of adverse events following immunisation (AEFI). Another would be the introduction of a no-fault compensation scheme for serious adverse events which can be confidently attributed to vaccination. An investigation into the unexpectedly high number of febrile convulsions in children aged less than 5 years after they had received the influenza vaccine in 2010 — in some cases, with devastating consequences4 — provided a forceful reminder that timely vaccine safety monitoring is needed in Australia.5 More active adverse event surveillance is certain to uncover more AEFI but many of these will only be coincidental, while others will be of a transient or relatively trivial nature. On rare occasions, a serious AEFI with long-term sequelae will be recognised. A decision will then need to be made on whether the vaccine was responsible for that serious event. The World Health Organization defines four categories of serious AEFI: hospital admission or prolongation of an existing hospital admission; permanent disability; any event that is life threatening; or death.6 Using these criteria, 8% (193/2396) of the AEFI reported by passive surveillance in Australia in 2009 were judged to be serious.7 However, unlike many countries where compensation schemes exist for adverse events attributed to a vaccine, Australia has no routine approach to making the assessment of attribution. Parents of children or adults who believe they deserve compensation for a serious adverse event that they attribute to a vaccine are therefore required to make their case through the adversarial legal system. This requires the demonstration that an individual or an organisation was at fault. However, fault is often difficult to demonstrate and an adverse event may be caused by vaccination through no fault of the vaccine manufacturer, the regulator or the person who administered the vaccine. We have previously argued that a Queensland child who developed transverse myelitis after receiving oral polio vaccine was an example of an adverse event following vaccination where no fault was attributable to any party.8,9 Despite detailed epidemiological evidence that was consistent in this case with the causal criteria for an AEFI promulgated by the Institute of Medicine of the National Academies in the United States,8 and despite laboratory evidence showing that the polio virus recovered from this child was similarly pathogenic to a polio virus that has been accepted as causing vaccine-associated paralytic polio,9 the polio expert committee concluded that the evidence was insufficient to support a causal relationship between the oral polio vaccine and transverse myelitis. As causality has not been accepted, this child has received no compensation. The general principles associated with this case raise a number of pertinent questions for Australia. First, should a child who may have been injured by a vaccine, which was endorsed and paid for by the community, be compensated by the community when the serious adverse event may be attributed to the vaccine? Second, what are the criteria for accepting an attributable relationship between receipt of the vaccine and a subsequent adverse event? Third, what is the best method for financing a compensation scheme? Each question may highlight a potential barrier to the implementation of a no-fault AEFI compensation scheme in Australia. By 2010, 19 countries around the world had implemented no-fault AEFI compensation, implicitly answering “yes” to the question of whether the community owes a duty of care to an individual injured by a vaccine.10 There is also a strong ethical argument for this position, based on the concept of redistributive justice. Any person who is injured while helping to protect the community — for instance, by contributing to herd immunity, such that there are sufficiently many people immunised to prevent widespread disease transmission within the community — should not bear the consequences of injury alone. In essence, the community owes a debt of gratitude to that person. Temporal association of an adverse event with receipt of a vaccine does not establish causality and the underlying notion of causation used in most compensation schemes is similar to that used in epidemiology.10 The World Health Organization has published guidelines on causality for an AEFI.11 An adverse event considered to be very likely or certainly due to a vaccine would comprise a “Clinical event with a plausible time relationship to vaccine administration, and which cannot be explained by concurrent disease or other drugs or chemicals”.11 To simplify and expedite determinations of causality in the US, a vaccine injury table is used to predetermine causality if a vaccine injury is included in the table.10 However, determining causation is a complex issue. Recognising this, most countries have a designated committee, comprising medical and legal members, which deliberates on the attributable relationship between receipt of the vaccine and subsequent adverse event.10 Concerns about funding a no-fault compensation scheme is another of the probable barriers to its implementation in Australia. Schemes are currently funded by one of four methods: a vaccine levy; compensation for AEFI as part of a much broader injury compensation scheme; specific AEFI compensation funded through general tax revenue; and funding in association with industry.10 Funding through a vaccine levy has been self-sustaining in the US. Despite compensation payments having been made to 2580 claimants since 1989, the compensation fund there has a surplus of about US$3 billion.12,13 No-fault vaccine-injury compensation programs are based on the premise that any adverse event attributable to vaccination is not due to the fault of a specific individual or organisation, but due to an unavoidable risk that is acknowledged as being associated with vaccines. Germany has been operating a no-fault AEFI compensation scheme for 50 years.10 France restricts its compensation to serious AEFI, since these are likely to have long-term implications for the injured party.10 Restricting compensation to events with long-term consequences, above a nominated clinical threshold, may be an acceptable model for Australia. We have previously argued that Australia should follow the lead of other advanced countries and implement a no-fault compensation scheme.14 We continue to argue that such a scheme, based on the ethical principle of redistributive justice, should form a cornerstone of Australia’s immunisation strategy. Disclaimer The views expressed are those of the authors and have not been endorsed by any institution or organisation with which the authors are affiliated or by any committees of which the authors are members.
Heath A Kelly BSc, MB BS, MPH · Clare Looker MB BS, MPH · David Isaacs MD, FRACP, FRCPCH
Socioeconomic disparities in stroke rates and outcome: pooled analysis of stroke incidence studies in Australia and New Zealand
Objective: To assess the influence of area-level socioeconomic status (SES) on incidence and case-fatality rates for stroke.Design, setting and participants: Analysis of pooled data for 3077 patients with incident stroke from three population-based studies in Perth, Melbourne, and Auckland between 1995 and 2003.Main outcome measures: Incidence and 12-month case-fatality rates for stroke.Results: Annual age-standardised stroke incidence rates ranged from 77 per 100 000 person-years (95% CI, 72–83) in the least deprived areas to 131 per 100 000 person-years (95% CI, 120–141) in the most deprived areas (rate ratio, 1.70; 95% CI, 1.47–1.95; P < 0.001). The population attributable risk of stroke was 19% (95% CI, 12%–27%) for those living in the most deprived areas compared with the least deprived areas. Compared with people in the least deprived areas, those in the most deprived areas tended to be younger (mean age, 68 v 77 years; P < 0.001), had more comorbidities such as hypertension (58% v 51%; P < 0.001) and diabetes (22% v 12%; P < 0.001), and were more likely to smoke (23% v 8%; P < 0.001). After adjustment for age, area-level SES was not associated with 12-month case-fatality rate.Conclusions: Our analysis provides evidence that people living in areas that are relatively more deprived in socioeconomic terms experience higher rates of stroke. This may be explained by a higher prevalence of risk factors among these populations, such as hypertension, diabetes and cigarette smoking. Effective preventive measures in the more deprived areas of the community could substantially reduce rates of stroke.
Emma L Heeley MSc, PhD · Jade W Wei BPharm · Kristie Carter PhD · Md Shaheenul Islam MB BS, MPH, MSc · Amanda G Thrift PhD · Graeme J Hankey MD · Alan Cass PhD · Craig S Anderson MD, PhD