Environmental health

Victorian legislation will help the health sector reduce emissions and adapt to climate change

Brett Sutton · Vanora Mulvenna · Daniel Voronoff · Tiernan Humphrys

The origins, scope and significance of the 2019–2020 Climate Health Western Australia Inquiry

Tarun S Weeramanthri · Sarah Joyce · Revle Bangor‐Jones

Reducing smoking during pregnancy among Aboriginal and Torres Strait Islander women is a national priority, but there has been little exploration of their experiences and desired support

Michelle Bovill

Clinical record A 42‐year‐old woman presented to the Sunshine Coast University Hospital, Queensland, with a 5‐day history of odynophagia, orthopnoea and rapid onset of neck swelling over 12 hours. She had returned one week prior from a year‐long trip to Central America, Sri Lanka and Indonesia. Relevant past medical history included nephrotic syndrome due to minimal change disease, use of prednisolone 2.5 mg daily and previous treatment with rituximab. Childhood vaccinations were reported, but she had no booster travel vaccinations. On examination, she had right‐sided neck swelling, consistent with “bull neck” (Box, A), and an exudative right tonsil with a haemorrhagic component (Box, B). The patient had several healed skin lesions and a 2 cm non‐healing ulcer on her buttock. Flexible nasendoscopy showed supraglottic oedema with a patent airway. The diagnosis of diphtheria was strongly considered, with differentials including peritonsillar abscess and tonsillitis. Computed tomography scan of the neck demonstrated peritonsillar phlegmon and oedema in the parapharyngeal space, pre‐vertebral fat and subcutaneous neck tissues. She was commenced on intravenous benzylpenicillin, lincomycin and dexamethasone, was placed on contact and droplet precautions, and was admitted to the intensive care unit. Multiple tissue and swab samples were taken from the pharyngeal membrane and the buttock wound and urgently sent to the laboratory for culture into selective media. She underwent elective intubation 24 hours later due to worsening laryngeal oedema. Tissue and swabs from the pharyngeal membrane and sacral wound grew Corynebacterium diphtheriae. Diphtheria antitoxin (DAT) 100 000 IU was administered 36 hours into her admission. The isolates were confirmed to be toxigenic by polymerase chain reaction.1,2 The patient was discharged from the intensive care unit on Day 6. On Day 7, she developed anterior T wave inversions on her electrocardiogram, with an elevated troponin value (0.39 μg/L; reference range, < 0.040 μg/L). Her cardiac enzymes showed serial improvement. She developed a moderate glossopharyngeal and vagal palsy, which resolved after 3 weeks, and peripheral neuropathy, which resolved after 4 months. The cardiac and neurological sequelae were thought to be complications of pharyngeal diphtheria. The local Public Health Unit and the infection management service identified 12 staff and seven close community contacts. All contacts had nasal and throat swabs taken, were treated with oral erythromycin and were vaccinated where appropriate.3 Staff were excluded from work until returning negative throat and nasal cultures at 48–72 hours. Discussion Diphtheria is an acute pharyngeal or cutaneous infection caused by toxigenic strains of C. diphtheriae — a gram‐positive, non‐motile, non‐encapsulated bacillus.4 The infection spreads by respiratory droplets or direct contact with nasopharyngeal secretions or skin lesions. The incubation period of diphtheria is commonly 2–5 days. Data from the World Health Organization show that diphtheria is endemic to South‐East Asia, including Indonesia, Malaysia and the Philippines.5 Our case illustrates the need for a thorough travel history and administration of timely antitoxin therapy in suspected diphtheria cases to limit diphtheria‐related neurological and cardiovascular consequences. Diphtheria is rare in Australia after the widespread use of the effective vaccine following World War II, with most cases associated with sporadic importations. There have been seven cases of diphtheria reported since 2001, including one that was fatal in 2011.6 Diphtheria affects the upper respiratory tract, presenting with sore throat and cervical lymphadenopathy; a coating membrane forms in about a third of cases. Simultaneous infection of the skin and respiratory tract is uncommon. Accumulation of the C. diphtheriae organism within the membrane along with fibrin debris result in the appearance of a white pseudomembrane.4 The pathognomonic bull neck is caused by superficial oedema of neck tissues and is associated with a more severe course and higher mortality. The diphtheria toxin is produced by toxigenic strains of the bacterium and affects the cardiovascular, renal and nervous systems via haematogenous spread. The toxin is bound on cell surface receptors and acts to arrest protein synthesis.7 Toxin‐producing infections have a mortality rate between 5% and 10%.8 Diphtheritic myocarditis occurs in 10–20% of patients with pharyngeal diphtheria manifesting as ST disturbance, corrected QT interval (QTc) prolongation, or heart block.9 Cardiac abnormalities are associated with extensive respiratory tract involvement and bull neck appearance as well as neurological sequelae, which occur in 75% of patients with severe respiratory disease.4 Cranial nerve neuropathy develops first; often presenting as swallowing difficulties and resulting in aspiration. DAT and antibiotics should be administered promptly upon clinical suspicion. Early administration of DAT reduces circulating toxin load and reduces clinical sequelae.3 Our patient received DAT at 36 hours, yet significant neurological sequelae were observed up to 4 months later. Penicillin and/or erythromycin are the antimicrobials of choice; however, resistance has been described.10 Lessons from practice Diphtheria should be suspected in patients presenting with pseudomembranous tonsillitis, significant neck swelling and relevant travel history. It is important for clinicians to liaise with their local laboratory and Public Health Unit in suspicious cases so appropriate investigations and follow‐up can be established. Timely administration of diphtheria antitoxin is imperative and should not be delayed awaiting laboratory confirmation. Booster vaccinations should be considered before travel, particularly in patients who may have waning immunity. Box – “Bull neck” characteristic of diffuse cervical lymphadenopathy with tracheal deviation (A). Pseudomembrane coating right tonsil, soft palate and uvula on presentation (B)

Sarah Grigg · David Hogan · F Shaun Hosein · Dean Johns · Amy Jennison · Shradha Subedi

Excellence in environmentally sustainable health care must be the goal of the Australian medical profession

Diana L Madden · Anthony Capon · Philip G Truskett

Objectives: To estimate the carbon footprint of five common hospital pathology tests: full blood examination; urea and electrolyte levels; coagulation profile; C‐reactive protein concentration; and arterial blood gases. Design, setting: Prospective life cycle assessment of five pathology tests in two university‐affiliated health services in Melbourne. We included all consumables and associated waste for venepuncture and laboratory analyses, and electricity and water use for laboratory analyses. Main outcome measure: Greenhouse gas footprint, measured in carbon dioxide equivalent (CO2e) emissions. Results: CO2e emissions for haematology tests were 82 g/test (95% CI, 73–91 g/test) for coagulation profile and 116 g/test (95% CI, 101–135 g/test) for full blood examination. CO2e emissions for biochemical tests were 0.5 g/test CO2e (95% CI, 0.4–0.6 g/test) for C‐reactive protein (low because typically ordered with urea and electrolyte assessment), 49 g/test (95% CI, 45–53 g/test) for arterial blood gas assessment, and 99 g/test (95% CI, 84–113 g/test) for urea and electrolyte assessment. Most CO2e emissions were associated with sample collection (range, 60% for full blood examination to 95% for coagulation profile); emissions attributable to laboratory reagents and power use were much smaller. Conclusion: The carbon footprint of common pathology tests was dominated by those of sample collection and phlebotomy. Although the carbon footprints were small, millions of tests are performed each year in Australia, and reducing unnecessary testing will be the most effective approach to reducing the carbon footprint of pathology. Together with the detrimental health and economic effects of unnecessary testing, our environmental findings should further motivate clinicians to test wisely.

Scott McAlister · Alexandra L Barratt · Katy JL Bell · Forbes McGain

In 2014, we reported in the MJA our findings, based on linked data for cervical screening and human papillomavirus (HPV) vaccination of women in Victoria, that participation of young women in cervical screening during 2010 and 2011 was significantly lower among HPV‐vaccinated than among unvaccinated women.1 In 2018, we had the opportunity to repeat the study at the national level as part of a broader data linkage study of cancer outcomes and screening behaviour across the three national cancer screening programs in Australia.2 In the original study (2014), the Australian Institute of Health and Welfare (AIHW) data linkage unit applied probabilistic name‐based linkage to HPV vaccination and cervical screening data. We acknowledged it was likely that some screened women who were vaccinated would be incorrectly identified as unvaccinated because many young women would have changed their names and addresses between vaccination and cervical screening. In the more recent study (2018), the AIHW again used probabilistic name‐based linkage, but first updated HPV vaccination and cervical screening data by obtaining histories of name and address changes from the Medicare Enrolment File. Medicare registrants’ details are updated when new data are provided to Medicare, the national health care scheme, and are recorded in new records with dates of change. The Australian Department of Human Services agreed to provide these data to the AIHW for data linkage purposes for our 2018 study. Our investigation was approved by the AIHW Ethics Committee (reference, EO 2014‐4‐130) and by state and territory human research ethics committees. After incorporating Medicare data, annual cervical screening rates for Victorian women aged 20–24 years or 25–29 years were higher during 2010 and 2011 for vaccinated than unvaccinated women,2 contrary to our 2014 findings.1 For 20–24‐year‐old Victorian women, the difference in rate changed from 10.1% lower to 14.7% higher for vaccinated women, and for 25–29‐year‐old women from 13.5% lower to 10.0% higher (Box). Our updated findings are consistent with findings from other countries of higher cervical screening participation among women who have been vaccinated against HPV.3,4,5 Incorporating the Medicare Enrolment File into the 2018 linkage was a test of proof of concept. Its successful use in this and similar studies has led to the AIHW data linkage unit granting ethics approval and relevant authorisations for employing the Medicare Enrolment File as a tool for improving the quality of other data linkage studies. The key message of our original study, however, remains unchanged. All women, whether vaccinated against HPV or not, should be encouraged to participate in cervical screening: the HPV vaccine does not protect against all HPV types, and many women in Australia were sexually active before they were vaccinated. While it is as yet unclear whether the association between vaccination and screening will persist for women who were routinely vaccinated at school, it is crucial that we focus on strategies that effectively engage women who do not currently participate in screening. Box – Estimated participation of Victorian women in cervical screening during 2010 and 2011, by HPV vaccination status and age group: 2014 and 2018 data linkage studies HPV = human papillomavirus.

Alison C Budd · Andrew Powierski · Theresa Chau · Marion Saville · Julia ML Brotherton

To the Editor: Climate change is this century's greatest global health threat. As the MJA considers the role of the health care sector in climate change, we urge readers to consider hospital food environments. Australia's health care system should be promoting diets that are healthy for both humans and the planet. A growing body of evidence suggests that healthier human diets have significant environmental co‐benefits. For example, reduced consumption of processed discretionary foods and red meats and increased consumption of fruits, vegetables and legumes have been shown to reduce the risk of certain non‐communicable diseases while also reducing diet‐related greenhouse gas emissions.1,2 Hospital food environments provide a useful intervention point to model and promote healthy, sustainable diets to Australians, as millions of meals are served to patients and their families in hospitals each year. Hospital food retailer guidelines have recently been developed by state governments and health care providers.3,4 To optimise health care food environments, a first step is to remove fast food outlets, vending machines and sugar‐sweetened beverages from hospitals. Inpatient food guidelines, however, are mostly outdated and sustainability is rarely considered. Inpatient food services should prioritise the delivery of fresh, locally sourced, unrefined foods with minimal packaging. Meals should adhere to dietary guidelines, be personalised to patients’ health needs, and minimise food waste. A recent audit by the Victorian Government into inpatient food services may provide an important opportunity to initiate reform.5 The Mater Group hospitals’ “at your request” room service exemplifies a cost‐effective food service model, showing improvements in patients’ nutrient intake, clinical outcomes, food waste reduction and patient satisfaction.6 Australia can also learn from the growing number of global initiatives to improve hospital food, including the New Zealand Ministry of Health's sustainability commitments, which include recommendations to encourage plant‐based eating, sustainable food sourcing and reductions in food waste.7 We should also look to innovative programs such as hospital rooftop gardens, hospital teaching kitchens, and traffic light labelling systems. To protect the health of humans and the planet, we urge state governments and health care providers to urgently evaluate hospital food quality, inpatient food services and retail food environments and implement new mandatory standards.

Genevieve Moseley · Luke Spajic · Georgia Behrens

Clinical record A 40‐year‐old woman of Karen ethnicity presented with 5 days of generalised abdominal pain. The pain was worsening and associated with vomiting in the 12 hours preceding presentation. She had been constipated for 5 weeks. There was no diarrhoea, no blood or mucous in the stool and no haematemesis. There were no sick family, friends or colleagues and no recent travel. She had an omnivorous diet, which had not changed recently, and worked casually at a vegetable farm. In the emergency department, vital signs were normal and the abdomen was mildly distended and tender. Initial blood tests showed a neutrophil count of 9.6 × 109/L (reference range [RR], 2.0–8.0 × 109/L), serum bicarbonate 22 mmol/L (RR, 22–32 mmol/L), normal renal function, and C‐reactive protein below 2.9 mg/L (RR, < 3.0 mg/L). Computed tomography of the abdomen and pelvis was consistent with colitis of the descending colon and ileus (Box 1). She was admitted for observation under the general surgical team. Five hours after admission, her condition rapidly deteriorated. Blood pressure was 80/40 mmHg, heart rate 129 beats per minute in sinus rhythm, and there was severe abdominal tenderness with generalised guarding. Repeat tests showed serum creatinine 175 μmol/L (RR, 60–110 μmol/L), bicarbonate below 10 mmol/L (RR, 22–32 mmol/L), blood pH 6.97 (RR, 7.35–7.45), and lactate 14.8 mmol/L (RR, < 1.5 mmol/L). At emergency surgery, colonoscopy and ileoscopy revealed mucosal inflammation affecting the distal 20 cm of terminal ileum, caecum, transverse and sigmoid colon, with patches of frank mucosal necrosis (Box 2). The bowel was grossly dilated, with small patches of full thickness caecal necrosis but no perforation. Subtotal colectomy, terminal ileectomy, and formation of an end ileostomy were performed, with resultant resolution of circulatory shock. Pathological examination demonstrated severe acute pancolitis and extensive mucosal necrosis (Box 3). Clostridium perfringens infection was suspected, due to a striking similarity to published cases.1,2C. perfringens was isolated from biopsy specimens of the necrotic colonic mucosa using selective culture media. The isolate expressed C. perfringens enterotoxin and α‐toxin, defined as toxinotype F.3 Postoperative management included vancomycin both orally and per rectum. Three months after the operation, she was pain‐free, with a normal appetite and functional state. Reversal of ileostomy is planned in coming months. Discussion C. perfringens is a gram‐positive bacillus that forms hardy spores, is ubiquitous in environmental soil and water, and can be part of normal bowel flora. Toxigenic strains commonly cause both foodborne and sporadic cases of acute, self‐limiting diarrhoea. The typical foodborne strain F produces C. perfringens enterotoxin and α‐toxin and was found in our patient.3 The organism exhibits the shortest known doubling time of any cell when grown at 42°C in cooked minced beef.4 Exposure to large inocula of toxigenic organisms may arise when meat is kept lukewarm before consumption. Enteric infections are characterised by adherence of organisms to small bowel mucosa before concurrent sporulation and release of toxin. This typically induces self‐limiting diarrhoea 10–12 hours after eating. Necrotising enterocolitis is a manifestation of C. perfringens enteric infection that is rare in high income countries. Some reported cases associate the condition with constipation, either pre‐existing due to medication side effects or induced by the high protein content of ingested contaminated meat. Constipation has been proposed to impair the usual expulsion of C. perfringens bacteria and spores, leading to mucosal necrosis and shock as opposed to the usual syndrome of transient diarrhoea. Mortality in case series is greater than 50%.1,2 Despite thorough assessment, the cause of our patient's constipation and means of exposure remain unclear. She most likely contracted the infection hours before the onset of her pain, 5 days before presentation. Exposure could have occurred during food preparation at home, meals with social groups, or via soil at her workplace. While rare in Australia, a type of C. perfringens necrotising enteritis was endemic throughout the 20th century in the Papua New Guinea highlands, caused by β‐toxin‐producing strains. Called “pigbel” in Tok Pisin, the disease is closely associated with traditional pig feasts. In the 1960s and 1970s, pigbel accounted for almost a quarter of paediatric deaths in highlands hospitals. Implementation of a β‐toxoid vaccine in 1979 resulted in an eightfold reduction in incidence and an even greater reduction in disease‐specific mortality.5 C. perfringens infection is an important differential diagnosis in cases of acute severe enteritis or colitis, particularly if accompanied by circulatory shock. Prompt operative intervention is necessary in such situations. In Papua New Guinea, toxoid vaccination has proven very successful. In Australia, food safety practices likely play the greatest role in controlling disease burden. Lessons from practice Toxigenic Clostridium perfringens type F commonly causes acute diarrhoea, with illness typically commencing hours after meat consumption. Cases are usually self‐limiting, and require symptomatic management only. Very rarely, toxigenic C. perfringens strains can cause fulminant bowel necrosis requiring emergency bowel resection, which may be associated with pre‐existing constipation. In the highlands of Papua New Guinea, necrotising enteritis has been a common cause of paediatric morbidity and mortality, where it is caused by a locally endemic strain of toxigenic C. perfringens. Box 1 – Coronal computed tomography image of the abdomen and pelvis with portal venous phase contrast, demonstrating mural thickening of the descending colon in the left lower quadrant and fluid‐filled distension of the transverse colon, ascending colon, and ileum Box 2 – Endoscopy images obtained immediately before laparotomy, showing mucosal necrosis of the ascending colon Box 3 – Macroscopic appearance of resected colon, demonstrating extensive mucosal necrosis and oedema

Harry N Walker · Kwee‐Chin Liew · Vicki Adams · Sarah Larcombe · Sonal S Nagra · Glenn Guest · Eugene Athan

An 80- year- old man presented with 2 days of fever and a widespread, itchy, nonblanching, erythematous rash involving more than 50% of body

David WJ Griffin · Genevieve E Martin · Catriona McLean · Allen C Cheng · Michelle L Giles

Ambient air quality in Australia is regulated by the National Environment Protection Measure (NEPM), which sets a maximum 24‐hour mean concentration of 50 μg/m3 for particulate matter less than 10 μm in diameter (PM10) and 25 μg/m3 for PM2.5. Each state and territory is required by the NEPM to annually report all breaches of this standard, including the sources of pollution.1 We analysed NEPM reports for Western Australia to identify days during 1 January 2002 – 31 December 2017 on which atmospheric particulate matter levels exceeded air quality standard levels, and classified them according to the most frequently reported sources of pollution: prescribed burns, wildfires, and other (crustal particles such as dust, wood smoke, and indeterminate). During 2008–2013, exceedances caused by smoke from prescribed burns, wildfires, and wood smoke were all recorded by the WA Department of Environment Regulation as “smoke haze”. For this period, we therefore applied a random forest algorithm, a machine learning method that uses a random sample of observations for known classifications to predict the classifications for new data.2 We included the variables month, day of the week, temperature, and pollution level as model predictors. To estimate background PM2.5 level, we obtained historical hourly values for PM10 and PM2.5 from the WA Department of Water and Environmental Regulation3 and calculated historical monthly means, excluding days on which particle levels exceeded the air quality standard. We estimated daily PM2.5 concentrations attributable to smoke events by subtracting the background PM2.5 level from measured daily values. Applying standard methods for assessing the health impact of air pollution,4 we estimated the numbers of premature deaths, hospitalisations for cardiovascular and respiratory problems, and emergency department presentations with asthma attributable to elevated PM2.5 levels. We used the value of statistical life (VSL)5 to estimate costs associated with premature mortality. The VSL is based on the willingness to pay for reduced risk of premature mortality, and does not take into account underlying health status, age, or life expectancy of individuals. Deaths associated with acute exposure to increased air pollution are more likely among people at greater risk because of advanced age or chronic illness.6 We estimated hospital service costs according to the mean cost of each episode of care as reported in the Independent Hospital Pricing Authority national cost data collection report7 and the Health Policy Analysis emergency care costing report.8 We also undertook a sensitivity analysis in which we excluded data for 2008–2013, when exceedances caused by smoke from prescribed burns, wildfires, and wood smoke were all recorded in NEPM reports as “smoke haze”. Further details on our methods, including underlying assumptions and limitations, are included in the online Supporting Information. During 2002–2017, particulate air pollution exceeded the national standard on 271 of 5844 days (4.6%), including 197 days (73%) attributable to prescribed burns or wildfires. We estimated that 41 (95% confidence interval [CI], 15–68) premature deaths, 99 (95% CI, 19–182) hospitalisations for cardiovascular problems and 174 (95% CI, 0–373) for respiratory conditions, and 123 (95% CI, 70–179) emergency department visits with asthma were attributable to elevated PM2.5 concentration (Box 1). Total estimated health costs were $188.8 million (95% CI, $68.1–311.1 million); $97.1 million (51%) was attributable to prescribed burns and $77.7 million (41%) to wildfires. Mean estimated health costs were lower on days affected by smoke from prescribed burns ($703 984; 95% CI, $254 064–$1.2 million) than those affected by wildfire smoke ($1.3 million; 95% CI, $475 000–$2.2 million), although more days were affected by prescribed burns (138) than by wildfires (59). The estimated smoke‐related costs of wildfires were highest in 2012 ($24.8 million); in many years, prescribed fires often accounted for most health‐related costs, peaking in 2017 ($24.1 million) (Box 2). In our sensitivity analysis excluding the period 2008–2013, the relative costs by source were similar (prescribed burns, 53% [$58.4 million]; wildfires, 38% [$41.6 million]; Supporting Information). Particulate matter in fire smoke is associated with adverse health outcomes,9 even at relatively low concentrations.10 Landscape fire smoke was the greatest contributor to excessive atmospheric particulate matter levels in WA during 2002–2017 and was associated with substantial health costs. Our estimates of the health impacts may be conservative, as we included only days when PM2.5 concentrations exceeded the national standard, excluding smoky days on which the air quality standard was not breached. Further, our selection of health outcomes did not encompass the total health burden attributable to smoke exposure. Our study highlights the different smoke‐related health effects and costs of infrequent severe wildfire and regular prescribed burning. While prescribed burning reduces the risk of wildfire, better understanding and incorporation into control strategies of the full health impacts of each type of fire are needed for sustainable fire management.11 Box 1 – Estimated health burden attributable to elevated PM2.5 concentrations, Western Australia, 2002–2017, by particulate matter source Outcome Estimated number of cases (95% confidence interval) Prescribed burns Wildfires Other Total Excess deaths (any cause) 21 (8–35) 17 (6–28) 3 (1–5) 41 (15–68) Hospital admissions, cardiovascular 51 (10–94) 41 (8–75) 7 (1–13) 99 (19–182) Hospital admissions, respiratory 89 (0–192) 72 (0–154) 13 (0–27) 174 (0–373) Emergency department attendances, asthma 63 (36–91) 51 (29–75) 9 (5–13) 123 (70–179) Box 2 – Estimated health costs tributable to elevated PM2.5 concentrations, Western Australia, 2002–2017, by particulate matter source

Nicolas Borchers Arriagada · Andrew J Palmer · David MJS Bowman · Fay H Johnston

Gaps in availability of both meningococcal ACWY and B vaccines exist for high risk groups Invasive meningococcal disease (IMD) is a serious disease and an emotive public health issue in Australia. In the early 2000s, IMD case numbers declined nationally by about 80%, from 688 in 2002 to 149 in 2013,1 due to a drop in serogroup C and B disease. The decline in serogroup C disease followed the comprehensive childhood meningococcal C vaccination program — free vaccination was available up to age 19 years — introduced in 2003.2 Simultaneously, but without clear cause in the absence of vaccination, meningococcal B (MenB) disease declined slowly from 1.49 cases per 100 000 population in 2003 to 0.47 in 2015 (293 and 112 cases respectively).3 Overall, the IMD incidence rose again after 2014, driven mainly by the emergence of serogroup W and, to a lesser extent, serogroup Y.1,4 Most serogroup W strains are close variants of the virulent ST‐11 clone initially identified in the United Kingdom and South America in 2009, which was associated with more frequent atypical clinical presentations, greater severity and increased mortality.1 Although the emergence of serogroups W and Y was a game changer, serogroup B still accounted for about half of all IMD cases in Australia between 2016 and 2018.4 Compared with some other vaccine‐preventable diseases, IMD is relatively rare, affecting about one in every 100 000 Australians, equating to an average of 250 cases per year between 2014 and 2018.1,4 However, the case fatality rate is high, and around 10–30% of survivors experience long term sequelae.3,5 Although IMD can occur at any age, it is more common in children aged less than 2 years (especially those aged < 12 months) and older adolescents (Box 1). Aboriginal and Torres Strait Islander (hereafter respectfully referred to as Indigenous) children aged up to 14 years are also disproportionately affected compared with non‐Indigenous children (Box 2). For example, rates of serogroup W IMD in Indigenous children were more than 30‐fold higher compared with non‐Indigenous children of the same age during 2016–2018 (Box 2). People with certain medical conditions also have a high risk of IMD.6 These conditions include asplenia; complement deficiency, which in some types the risk is up to 10 000 times greater than in the general population;7 and use of eculizumab, which is a monoclonal antibody directed against complement and is used for treating paroxysmal nocturnal haemoglobinuria and atypical haemolytic uraemic syndrome. Increased use of quadrivalent meningococcal conjugate vaccines Three brands of quadrivalent meningococcal conjugate (MenACWY) vaccines are available in Australia: Menactra (Sanofi), Menveo (GlaxoSmithKline) and Nimenrix (Pfizer). These quadrivalent vaccines include a capsular polysaccharide from each ACWY serogroup conjugated to a carrier protein, superseding the less immunogenic polysaccharide‐only vaccines previously used. The rapid rise of serogroups W and Y disease prompted all states and territories to fund MenACWY vaccination programs in 2017 and 2018 as an outbreak response.8 These programs varied but predominantly targeted adolescents aged 15–19 years, aiming to both directly prevent disease and to interrupt community transmission of meningococci through reduced acquisition of nasopharyngeal carriage, which is most prevalent in this age group.9,10 Some jurisdictions also implemented time‐limited vaccination programs covering select age groups, from infancy up to older adolescence, to control serogroup W outbreaks. The most notable of these outbreaks began in September 2017 in the Northern Territory and spread to nearby communities in central Australia, including regions in Western Australia, Queensland and South Australia. Indigenous children aged less than 10 years living in remote communities were primarily affected, with 19 cases within a few months.11 Meningococcal B vaccine use in Australia The modes of transmission, pathogenesis and treatment of serogroup B IMD are the same as for IMD caused by other serogroups, although the case fatality rate appears lower for serogroup B (6.9%) than for serogroups W, C and Y (12.8%, 12.0% and 10.8% respectively).12 However, the development of a vaccine against serogroup B disease was problematic for decades because serogroup B capsular polysaccharide is cross‐reactive with human tissues (an autoantigen) and thus poorly immunogenic.13 Two MenB vaccines, developed using novel recombinantly derived protein antigens common to many serogroup B strains, are now available in Australia: Bexsero (GlaxoSmithKline), since 2013, and Trumenba (Pfizer), since 2017. Trumenba is only registered for use from 10 years of age, whereas Bexsero can be used from 6 weeks of age. Both MenB vaccines have a high cost (around $100 per dose) and require multiple doses. Bexsero also causes higher rates of fever in young children than other vaccines included in the National Immunisation Program (NIP), necessitating the use of prophylactic paracetamol around the time of immunisation.6 Data on the benefits of MenB vaccine use are gradually accumulating, predominantly from the UK, which is the only country to have formally evaluated an ongoing funded population‐based program. Infants in the UK have been offered a three‐dose course of Bexsero (scheduled at ages 2, 4 and 12 months) since 2015. New data from the UK over 3 years estimate vaccine effectiveness against serogroup B IMD to be 52.7% (95% CI, −33.5 to 83.2) for a two‐dose primary schedule for infants, and 59.1% (95% CI, −31.1 to 87.2) for a two‐dose primary schedule followed by a booster dose at one year.14 However, Bexsero does not appear to have an impact on nasopharyngeal carriage of serogroup B,9 which implies that herd immunity (indirect protection in unvaccinated individuals) would be limited or absent despite population‐based vaccination.9 In addition, for both vaccines, protection against only around three‐quarters of all circulating MenB strains is predicted, based on in vitro assays.15 To date, the use of MenB vaccines in Australia has been limited in the absence of NIP funding. In October 2018, in the context of higher serogroup B IMD incidence rates compared with other parts of Australia, the South Australian government introduced the only state‐funded MenB vaccination program for young children, expanding to adolescents in February 2019.8 In 2020, a population‐level study of adolescent MenB vaccination in the Northern Territory will commence to explore its impact on gonorrhoea — a high incidence sexually transmitted disease caused by the related organism Neisseria gonorrhoea — as well as on serogroup B IMD (Helen Marshall, Professor in Vaccinology and National Health and Medical Research Council Practitioner Fellow, Robinson Research Institute, University of Adelaide, Australia, personal communication, January 2020). Assessment and introduction of meningococcal vaccines to Australia's National Immunisation Program Both equity and cost‐effectiveness are important considerations when approaching decision making regarding vaccine incorporation into immunisation programs. To be added to the Australian NIP, vaccines require a comprehensive assessment and must be recommended as cost‐effective by the Pharmaceutical Benefits Advisory Committee (PBAC); this is based on economic modelling, typically undertaken by the vaccine manufacturer.16 With a low IMD incidence (one per 100 000), relatively small numbers of deaths, and trends in serogroup incidence being difficult to predict, the accurate assessment of the cost‐effectiveness of both types of meningococcal vaccines (MenACWY and MenB) has been challenging. Low incidence rates have meant reliance on immunologic correlates of protection to predict vaccine impact (randomised placebo‐controlled efficacy studies are not feasible for such rare outcomes) and a limited number of post‐market vaccine effectiveness estimates. Other key uncertainties include the duration of protection and the magnitude of any herd protection effect, particularly for MenB vaccines, for which evidence is showing that there is no effect on nasopharyngeal meningococcal carriage.9 These uncertainties, together with the high cost of the MenB vaccines in particular, provide challenges for the value for money assessment necessary to underpin vaccine introduction into long term programs. In 2018, the MenACWY vaccine Nimenrix replaced the meningococcal serogroup C vaccine on the NIP at 12 months of age, and was also added to the NIP for use in a single birth cohort of adolescents aged 14–16 years from early 2019, replacing jurisdictionally funded programs.8 This is expected to provide direct protection to vaccinated individuals as well as some indirect protection to unvaccinated people over time.17 The potential to fund the MenACWY vaccine for certain high risk groups with underlying medical conditions through the NIP has also been flagged in a recent positive PBAC recommendation,18 which is under active consideration by the Australian Government. The Bexsero MenB vaccine was assessed by the PBAC on three occasions between 2013 and 2015, but was deemed as not being cost‐effective at the manufacturer's proposed price.19 In November 2019, following another manufacturer application, the PBAC recommended the NIP inclusion of Bexsero for Indigenous infants (with a catch‐up to 2 years of age) and for anyone with certain medical conditions (asplenia, complement deficiency, and eculizumab treatment). However, once again, the use of the vaccine in a broader population‐based program for infants and adolescents was not considered cost‐effective.20 The implementation of these recommendations is under active consideration by the Australian Government. Gaps in the prevention of meningococcal disease in Australia The Australian immunisation handbook recommends that any person who wants to protect themselves against invasive meningococcal disease can receive MenACWY and MenB vaccines from as early as 6 weeks of age.6 Box 3 shows groups particularly recommended for vaccination based on their higher risk of disease, compared with current and anticipated funded meningococcal vaccine programs. New proposed and existing funded programs are a substantial achievement and will provide protection to many individuals most at risk from vaccine‐preventable meningococcal strains. However, some equity gaps remain. It will take time to accrue the benefits of reduced MenACWY disease incidence and disease transmission across the population when vaccinating only at ages one and 15 years, especially without including all infants in the NIP‐funded program. It is possible that the disparity in IMD rates between Indigenous and non‐Indigenous children may persist for years, particularly for serogroup B disease, in the absence of herd immunity and of an adolescent program funded by the NIP. Assessing program impact on disease, particularly in jurisdictions where wider populations did, or continue to, receive state‐funded vaccines (against MenACWY or MenB disease), such as Western Australia, Tasmania and South Australia,8 is essential to evaluate evidence of benefit. The remaining access gaps are very challenging to address for high cost vaccines that are not offered at cost‐effective prices by the manufacturer. Other initiatives, such as ensuring that health services fund vaccination of persons living with human immunodeficiency virus and of at‐risk laboratory workers (two groups not included in the NIP), and addressing the social determinants of health that underpin high rates of meningococcal disease (and other vaccine‐preventable diseases), are also important.21 Conclusion Australia has progressively implemented funded vaccination programs for various high risk groups using MenACWY and MenB vaccines over the past 5 years. The anticipated expansion of NIP funding to include medical at‐risk groups for both vaccines and to include young Indigenous children for MenB vaccine, in addition to established MenACWY programs, should be effective over time to protect those most at risk of disease. Close monitoring of emerging data on the duration of vaccine protection from Australia and internationally is needed, particularly for individuals with underlying medical conditions whose risk is enduring. It remains challenging that for one disease, IMD, we must use two vaccines; while at least one pentavalent vaccine (MenABCWY) is under development, it is years away from use, and the assessment of cost‐effectiveness is equally uncertain. This rare but deadly disease will continue to challenge; clinicians should remain aware and discuss vaccination options against both MenB and MenACWY disease with their patients. Box 1 – Invasive meningococcal disease (IMD) notification rates by serogroup and age group (Australia, 2016–2018) The graph shows the rate of cases of IMD notified to the National Notifiable Diseases Surveillance System between 1 January 2016 and 31 December 2018. The total cases include all notified cases of IMD, including serogroups B, C, E, W, Y and unknown serogroup. There were no cases of serogroup A in this period. Box 2 – Average annual notification rates of invasive meningococcal disease (IMD) for Aboriginal and Torres Strait Islander people compared with non‐Indigenous people, by age group and serogroup (Australia, 2016–2018) RR = rate ratio. The graph shows the rate of cases of serogroup B and W IMD notified to the National Notifiable Diseases Surveillance System between 1 January 2016 and 31 December 2018. Box 3 – Australian recommendations for meningococcal vaccination and funded programs*† Recommendations Funded programs for MenB vaccines‡ Funded programs for MenACWY vaccines‡ Overall AIH recommendation Any person who wants to protect themselves against invasive meningococcal disease can receive MenACWY and MenB vaccines from as early as 6 weeks of age No funded programs that cover all age groups No funded programs that cover all age groups Specific AIH recommendations for high risk groups§ All individuals in particular age groups (6 weeks to 4 years and 15–19 years) State/territory: South Australia: 6 weeks to 12 months of age, with catch‐up to 4 years of age8 Northern Territory: to be provided for adolescents from early 2020 as part of an NHMRC‐funded research study¶ NIP: One dose at age 12 months One school‐based cohort (age ~ 15–16 years)8 State/territory: Various current and previous programs — for further detail refer to summary document8 or individual health department websites Aboriginal and Torres Strait Islander people (6 weeks to 19 years of age) NIP: Nil, but anticipated it will likely be included for infants, with catch‐up to 2 years of age20 NIP: One dose at age 12 months One school‐based cohort (age ~ 15–16 years)8 State/territory: South Australia: 6 weeks to 12 months of age, with catch‐up to 4 years of age8 Northern Territory: to be provided for adolescents from early 2020 as part of an NHMRC‐funded research study¶ State/territory: Various current and previous programs — for further detail refer to summary document8 and individual health department websites High risk due to medical condition (asplenia/hyposplenia, complement deficiency, eculizumab use, HIV, post‐HSCT; all people aged ≥ 6 weeks) NIP: Nil, but anticipated it will be included for individuals with asplenia/hyposplenia, complement deficiency, eculizumab use20 NIP: Nil, but anticipated it will be included for individuals with asplenia/hyposplenia, complement deficiency, eculizumab use20 Other: Some individual hospitals or local health services may fund the vaccine for patients with HIV or HSCT Other: Some individual hospitals or local health services may fund the vaccine for patients with HIV or HSCT Other risk factors (young adults aged 20–24 years who smoke or live in close quarters; eg, military barracks or university residential accommodation) Nil (self‐funded) Nil (self‐funded) Laboratory workers at risk Nil (may be employer‐funded) Nil (may be employer‐funded) Travellers to endemic areas Nil (self‐funded) Nil (self‐funded) AIH = Australian immunisation handbook; HIV = human immunodeficiency virus; HSCT = haematopoietic stem cell transplant; NHMRC = National Health and Medical Research Council; MenACWY = serogroups A, C, W and Y meningococci; MenB = serogroup B meningococcus; NIP = National Immunisation Program. * Adapted from the AIH6 and other referenced sources. † Note that the number of doses recommended varies by specific group — refer to the AIH for details. ‡ As of 17 January 2020. § Recommendations are for both MenACWY and MenB vaccines. ¶ Helen Marshall, Professor in Vaccinology and NHMRC Practitioner Fellow, Robinson Research Institute, University of Adelaide, Australia, personal communication, January 2020.

Cyra Patel · Clayton K Chiu · Frank H Beard · Nigel W Crawford · Kristine Macartney

Objectives: To describe the first isolation and sequencing of SARS‐CoV‐2 in Australia and rapid sharing of the isolate. Setting: SARS‐CoV‐2 was isolated from a 58‐year‐old man from Wuhan, China who arrived in Melbourne on 19 January 2020 and was admitted to the Monash Medical Centre, Melbourne from the emergency department on 24 January 2020 with fever, cough, and progressive dyspnoea. Major outcomes: Clinical course and laboratory features of the first reported case of COVID‐19 (the illness caused by SARS‐CoV‐2) in Australia; isolation, whole genome sequencing, imaging, and rapid sharing of virus from the patient. Results: A nasopharyngeal swab and sputum collected when the patient presented to hospital were each positive for SARS‐CoV‐2 (reverse transcription polymerase chain reaction). Inoculation of Vero/hSLAM cells with material from the nasopharyngeal swab led to the isolation of SARS‐CoV‐2 virus in culture. Electron microscopy of the supernatant confirmed the presence of virus particles with morphology characteristic of viruses of the family Coronaviridae. Whole genome sequencing of the viral isolate and phylogenetic analysis indicated the isolate exhibited greater than 99.99% sequence identity with other publicly available SARS‐CoV‐2 genomes. Within 24 hours of isolation, the first Australian SARS‐CoV‐2 isolate was shared with local and overseas reference laboratories and major North American and European culture collections. Conclusions: The ability to rapidly identify, propagate, and internationally share our SARS‐CoV‐2 isolate is an important step in collaborative scientific efforts to deal effectively with this international public health emergency by developing better diagnostic procedures, vaccine candidates, and antiviral agents.

Leon Caly · Julian Druce · Jason Roberts · Katherine Bond · Thomas Tran · Renata Kostecki · Yano Yoga · William Naughton · George Taiaroa · Torsten Seemann · Mark B Schultz · Benjamin P Howden · Tony M Korman · Sharon R Lewin · Deborah A Williamson · Mike G Catton

Some patients may not benefit from inpatient rehabilitation, but numerous factors must be considered

Ian D Cameron

Objective: To investigate changes in sales to pharmacies of over‐the‐counter (OTC) and prescription analgesics, cold and flu products, and cough suppressants after the rescheduling of codeine as a prescription only medicine in February 2018. Design: Interrupted time series analysis of sales to pharmacies. Setting: Pharmaceutical sales to community pharmacies in Australia, March 2015 – March 2019. The period January 2017 (month after rescheduling was announced) to January 2018 (month before rescheduling was implemented) was excluded from the time series analysis. Main outcome measures: Monthly pack and tablet sales per 10 000 population of OTC and prescription analgesics, cold and flu products, and cough suppressants. Results: During 2016, 7586 packs and 248 127 tablets of OTC codeine per 10 000 population were sold to pharmacies; in the 14 months after rescheduling, a small level increase in monthly prescription codeine sales was evident (2247 tablets/capsules per 10 000 population; 95% CI, 1231–3264 per 10 000 population). Monthly OTC analgesic sales increased by 258 (95% CI, 151–365) packs per 10 000 population and 37 856 (95% CI, 26 143–49 569) tablet/capsules per 10 000 population. Monthly sales of single ingredient paracetamol (41 415 [95% CI, 31 374–51 456] tablets/capsules per 10 000 population), ibuprofen (1392 [95% CI 916–1868] tablets/capsules per 10 000 population), paracetamol/ibuprofen (1618 tablets [95% CI, 1567–1669] tablets/capsules per 10 000 population), and other paracetamol combinations (233 [95% CI, 112–353] tablets/capsules per 10 000 population) all increased, but not those of prescription analgesic products not containing codeine. Rises for OTC cold/flu products containing the opioid derivative dextromethorphan were small; sales of OTC cough suppressants containing opioid derivatives (dextromethorphan, pholcodine, dihydrocodeine) did not change. Conclusions: The rescheduling of codeine was followed by increased sales to pharmacies of paracetamol, ibuprofen, and paracetamol combination products. While these products carry no risk of dependence, their inappropriate use is also associated with harms that warrant adverse event monitoring.

Andrea L Schaffer · Rose Cairns · Jared A Brown · Natasa Gisev · Nicholas A Buckley · Sallie‐Anne Pearson

Inclusion of the right to health in Queensland's Human Rights Act is historic but not without challenge In February 2019, the Queensland Parliament passed the Human Rights Act 2019, which took effect on 1 January 2020. Its introduction makes Queensland the third Australian jurisdiction to implement human rights legislation, after the Australian Capital Territory and Victoria in 2004 and 2006, respectively. While the Queensland Act is based on a model of rights legislation broadly consistent with the Victorian and ACT models, it differs in its inclusion of the right to health services (section 37): Every person has the right to access health services without discrimination. A person must not be refused emergency medical treatment that is immediately necessary to save the person's life or to prevent serious impairment to the person.1 The inclusion of section 37 is historic. The right to health is made subject to law on Australian shores and a state/territory government is finally accountable, by law, to protect and promote the enjoyment of the highest attainable standard of physical and mental health. Rights language is part of Australia's public health vernacular, evidenced by the Australian Charter of Healthcare Rights.2 However, unless such rights are expressed in domestic law, then right to health principles and policies are important words on paper without overt legal consequence for effective monitoring and accountability.3,4 As Australia lacks a legal tradition regarding the right to health, the introduction of section 37 creates interpretive challenges for the new Queensland Human Rights Commission (QHRC). The right to health has received limited robust attention in both Australian schools of public health and law, as well as in Australian public health‐related literature.5 The QHRC, and Queensland's courts and tribunals, will likely look to United Nations (UN) commentary on the right to health, and to overseas jurisprudence and scholarship for guidance on section 37's emergent framing.3,6 With the right to health found in over 100 national constitutions and the UN Special Rapporteur on the right to health issuing annual reports, guidance is available.7,8 Health service obligations and remedies under the new Act Queensland government departments and public employees will have a responsibility to protect and promote the human rights of Queensland individuals, and in their health service delivery and decision making, act in a way consistent with their obligations under the Act.1 Health agencies that fit the Act's “public entity” criteria are also bound to comply with the Act. If an individual alleges a section 37 violation, they should make a complaint to the government agency or public entity, which must respond within 45 business days.1,6 If an inadequate or no response is received, the individual — or two or more people jointly — can lodge a complaint with the QHRC.1 Given that the Act's regulatory model favours discussion, rights awareness raising and education, the QHRC will aim to pragmatically resolve section 37 disputes. Monetary damages will not be available.6 In the case of judicial review, a person might have the original decision quashed or referred back to the original decision maker for redetermination.6 In certain circumstances, pending legal advice, a section 37 complainant might have grounds to pursue a distinctly separate medical negligence cause of action if a health professional or service provider breaches their common law duty of care and the complainant has sustained pain and suffering, loss or injury.9 Some grievances against health service providers (notably private providers) can continue to be dealt with by the Health Ombudsman under Queensland's Health Ombudsman Act 2013, and the QHRC may indeed refer complaints to the Health Ombudsman (with the complainant's consent).1,10 However, potential complainants under either Act should be aware the objectives of both Acts markedly differ. The Health Ombudsman Act emphasises that the health and safety of the public are paramount, thereby framing health through a health security lens at the population level, whereas the Human Rights Act takes an individual level approach: the enjoyment of the highest attainable standard of physical and mental health of each and every person in Queensland is paramount (Box 1). Additionally, the Health Ombudsman Act does not recognise the special importance that human rights — and by extension, health and human rights and accessible, non‐discriminatory health service provision — has for Queensland's Aboriginal peoples and Torres Strait Islander peoples.1 On this point, there is no reason why the definition of health services in section 37(1) could not be interpreted to integrate a culturally responsive meaning for Queensland's Indigenous peoples, consistent with the UN Declaration on the Rights of Indigenous Peoples (Box 2).11 Interpreting section 37 and health rights protections found elsewhere in the Act The Act takes a narrow approach to interpreting the right to health Section 37 is modelled on the right to health in article 12 of the International Covenant on Economic, Social and Cultural Rights.12 The UN Committee responsible for the Covenant stated in General Comment No. 14 that article 12 contains two elements: the right to access health services; and the right to access the underlying determinants of health, or the underlying factors that promote conditions in which people can lead a healthy life.3 Regarding the first element of what accessible, non‐discriminatory health services might look like for section 37 achievement, General Comment No. 14 provides the QHRC with instruction (Supporting Information).3 The Queensland Parliament has clarified it will only adopt the first element of article 12 of the International Covenant, which protects right to health service access; section 37 will not extend to include Queenslanders’ right to the broader health determinants. By limiting section 37 to questions of access to emergency medical treatment and non‐discriminatory health service provision, Parliament cautiously chose not to conflate the parameters of section 37. For some right to health academic specialists, this measured approach is prudent.13 Although section 37 claims are not to incorporate the determinants of health, complainants may nevertheless lodge separate or concurrent claims that capture certain health determinants, such as the right to culture (sections 27 and 28). Public health practitioners are well aware that culture is a significant health determinant.14 Housing is also a major determinant of health, and a housing rights claim (that causally impacts a claimant's health and wellbeing) might be realised under section 24 (property rights). Claims that seek to protect and promote the rights of individuals and communities to access the determinants of health relating to food and water could be sought under the right to life (section 16). This is because, per the explanatory notes to the Human Rights Bill 2018 (Qld), this right reflects the positive obligation on states “to take positive steps to protect the lives of individuals through, for example … positive measures to address other threats to life such as malnutrition and infant mortality” (emphasis added).6 With this in mind, section 16 allegations that identify a compelling food or water security nexus that threatens the right to life could be made. However, the QHRC can refuse to deal with a complaint it considers “frivolous, trivial, vexatious, misconceived or lacking in substance”.1 The protection of other health rights elsewhere in the new Act As highlighted above, the content of section 37 claims will likely raise other rights contraventions. It is foreseeable, for example, that a section 25 right to privacy breach by a health service provider could directly or indirectly create a section 37 access to health service violation (and vice versa). Further, a section 37 contravention, or its ramifications, may be so egregious that the complainant could rationally argue that they have experienced a breach of their section 17(b) right not to be treated in a cruel, inhuman or degrading way by the health service. Section 17(c) also protects and promotes an individual's health and human right to “not be … subjected to medical or scientific experimentation or treatment without the person's full, free and informed consent”.1 Certainly, in some cases, a fine line will arise between informed consent to medical treatment and health service access under section 37. The Act also covers reproductive health and rights. Section 106 clarifies that the Act “does not affect laws about termination of pregnancy”, thereby referring to and upholding the Termination of Pregnancy Act 2018 (Qld). According to Queensland Health, that Act “ensures termination of pregnancy is treated as a health issue rather than a criminal issue” and “supports a woman's right to health, including reproductive health and autonomy”.15 Final comments Queensland Health already has antidiscrimination policies and protocols for its staff and for its patients and clients. Therefore, compliance with section 37 and the Act's wider provisions should not be onerous for government and many other public health service agencies bound by the new Act. However, if international right to health experience can teach Queensland anything, it is that government response to allegations of section 37 violations should not be reactive and visible at QHRC conciliation meetings alone.4 Advancing the right to health for all Queenslanders will not occur in legal silos but in complement with planned educational and promotional activities that help build a culture in the Queensland public sector and broader community that respects and promotes health and human rights, as well as promotes a dialogue about the nature, meaning and scope of health rights for Queensland's most important asset, its human capital.1,6 This will require the engagement of both government and non‐government stakeholders, as well as community members, beyond the health sector. Box 1 – Objectives and principles of the Human Rights Act 2019 (Qld) and Health Ombudsman Act 2013 (Qld) Human Rights Act 2019 Health Ombudsman Act 2013 Main objects: section 3* Main objects: section 3 † to protect and promote human rights; and to help build a culture in the Queensland public sector that respects and promotes human rights; and to help promote a dialogue about the nature, meaning and scope of human rights. to protect the health and safety of the public; and to promote— professional, safe and competent practice by health practitioners; and high standards of service delivery by health service organisations; and to maintain public confidence in the management of complaints and other matters relating to the provision of health services. Preamble* Paramount guiding principle: section 4 † In enacting this Act, the Parliament of Queensland recognises— The inherent dignity and worth of all human beings. The equal and inalienable human rights of all human beings. Human rights are essential in a democratic and inclusive society that respects the rule of law. Human rights must be exercised in a way that respects the human rights and dignity of others. Human rights should be limited only after careful consideration, and should only be limited in a way that can be justified in a free and democratic society based on human dignity, equality, freedom and the rule of law. Although human rights belong to all individuals, human rights have a special importance for the Aboriginal peoples and Torres Strait Islander peoples of Queensland, as Australia's first people, with their distinctive and diverse spiritual, material and economic relationship with the lands, territories, waters, coastal seas and other resources with which they have a connection under Aboriginal tradition and Ailan Kastom. Of particular significance to Aboriginal peoples and Torres Strait Islander peoples of Queensland is the right to self‐determination. The main principle for administering this Act is that the health and safety of the public are paramount. Without limiting subsection (1), the health and safety of the public is the main consideration for— the health ombudsman, when deciding what relevant action to take to deal with a complaint or other matter; and the director of proceedings, when deciding whether to refer a matter to QCAT; and QCAT, when deciding a matter referred to it under this Act. QCAT = Queensland Civil and Administrative Tribunal. * Reproduced from https://www.legislation.qld.gov.au/view/html/asmade/act-2019-005;8 † Reproduced from https://www.legislation.qld.gov.au/view/html/inforce/current/act-2013-036.10 Box 2 – The right to health: article 24 of the United Nations Declaration on the Rights of Indigenous Peoples* Indigenous peoples have the right to their traditional medicines and to maintain their health practices, including the conservation of their vital medicinal plants, animals and minerals. Indigenous individuals also have the right to access, without any discrimination, to all social and health services. Indigenous individuals have an equal right to the enjoyment of the highest attainable standard of physical and mental health. States shall take the necessary steps with a view to achieving progressively the full realization of this right. * Reproduced from https://www.un.org/development/desa/indigenouspeoples/wp-content/uploads/sites/19/2018/11/UNDRIP_E_web.pdf.11 Declarations are not ratified. Adopted by the UN General Assembly on 17 September 2007. Supported by the Australian Government on 3 April 2009.

Claire E Brolan

If I am allowed to anaesthetise again, I'll share a few quiet reassuring words with my patients I had spent the past 25 years working in hospitals, intensive care units (ICUs) and theatres. So many thousands of operations on so many patients, and yet here I was, fearful and frankly embarrassed. I lay motionless, face fixed in an unconvincing grin for the benefit of former colleagues as I floated past them, a single off‐white sheet covering my goosebumps. Just another patient this time. Paraded down the corridor; relatives and staff trying to guess whether you were haemorrhoids or a vasectomy. I was no longer the operating room DJ, “gasman” and “wannabe comedian”. Rather than choosing a playlist and sipping the first of many espressos that morning, I had stiffly, illegibly signed a consent form and wet my parched lips from a plastic cup. The last time consent for surgery had been requested, it had been during an emergency helicopter flight, given by my shell‐shocked wife, thousands of miles away. She had tearfully agreed to the trauma team's plans to stabilise my broken neck and jaw, sew my ear back on and drain my exploded right chest, ruptured lung and kidney. The good news was that the pulverised hands and multiple lumbar fractures could wait for another day. It hadn't been clear at that stage if walking was going to be an option, nor whether the brutal deceleration would take a longer term toll upon my brain. It would be a week in the ICU, ventilated and restrained, plus many months of interminable rehabilitation before anyone would know for certain. I remembered accelerating down that long steep hill into Apollo Bay, tucking low on the frame, not even having to pedal to gain speed rapidly, looking ahead for the group I had lost contact with. I flew past other riders, cautiously feathering their brakes on the descent. My eyes watered in the chill jet stream and the bike's carbon wheels chattered on the gleaming tarmac. Then darkness. Silence. Darkness. A large, calloused hand gently, insistently squeezed mine. Like waking from a deep restful sleep, I realised that I had been aware of the pressure on my palm for some time before I understood to try to respond. Slowly, hesitantly, I opened my eyes. The voice was deep, resonant and strangely familiar. It was my son. The brain damage that I sustained on that cold morning in Melbourne, head on into a street pole at 65 km/h tossed me onto the other side of life's road. Each of us doctors spends our training and junior years formulating our own personal and crucially professional identity. Born from repetitive, regular crises of confidence through patient deaths, personal errors and sometimes just promotion to the next terrifying level of responsibility. It wasn't so much learning what to do to be a competent doctor; it was more learning what it was to be a doctor, how we saw ourselves and how society regarded us. I realised that I could no longer muster that theatre blues’ confidence, that surgical squad strut. Laying on a theatre trolley, in a queue for the lifts, I was just another tremulous punter, nervous about the loss of control. I was most afraid of the drug‐induced, return to the darkness. The maxillofacial surgeon had asked me, many weeks after the plates and metalwork had been screwed in, between loosening yanks on the wires holding my face together, if I remembered the accident. I gargled denial noises, my mouth jammed open. “That's a good job,” she laughed. “What a mess!” Operating lists had been my working day and I missed them and my colleagues too, diligent and quirky, good‐hearted and generous. I watched them quietly busy around me, hushed and focused as they made their last detailed preparations. Part of me was ashamed that I knew so little about each of them individually, especially since so many had spontaneously sought me out, given me support and warmth during my months in rehabilitation. Perhaps there was more to medicine than just caring for people. Health teams build something together. Trust, empathy, a united resolve to do the best we can. It looked simple enough when you saw staff doing the same operation a thousand times, but it was the commitment to excellence and good outcomes that defined these humble, generous people. Many of the staff knew me that day as I arrived in the cool clinical space, air conditioner humming, the last stop before the deep dive. A familiar face checked me in for the final time. Knowing her well as I did, I was fleetingly relieved that it was my arm, and not some more delicate area that had been crushed as I was catapulted from the bike. I lay there quietly and felt the emotions rise again, tears welling up. The crash trauma and the rehabilitation had made me afraid of the absence, the journey into that anaesthetic void. I could picture the theatre scene on the day of the accident. Probably not much different to today really. Relaxed, professional and all quite routine. Shredded Lycra, chest drains, ruptured organs and the rest. Sometimes, when I had been the boss, patients would get worried when I told them that things were routine. That wasn't to say we weren't concentrating, it's just that we had done it many times before. I would deliberately avoid the patient's back story just to keep my own anxiety at bay, ignore the injustice and bypass the random cruelty of their situation. Just put an airway into them and keep them asleep while the damaged bits got sorted. No doubt, when they lay my broken body onto a theatre table after the crash, it was much the same. Maybe some passing banter about the weekend's footy results, the crappy Melbourne weather and “middle‐aged men in Lycra” who really should know better. How ironic it would have been had I not hit the pole with my chin, but with my forehead and pithed my brain. Imagine the plaudits for the State Medical Director for DonateLife who felt so impassioned about saving other people's lives through organ donation, that he selflessly became a donor himself. Surely at least an Order of Australia for me? It could have been one of my team informing my family, hands held tight, that their husband and father was not going to make it but that he could save other people's lives. Drugs now flowed into a vein. I often tried to excel at the flippant and the ridiculous in the face of the worst of emergency situations, but not today, not on the other side, a scared patient. “Another one bites the dust” had always got a giggle if I played it from my Spotify favourites, just before sleep time. I used to jokingly tell patients before I put them under that being worried was quite understandable and that if anything bad happened, they would never know because they'd be dead. Strangely, that didn't seem funny anymore. Perhaps if I am allowed to anaesthetise again, once my brain is straight, I'll just share a few quiet reassuring words with my patients, tell them that it's okay to be frightened, that they're safe and that I won't leave their side until they awake. I used to pat myself on the back when a patient left my ICU. Now I have seen that leaving the ICU is not the end of the journey but the start of a new journey. I tried to explain through the mist of my confusion to the nurse caring for me that without her company and support, I wouldn't have survived. She started to cry. I hadn't meant to upset her but I wanted her to know that I was grateful. The outpatients’ clinic since then has been shocking and revelatory. I was the only one not in a wheelchair and for that I felt terrible guilt. Proper patients with proper injuries, courage and optimism by the bucketload have been a sombre reminder of what might have been. I have no memory of those first few steps, my wife's tears or the cheers from my hemiplegic room‐mate as I edged back onto my bed for a well earned rest. Because of the brain injuries, the thought of anaesthetising someone now fills me with an unfamiliar fear. It took me all my waking hours to craft this cast‐iron professional identity of mine and an instant to fatally fracture it. I even had the Rod of Asclepius tattooed on my biceps on my 50th birthday just to affirm a life's commitment to medicine. The supreme irony that I may never practise again and the loss of that coveted persona have been the most traumatic part. Who am I now? I used to be a doctor until that day on the Great Ocean Road. Not anymore. Perhaps one day I will accept the crash and its consequences; move on with my life. Not quite yet.

Bruce Powell

Weather conditions conducive to extreme bushfires are becoming more frequent as a consequence of climate change.1 Such fires have substantial social, ecological, and economic effects, including the effects on public health associated with smoke, such as premature mortality and exacerbation of cardio‐respiratory conditions.2,3 During the final quarter of 2019 and the first of 2020, bushfires burned in many forested regions of Australia, and smoke affected large numbers of people in New South Wales, Queensland, the Australian Capital Territory and Victoria. The scale and duration of these bushfires was unprecedented in Australia. We undertook a preliminary evaluation of the health burden attributable to air pollution generated by bushfires during this period. Using standard methods for assessing the health impact of air pollution,4 we estimated the numbers of excess deaths, hospitalisations for cardiovascular and respiratory problems, and emergency department presentations with asthma in NSW, Queensland, the ACT and Victoria between 1 October 2019 and 10 February 2020 that could be attributed to bushfire smoke exposure. We estimated population exposure to particulate matter less than 2.5 μm in diameter (PM2.5) for the regions of NSW, Queensland, the ACT and Victoria for which publicly available air quality monitoring data were available (for about 90% of the total population of these states). Data were obtained from the NSW Department of Planning, Industry and Environment,5 the Queensland Department of Science,6 ACT Health,7 and the Environmental Protection Agency Victoria.8 We defined bushfire smoke‐affected days as days on which the 24‐hour mean PM2.5 concentration exceeded the 95th percentile of historical daily mean values for individual air quality stations. We estimated daily mean PM2.5 levels by Statistical Area Level 2 (SA2), using station level data whenever at least one monitoring station was within 100 km of the SA2 centroid, and applying inverse distance weighting.9 Published population and health data from the Australian Bureau of Statistics,10,11 the Australian Institute of Health and Welfare,12,13,14,15 and the NSW Ministry of Health were used.16 We quantified health outcomes by combining baseline incidence rates12,13,14,15 for each health outcome with daily exposure data and applying the relevant exposure–response risk coefficients for each outcome.17,18 We also conducted sensitivity analyses with different PM2.5 thresholds for defining bushfire smoke‐affected days. Further methodological details, including underlying assumptions and limitations, are included in the online Supporting Information. Our analysis of publicly available aggregated data did not require ethics approval. During the study period, PM2.5 concentrations exceeding the 95th percentile of historical daily mean values were recorded by at least one monitoring station in the study area on 125 of 133 days (Box 1). We estimated that bushfire smoke was responsible for 417 (95% CI, 153–680) excess deaths, 1124 (95% CI, 211–2047) hospitalisations for cardiovascular problems and 2027 (95% CI, 0–4252) for respiratory problems, and 1305 (95% CI, 705–1908) presentations to emergency departments with asthma (Box 2). Applying lower thresholds for defining bushfire smoke‐affected days (no threshold, 90th percentile of historical values) did not markedly alter our findings; a higher threshold (99th percentile) reduced the estimates by about 20%. The highest population‐weighted PM2.5 exposure level, 98.5 μg/m3 on 14 January 2020 (Box 1), exceeded the national air quality 24‐hour standard (25 μg/m3)19 and was more than fourteen times the historical population‐weighted mean 24‐hour PM2.5 value of 6.8 μg/m3. We have estimated the excess health burden during 19 weeks’ continuous fire activity in the states most severely affected by smoke. Our estimates are based on air quality data from monitoring stations in the four eastern states — that is, we did not include data for smoke from all extreme fires in Australia during the study period — and we did not attempt to estimate health effects for which exposure–response relationships are less well characterised, such as primary health care attendances and ambulance calls. Detailed epidemiological analysis of more comprehensive exposure estimation and empirical health data will provide more complete information about the harms attributable to the severe air pollution associated with these unprecedented fires, but our findings indicate that the smoke‐related health impact was substantial. Smoke is just one of many problems that will intensify with the increasing frequency and severity of major bushfires associated with climate change. Expanded and diversified approaches to bushfire mitigation and adaptation to living in an increasingly hot and fire‐prone country are urgently needed.20 Box 1 – Population‐weighted PM2.5 levels, New South Wales, Queensland, the Australian Capital Territory and Victoria, 1 October 2019 – 10 February 2020* * Data by state are included in the online Supporting Information. Box 2 – Estimated health burden attributable to bushfire smoke, Queensland, New South Wales, the Australian Capital Territory and Victoria, 1 October 2019 – 10 February 2020 Outcome Estimated number of cases (95% confidence intervals) Queensland New South Wales Australian Capital Territory Victoria Total Excess deaths (any cause) 47 (17–77) 219 (81–357) 31 (12–51) 120 (44–195) 417 (153–680) Hospital admissions, cardiovascular 135 (25–246) 577 (108–1050) 82 (15–149) 331 (62–602) 1124 (211–2047) Hospital admissions, respiratory 245 (0–513) 1050 (0–2204) 147 (0–308) 585 (0–1227) 2027 (0–4252) Emergency department attendances, asthma 113 (61–165) 702 (379–1026) 89 (48–131) 401 (217–586) 1305 (705–1908)

Nicolas Borchers Arriagada · Andrew J Palmer · David MJS Bowman · Geoffrey G Morgan · Bin B Jalaludin · Fay H Johnston

Screening guidelines specific to the needs of Australia’s Indigenous population are needed

Nicole Lowres · Ben Freedman

The evidence from real world implementation is compelling

Mike Daube · Julia Stafford

Information on COVID‐19 and its impact is being updated constantly and Australia must continue to be prepared at all levels of the health care system An outbreak of a novel coronavirus, formally named severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and causing coronavirus disease 2019 (COVID‐19), emerged in the city of Wuhan in Hubei province in central China in December 2019. The first cases were noted as a cluster of patients with pneumonia who were all linked to a live animal market, and testing found the presence of a previously unknown coronavirus. Coronaviruses are a group of viruses that affect both animals and humans, and several (OC43, 229E, HKU1 and NL63) are a cause of the common cold.1,2 However, two coronaviruses previously caused significant outbreaks associated with more severe disease: the SARS coronavirus in 2002–2003 and the Middle East respiratory syndrome coronavirus that emerged in 2012.1,2 In contrast to previous outbreaks, the rapid sharing of viral sequences enabled laboratories worldwide to develop diagnostic tests within weeks of discovery of the pathogen.3 An Australian laboratory subsequently isolated the virus from a clinical sample (the first to do so outside of China), and rapidly shared this virus with relevant global agencies, further aiding diagnostic, therapeutic and vaccine development efforts. Information on the new virus and its impact is being updated constantly. While ascertainment of the milder end of the disease spectrum varies between countries,4 the age‐specific severity profile appears to be relatively consistent.5 Age is clearly an important risk factor — there have been few severe cases reported in children, and a high case fatality risk in the elderly. However, it is not clear whether comorbidities reflect the age group affected or whether they are risk factors for severe disease.6,7 Early studies using data before the institution of public health interventions in China suggest that SARS‐CoV‐2 is as transmissible as SARS coronavirus and probably more transmissible than influenza viruses.8,9 Emerging data suggest that viral load is highest around the onset of illness in milder cases, and transmission may occur during this pre‐symptomatic period.10,11,12 Careful analysis of early data suggests that the mean incubation period is 6 days, with a range of up to 14 days.13 There have been a considerable number of large clusters associated with large events, including religious communities, weddings, business meetings, closed communities, dormitories and cruise ships.14,15,16,17 The importance of infection control is also reinforced by a report that 41% of cases in Wuhan were acquired nosocomially (including 40 health care workers and 17 patients).6 Since the World Health Organization was first notified of this new pathogen, more than 2 million cases and over 130 000 deaths have been reported globally. On 16 April 2020, there were 6462 confirmed cases of COVID‐19 in Australia, including 63 deaths. After early outbreaks in Asia, the hardest hit countries currently are the United States and in Europe. There is great concern about low and middle income countries with limited diagnostic and public health capacity. The public health, political and societal ramifications have been considerable, with disruptive interventions that would have been unthinkable even a few months ago. Ultimately, a vaccine will be required; at the time of writing, 60 vaccine candidates have been developed, including three entering human trials (https://vac-lshtm.shinyapps.io/ncov_vaccine_landscape/). For clinicians, the main considerations are the clinical management of patients with suspected COVID‐19 but also systems to facilitate the identification of potential cases and to permit safe assessment and referral as appropriate. The experience with SARS and Middle East respiratory syndrome also reinforces the need for health services (both internationally and within Australia) to promptly identify patients with suspected infection and implement effective infection control measures, including adequate protection of health care workers. Based on clinical features, it can be difficult to distinguish patients with COVID‐19 from those with other respiratory viral infections, including influenza. Although the original case series described fever in almost all patients,7 further experience has noted cases with only respiratory symptoms, and even a small proportion with gastrointestinal symptoms.6 This has resulted in constant changes to case definitions, initially limited to febrile respiratory infections in travellers, but now including the full spectrum of illness in patients with broader epidemiological risk factors. Clinicians should refer to current information to guide testing and management (Box 1). Nucleic acid assays for SARS‐CoV‐2 are available at all Australian reference laboratories and commercial tests are now available in diagnostic laboratories. Compared with other countries, Australia has now performed a proportionately large amount of testing per capita.18 However, the sheer scale of testing has placed extraordinary pressure on supply chains for essential components required for laboratory testing, both in Australia and globally. Current World Health Organization advice is to test patients who meet the case definition for COVID‐19, regardless of whether another respiratory virus is detected, as co‐infections may occur.19 In recent weeks, surveillance for COVID‐19 has expanded to include a much broader range of risk factors to ensure capture of community transmissions. The role of serological assays (particularly point‐of‐care testing) in the overall public health response to COVID‐19 has yet to be defined, although peak bodies such as the Royal College of Pathologists note that there is no role for point‐of‐care assays in the diagnosis of acute COVID‐19.20 Lessons of the past are instructive for Australia, particularly the experience in Canada with its similar federated government and comparable health care system. In 2003, an outbreak of SARS coronavirus in Toronto infected 438 people and caused 44 deaths, including many health care workers. Following this public health disaster, two important reviews were conducted: the National Advisory Committee on SARS and Public Health,21 and Ontario's SARS Commission.22 The former reinforced the need for a strong and adequately funded nationally coordinated public health and laboratory system and led to the establishment of the Public Health Agency of Canada. The SARS Commission made detailed recommendations, including endorsing the “importance of the precautionary principle that reasonable efforts to reduce risk need not await scientific proof [which] was demonstrated over and over during SARS”.22 It made recommendations regarding clear governance, preparing for the need for unexpected interventions (including the closure of three hospitals to control the outbreak), effective distribution of outbreak alerts and directives, the need for effective crisis communication, and the value of robust and timely surveillance. With the involvement of health care workers as cases, the Commission highlighted the need to listen to frontline workers and unions and ensure a robust safety culture and effective infection control. We have many more information (and misinformation) sharing tools than were available in 2003. It has been breathtaking to watch the scientific process unfold in almost real time. Rapid genomic sequencing and online databases are being used to generate and analyse primary data. Preprint servers and rapid review in traditional journals are quickly publishing research findings. Research centres and platforms are responding to rapidly collect data and evaluate interventions. Social media and traditional media platforms are disseminating public health messages and findings. However, the fundamental structure of our public health care system remains unchanged, with the same channels of formal communication and direction through jurisdictions and national networks. A future review should consider whether surveillance and response for all infectious disease threats could be better coordinated by a centralised national agency. There are still many major unresolved clinical and public health issues (Box 2). Clear communication to the public and to clinicians has been difficult, particularly with constantly changing epidemiology and evidence. Australia was not significantly challenged by the two previous zoonotic coronavirus outbreaks, but this global crisis has now significantly disrupted the lives of all Australians. With thousands of cases reported in Australia, public health authorities, governments at all levels, researchers and clinicians, laboratories and the community need to continue to work together in a timely and transparent manner to ensure an effective response. Box 1 – Useful sources of official information* Australian information Australian Government Department of Health: https://www.health.gov.au/health-topics/novel-coronavirus Smart Traveller: https://www.smartraveller.gov.au/ Jurisdictional health department sites: New South Wales: https://www.health.nsw.gov.au/Infectious/diseases/Pages/coronavirus.aspx; Victoria: https://www.dhhs.vic.gov.au/coronavirus; Australian Capital Territory: https://www.health.act.gov.au/health-professionals/chief-health-officer-alerts; Tasmania: https://www.coronavirus.tas.gov.au/; South Australia: https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/clinical+resources/clinical+topics/infectious+disease+control/novel+coronavirus+%282019-ncov%29+infection+for+health+professionals/novel+coronavirus+%282019-ncov%29+infection+information+for+health+professionals; Western Australia: https://ww2.health.wa.gov.au/Articles/A_E/Coronavirus; Northern Territory: https://coronavirus.nt.gov.au/; Queensland: https://www.qld.gov.au/health/conditions/health-alerts/coronavirus-covid-19 International situation reports and resources World Health Organization: https://www.who.int/csr/don/12-january-2020-novel-coronavirus-china/en/ United States Centers for Disease Control and Prevention: https://www.cdc.gov/coronavirus/2019-ncov/index.html European Centre for Disease Prevention and Control: https://www.ecdc.europa.eu/en/coronavirus * Websites viewed April 2020. Box 2 – Major unresolved clinical and public health issues Clinical Optimal samples for diagnostic testing (upper versus lower respiratory tract samples) Utility of existing and investigational antiviral agents and other treatments Host risk factors associated with poor clinical outcomes Public health and control The long term public health strategy for control to minimise morbidity and mortality, but taking into account broader impacts of health, the economy and society The optimal mix of case finding and isolation, contact tracing and quarantine, social distancing and personal hygiene Optimal, yet pragmatic, infection control measures to prevent infections in health care facilities and residential aged care facilities

Allen C Cheng · Deborah A Williamson

Percutaneous coronary intervention with stent implantation (PCI‐S) has revolutionised the management of patients with coronary artery disease at high risk of myocardial infarction and stroke.1 Dual antiplatelet therapy (aspirin with clopidogrel, prasugrel or ticagrelor) is superior to aspirin alone for preventing atherothrombotic events, including stent thrombosis, in patients undergoing PCI‐S,2 and is recommended by Australian guidelines.3 We analysed de‐identified, linked Pharmaceutical Benefits Scheme (PBS) and Medicare Benefits Schedule (MBS) data for a 10% random sample of Medicare beneficiaries provided by the Australian Department of Health, to quantify rates of antiplatelet drug dispensing within 30 days of PCI‐S. We included all patients with MBS claims for PCI‐S (items 38306, 38312, 38318) between 1 January 2013 and 30 September 2014. MBS data on PCI‐S procedures are available only for private patients, who account for about 45% of PCI‐S procedures in Australia.4 The medicines of interest for our analysis were clopidogrel and clopidogrel/aspirin (Anatomical Therapeutic Chemical [ATC] codes B01AC04 and B01AC30), ticagrelor (ATC code B01AC24), and prasugrel (ATC code B01AC22). Aspirin alone was not examined because over‐the‐counter use is not captured in PBS claims data. We assessed the association of several factors with antiplatelet medication dispensing within 30 days of PCI‐S, expressed as odds ratios, by logistic regression modelling. The New South Wales Population and Health Services Research Ethics Committee approved the study (Cancer Institute NSW reference, 2013/11/494). Of 2869 patients who underwent PCI‐S during the study period, 2592 (90%) were dispensed antiplatelet drugs within 30 days of the procedure. Dispensing was more frequent for concessional PBS beneficiaries, patients who had not undergone PCI‐S in the preceding year, patients not dispensed antiplatelet drugs during the preceding six months, and patients dispensed proton pump inhibitors within 30 days of the procedure. Antiplatelet therapy was also more frequent among patients from Victoria or Tasmania, Queensland, and Western Australia than for those from NSW or the Australian Capital Territory (Box). Our findings indicate that 10% of patients undergoing PCI‐S did not receive guideline‐recommended dual antiplatelet therapy within 30 days of their procedure. Cost may have been a barrier, as antiplatelet therapy was less frequent among general than concessional PBS beneficiaries; the maximum out‐of‐pocket cost for any single PBS item in 2013 was $5.90 for concessional beneficiaries, but $36.10 for general beneficiaries, and general beneficiaries may have already experienced significant out‐of‐pocket costs for both health insurance and their procedure. In most states, the Public Hospitals Pharmaceutical Reform Agreement6 ensures that PBS‐subsidised medications can be dispensed to patients when they are discharged from hospital. NSW and the ACT, however, do not participate in this agreement; patients are discharged from public hospitals with unsubsidised medicines sufficient for only 2–7 days, after which they must visit a community doctor for prescribing of PBS‐subsidised medications. This inconvenience may contribute to the lower 30‐day dispensing rate in these jurisdictions. We were unable to evaluate the long term clinical effect of antiplatelet therapy as the analysed datasets do not include information about hospital admissions. The number of PCI‐S procedures in Australia increased from 24 500 MBS claims in 2013 to 29 000 in 2018 (http://medicarestatistics.humanservices.gov.au/statistics/mbs_item.jsp), and the number of patients at risk of early stent thrombosis may also have grown. Why some patients undergoing PCI‐S are not receiving dual antiplatelet therapy directly after their procedure should be further investigated. Box – Characteristics of patients undergoing percutaneous coronary intervention with stent implantation (PCI‐S) in Australia, and their association with dual antiplatelet therapy within 30 days of PCI‐S Number of patients Odds ratio (95% confidence interval) Underwent PCI‐S Antiplatelet therapy within 30 days Univariate models Multivariate model Total number of patients undergoing PCI‐S 2869 2592 (90%) Age (years) 18–54 351 (12%) 307 (87%) 1 1 55–64 711 (25%) 640 (90%) 1.29 (0.87–1.93) 1.26 (0.83–1.91) 65–74 965 (34%) 879 (91%) 1.47 (0.99–2.16) 1.17 (0.76–1.81) 75–84 660 (23%) 605 (92%) 1.58 (1.04–2.40) 1.09 (0.66–1.81) 85 or more 182 (6%) 161 (88%) 1.10 (0.63–1.91) 0.83 (0.66–1.60) Sex Women 670 (23%) 604 (90%) 1 1 Men 2199 (77%) 1988 (90%) 0.97 (0.73–1.30) 0.86 (0.63–1.18) State where PCI‐S was undertaken New South Wales/Australian Capital Territory 1121 (39%) 986 (88%) 1 1 Victoria/Tasmania 752 (26%) 694 (92%) 1.64 (1.19–2.26) 1.56 (1.12–2.17) South Australia/Northern Territory 147 (5%) 129 (88%) 0.98 (0.58–1.66) 0.94 (0.55–1.60) Queensland 549 (19%) 504 (92%) 1.53 (1.08–2.19) 1.47 (1.02–2.13) Western Australia 300 (10%) 279 (93%) 1.82 (1.13–2.94) 2.14 (1.28–3.59) PBS patient category General 1453 (51%) 1293 (89%) 1 1 Concessional 1404 (49%) 1299 (93%) 1.53 (1.18–1.98) 1.63 (1.18–2.26) Previous PCI‐S Preceding 12 months 234 (8%) 199 (85%) 1 1 None 2635 (92%) 2393 (91%) 1.74 (1.19–2.55) 1.41 (0.93–2.13) Previous antiplatelet therapy Preceding 6 months 1135 (40%) 995 (88%) 1 1 None 1734 (60%) 1597 (92%) 1.64 (1.28–2.10) 1.96 (1.45–2.64) Anticoagulant therapy within 30 days of PCI‐S No 84 (3%) 77 (92%) 1 1 Yes 2785 (97%) 2515 (90%) 1.18 (0.54–2.59) 1.04 (0.47–2.33) Proton pump inhibitor therapy within 30 days of PCI‐S No 1002 (35%) 931 (93%) 1 1 Yes 1867 (65%) 1661 (89%) 1.63 (1.23–2.16) 1.42 (1.05–1.92) Comorbid conditions (six months before PCI‐S) None 196 (7%) 169 (86%) 1 1 1 180 (6%) 165 (92%) 1.76 (0.90–3.42) 1.47 (0.72–3.01) 2 259 (9%) 234 (90%) 1.50 (0.84–2.67) 1.34 (0.71–2.56) 3 389 (14%) 356 (92%) 1.72 (1.00–2.96) 1.54 (0.84–2.82) 4 452 (16%) 395 (87%) 1.11 (0.68–1.81) 1.01 (0.57–1.79) 5 or more 1393 (49%) 1273 (91%) 1.70 (1.08–2.65) 1.56 (0.88–2.75) PBS = Pharmaceutical Benefits Scheme. *Patients were classified as concessional beneficiaries if all PBS dispensing was concessional during year preceding and the three months following the PCI‐S procedure. †Based on RxRisk comorbidity indices.5

Benjumin Hsu · Michael O Falster · Andrea L Schaffer · Sallie Pearson · Louisa Jorm · David B Brieger

Misgendering negatively affects the mental and physical health of trans individuals

Irene J Dolan · Penelope Strauss · Sam Winter · Ashleigh Lin

The balance between benefits and risks could be improved if effective risk-based screening protocols were developed

David M Roder · Elizabeth Buckley

Ongoing population- level strategies are needed to further reduce lead exposure

Mark P Taylor · Bruce P Lanphear