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AbstractCumulus‐intact and ‐denuded unfertilized oocytes from two mouse strains were exposed to 1.5 m ethanol (EtOH) or two cryoproteclant solutions, 1.5 M propanediol (PROH) or 1.5 M dimethylsulfoxide (DMSO), for 4.5 min at 27°C, and the proportion of activating or degenerating oocytes studied. Exposure to DMSO did not significantly increase activation above that of oocytes not exposed to DMSO. Treatment of oocytes in PROH resulted in the activation of up to 87% of viable oocytes. This was significantly higher (P <01) than in control oocytes and comparable to the rate of activation after treatment with EtOH (59–96% activation). In solutions at 1°C, 47% of control oocytes were activated, which was not significantly different from the rate of activation in EtOH (36%) or PROH (50%) at 1°C. Following treatment with PROH, up to 87% of oocytes degenerated within a period of 6 h in vitro. The age of the oocytes (h post hCG) and the time of cumulus removal with the enzyme hyaluronidase, relative to the time of exposure to the chemicals, influenced the level of degeneration in most groups. Significantly fewer oocytes degenerated when cumulus cells were removed before treatment (0–31%) than when the cumulus was left intact throughout the treatment and 6 h culture period (10–87%). Exposure to PROH at 1°C reduced oocyte degeneration to 5%. We conclude that PROH causes significantly greater losses of oocytes as a result of parthenogenetic activation and degeneration than of exposure to DMSO.

The accuracy and reliability of a rapid blood alcohol estimation by means of a breath alcohol analyser has been evaluated under casualty department conditions in a series of 646 road-crash victims managed at the Dandenong and District Hospital. A higher correlation (r = 0.91) was found between the breath alcohol analyser readings in 633 casualties and those obtained by blood analysis in the police laboratory. In 13 unconscious casualties in whom a nasal breath test was performed, the correlation was lower (r = 0.76). In six casualties, the breath alcohol analyser readings showed lower alcohol concentrations than the legal limit of 0.05 g/100 mL (10.9 mmol/L), but blood analysis detected an illegal concentration. Further evaluation of the accuracy of the breath alcohol analyser in other casualty departments is necessary before it can be recommended as a screening device in States which have legislated for compulsory blood alcohol tests in adult road casualties.

Alcohol outlets tend to be located in lower income areas, exposing lower income populations to excess risks associated with alcohol sales through these establishments. The objective of this study was to test two hypotheses about the etiology of these differential exposures based on theories of the economic geography of retail markets: (a) outlets will locate within or near areas of high alcohol demand, and (b) outlets will be excluded from areas with high land and structure rents.Data from the 2010 National Drug Strategy Household Survey were used to develop a surrogate for alcohol demand (i.e., market potential) at two census geographies for the city of Melbourne, Australia. Bayesian conditional autoregressive Poisson models estimated multilevel spatial relationships between counts of bars, restaurants, and off-premise outlets and market potential, income, and zoning ordinances (Level 1: n = 8,914).Market potentials were greatest in areas with larger older age, male, English-speaking, high-income populations. Independent of zoning characteristics, greater numbers of outlets appeared in areas with greater market potentials and the immediately surrounding areas. Greater income excluded outlets in local and surrounding areas.These findings are consistent with the hypothesis that alcohol outlets are located in areas with high demand and are excluded from high-income areas. These processes appear to take place at relatively small geographic scales, encourage the concentration of outlets in specific low-income areas, and represent a very general economic process likely to take place in communities throughout the world.

Background: Alcohol use is a key preventable risk factor for serious injury. To effectively prevent alcohol-related injuries, we rely on the accurate surveillance of alcohol involvement in injury events. This often involves the use of administrative data, such as International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, Australian Modification (ICD-10-AM) coding. Objective: To evaluate the completeness and accuracy of using administrative coding for the surveillance of alcohol involvement in major trauma injury events by comparing patient blood alcohol concentration (BAC) with ICD-10-AM coding. Method: This retrospective cohort study examined 2918 injury patients aged ≥18 years who presented to a major trauma centre in Victoria, Australia, over a 2-year period, of which 78% ( n = 2286) had BAC data available. Results: While 15% of patients had a non-zero BAC, only 4% had an ICD-10-AM code suggesting acute alcohol involvement. The agreement between blood alcohol test results and ICD-10-AM coding of acute alcohol involvement was fair ( κ = 0.33, 95% confidence interval: 0.27–0.38). Of the 341 patients with a non-zero BAC, 82 (24.0%) had ICD-10-AM codes related to acute alcohol involvement. Supplementary factors Y90 Evidence of alcohol involvement determined by blood alcohol level codes, which specifically describe patient BAC, were assigned to just 29% of eligible patients with a non-zero BAC. Conclusion: ICD-10-AM coding underestimated the proportion of alcohol-related injuries compared to patient BAC. Implications: Given the current role of administrative data in the surveillance of alcohol-related injuries, these findings may have significant implications for the implementation of cost-effective strategies for preventing alcohol-related injuries.

Epidemic thunderstorm asthma (ETSA) is due to a complex interaction of environmental and individual susceptibility factors, with outbreaks reported globally over the last four decades. Australia has been particularly susceptible with nearly half of episodes reported internationally, culminating in the catastrophic Melbourne 2016 event.Reported ETSA episodes are reviewed for common environmental and meteorological risk factors. Allergen aerobiology interaction with thunderstorm activity and rapid weather condition changes is examined. Assessment of the clinical and immunological data highlights risk factors for ETSA presentation, hospital admission, and intensive care admission. Risk factors associated with ETSA deaths are evaluated. Public health strategies, as well as pharmacological and immunological management approaches to reduce individual susceptibility and prevent ETSA are discussed.Improved understanding of the specific meteorological factors predisposing to the greatest risk of ETSA to improve forecasting is required. Better monitoring of aeroallergen levels in areas of greatest geographic risk, with further research into allergen aerobiology underpinning mechanisms of allergen exposure is needed. The role of climate change in increasing the risk of ETSA outbreaks requires further research. Public awareness and education are required to reduce exposure, and to improve uptake of pharmacological and immunological risk reduction and preventive strategies.

AbstractHigh surrounding road density could increase traffic-related air pollution, noise and the risk of traffic injuries, which are major public health concerns for children. We collected geographical data for all childcare centers (16,146) in Australia and provided the data on the road density surrounding them. The road density was represented by the child care center’s nearest distance to main road and motorway, and the length of main road/motor way within 100~1000-meter buffer zone surrounding the child care center. We also got the data of PM2.5 concentration from 2013 to 2018 and standard Normalized Difference Vegetation Index (NDVI) data from 2013 to 2019 according to the longitude and latitude of the child care centers. This data might help researchers to evaluate the health impacts of road density on child health, and help policy makers to make transportation, educational and environmental planning decisions to protect children from exposure to traffic-related hazards in Australia.

Heat exposure is an important but underappreciated risk factor contributing to cardiovascular disease. Warming temperatures might therefore pose substantial challenges to population health, especially in a rapidly aging population. To address a potential increase in the burden of cardiovascular disease, a better understanding of the effects of ambient heat on different types of cardiovascular disease and factors contributing to vulnerability is required, especially in the context of climate change. This study reviews the current epidemiological evidence linking heat exposures (both high temperatures and heatwaves) with cardiovascular disease outcomes, including mortality and morbidity.In this systematic review and meta-analysis, we searched PubMed, Embase, and Scopus for literature published between Jan 1, 1990, and March 10, 2022, and evaluated the quality of the evidence following the Navigation Guide Criteria. We included original research on independent study populations in which the exposure metric was high temperatures or heatwaves, and observational studies using ecological time series, case crossover, or case series study designs comparing risks over different exposures or time periods. Reviews, commentaries, grey literature, and studies that examined only seasonal effects without explicitly considering temperature were excluded. The risk estimates were derived from included articles and if insufficient data were available we contacted the authors to provide clarification. We did a random-effects meta-analysis to pool the relative risk (RR) of the association between high temperatures and heatwaves and cardiovascular disease outcomes. The study protocol was registered with PROSPERO (CRD42021232601).In total, 7360 results were returned from our search of which we included 282 articles in the systematic review, and of which 266 were eligible for the meta-analysis. There was substantial heterogeneity for both mortality (high temperatures: IThis review strengthens the evidence on the increase in cardiovascular disease risk due to ambient heat exposures in different climate zones. The widespread prevalence of exposure to hot temperatures, in conjunction with an increase in the proportion of older people in the population, might result in a rise in poor cardiovascular disease health outcomes associated with a warming climate. Evidence-based prevention measures are needed to attenuate peaks in cardiovascular events during hot spells, thereby lowering the worldwide total heat-related burden of cardiovascular disease-related morbidity and death.Australian Research Council Discovery Program.

ABSTRACTAimTo describe the assignment of International Classification of Disease (ICD)‐10 alcohol codes as underlying or contributory causes of death by the Australian Bureau of Statistics during mortality coding for suicides according to the blood alcohol concentration (BAC) detected at autopsy.DesignPopulation‐based case‐series descriptive analysis.Setting and participantsData for all alcohol‐related (Alc+) suicide deaths (aged 15+) in Australia from 2010–2015 (n = 3132) from the National Coronial Information System.MeasurementsAlc+ suicides were categorised as those with a post‐mortem BAC ≥0.05 g/100 mL. The outcome variable was whether the case was assigned an ICD‐10 alcohol code (F10.0–F10.9, R78.0, T51, X45 and/or X65). We estimated OR for the assignment of codes in Alc+ suicides using BAC as the key predictor. We also examined several covariates that have been implicated in the risk of Alc+ suicides.FindingsAn ICD‐10 alcohol code was assigned during the mortality coding process in 47.6% (n = 1491) of Alc+ suicides. Higher BAC was associated with higher odds of having a code assigned; cases with a BAC over 0.20 g/100 mL over were twice as likely to have an alcohol code assigned (adjusted OR [AOR] = 2.06, 95% CI = 1.59, 2.67) compared with cases with a BAC of 0.050–0.075 g/100 mL. Compared with New South Wales, higher likelihood of code assignment was found in Northern Territory (AOR = 3.85, 95% CI = 2.32, 6.63) and Western Australia (AOR = 2.89, 95% CI = 2.27, 3.68). Compared with 15–24 year olds, 25–44 (AOR = 0.79, 95% CI = 0.63, 0.99) and 65–84 year olds (AOR = 0.63, 95% CI = 0.43, 0.93) were less likely to have a code assigned.ConclusionsAn ICD‐10 alcohol code was not assigned as an underlying or contributory cause of death in over half of suicides in Australia (2010–2015) with a BAC ≥0.05 g/100 mL. The higher the BAC detected at autopsy, the more likely cases were to be assigned an alcohol code during the mortality coding process.