Objectives: To describe the epidemiology and toxicity of caffeinated energy drink exposures in Australia. Design, setting and subjects: Retrospective observational study analysing data from calls regarding energy drink exposures recorded in the database of an Australian poisons information centre over 7 years to 2010. Main outcome measures: Type of exposure; co‐ingestants; symptoms reported; and reported hospitalisations. Results: Callers reported 297 exposures to energy drinks, which showed an increasing annual trend from 12 in 2004 to 65 in 2010. Median age for the 217 subjects with recreational exposure was 17 years (interquartile ratio [IQR], 15–21; range, 11–60) and 57% were male. One hundred recreational users co‐ingested other substances, predominantly alcohol (50) or other caffeinated products (44). The number of energy drinks consumed in one session varied greatly (median, 5 units; IQR, 3–8; range, 1–80). Most subjects who reported recreational use reported experiencing symptoms (87%). The most common symptoms were palpitations, agitation, tremor and gastrointestinal upset. Twenty‐one subjects had signs of serious cardiac or neurological toxicity, including hallucinations, seizures, arrhythmias or cardiac ischaemia. At least 128 subjects (57 with no co‐ingestants) required hospitalisation. Conclusions: Reports of caffeine toxicity from energy drink consumption are increasing, particularly among adolescents, warranting review and regulation of the labelling and sale of these drinks. Educating adolescents and increasing the community's awareness of the hazards from energy drinks is of paramount importance.
Volunteer subjects recalled their recent phone use with moderate systematic error and substantial random error. This large random error can be expected to reduce the power of the Interphone study to detect an increase in risk of brain, acoustic nerve, and parotid gland tumours with increasing mobile phone use, if one exists.
Most studies of mobile phone use are case-control studies that rely on participants' reports of past phone use for their exposure assessment. Differential errors in recalled phone use are a major concern in such studies. INTERPHONE, a multinational case-control study of brain tumour risk and mobile phone use, included validation studies to quantify such errors and evaluate the potential for recall bias. Mobile phone records of 212 cases and 296 controls were collected from network operators in three INTERPHONE countries over an average of 2 years, and compared with mobile phone use reported at interview. The ratio of reported to recorded phone use was analysed as measure of agreement. Mean ratios were virtually the same for cases and controls: both underestimated number of calls by a factor of 0.81 and overestimated call duration by a factor of 1.4. For cases, but not controls, ratios increased with increasing time before the interview; however, these trends were based on few subjects with long-term data. Ratios increased by level of use. Random recall errors were large. In conclusion, there was little evidence for differential recall errors overall or in recent time periods. However, apparent overestimation by cases in more distant time periods could cause positive bias in estimates of disease risk associated with mobile phone use.
ObjectivesThe objective of this study was to examine the associations of brain tumours with radio frequency (RF) fields from mobile phones.MethodsPatients with brain tumour from the Australian, Canadian, French, Israeli and New Zealand components of the Interphone Study, whose tumours were localised by neuroradiologists, were analysed. Controls were matched on age, sex and region and allocated the ‘tumour location’ of their matched case. Analyses included 553 glioma and 676 meningioma cases and 1762 and 1911 controls, respectively. RF dose was estimated as total cumulative specific energy (TCSE; J/kg) absorbed at the tumour's estimated centre taking into account multiple RF exposure determinants.ResultsORs with ever having been a regular mobile phone user were 0.93 (95% CI 0.73 to 1.18) for glioma and 0.80 (95% CI 0.66 to 0.96) for meningioma. ORs for glioma were below 1 in the first four quintiles of TCSE but above 1 in the highest quintile, 1.35 (95% CI 0.96 to 1.90). The OR increased with increasing TCSE 7+ years before diagnosis (p-trend 0.01; OR 1.91, 95% CI 1.05 to 3.47 in the highest quintile). A complementary analysis in which 44 glioma and 135 meningioma cases in the most exposed area of the brain were compared with gliomas and meningiomas located elsewhere in the brain showed increased ORs for tumours in the most exposed part of the brain in those with 10+ years of mobile phone use (OR 2.80, 95% CI 1.13 to 6.94 for glioma). Patterns for meningioma were similar, but ORs were lower, many below 1.0.ConclusionsThere were suggestions of an increased risk of glioma in long-term mobile phone users with high RF exposure and of similar, but apparently much smaller, increases in meningioma risk. The uncertainty of these results requires that they be replicated before a causal interpretation can be made.
Background and aims Globally, codeine is the most‐used opioid. In December 2016, Australia announced that low‐strength codeine (≤ 15 mg) would be re‐scheduled and no longer available for purchase over‐the‐counter; this was implemented in February 2018. We aimed to evaluate the effect of this scheduling change on codeine misuse and use and misuse of other opioids. Design and setting Interrupted time–series analysis of monthly opioid exposure calls to New South Wales Poisons Information Centre (NSWPIC, captures 50% of Australia's poisoning calls), January 2015– January 2019 and monthly national codeine sales, March 2015–March 2019. We incorporated a washout period (January 2017 – January 2018) between the announcement and implementation, when prescriber/consumer behaviour may have been influenced. Participants Intentional opioid overdoses resulting in a call to NSWPIC. Measurements We used linear segmented regression to identify abrupt changes in level and slope of fitted lines. Codeine poisonings and sales were stratified into high strength (> 15 mg per dose unit) and low strength (≤ 15 mg). Only low‐strength formulations were re‐scheduled. Findings We observed an abrupt −50.8 percentage [95% confidence interval (CI) = −79.0 to −22.6%] level change in monthly codeine‐related poisonings and no change in slope in the 12 months after February 2018. There was no increase in calls to the NSWPIC for high‐strength products, level change: –37.2% (95% CI = −82.3 to 8%) or non‐codeine opioids, level change: –4.4% (95% CI = −33.3 to 24.4%). Overall, the re‐scheduling resulted in a level change in opioid calls of −35.8% calls/month (95% CI = −51.2 to −20.4%). Low‐strength codeine sales decreased by 87.3% (95% CI = −88.5 to −85.9%), with no increase in high‐strength codeine sales in the 14 months following re‐scheduling, −4.0% (95% CI = −19.6 to 14.6%). Conclusions Codeine re‐scheduling in Australia appears to have reduced codeine misuse and sales.
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