Australian Institute of Health and Welfare

OBJECTIVE: To assess the cancer risk in children and adolescents following exposure to low dose ionising radiation from diagnostic computed tomography (CT) scans. DESIGN: Population based, cohort, data linkage study in Australia. COHORT MEMBERS: 10.9 million people identified from Australian Medicare records, aged 0-19 years on 1 January 1985 or born between 1 January 1985 and 31 December 2005; all exposures to CT scans funded by Medicare during 1985-2005 were identified for this cohort. Cancers diagnosed in cohort members up to 31 December 2007 were obtained through linkage to national cancer records. MAIN OUTCOME: Cancer incidence rates in individuals exposed to a CT scan more than one year before any cancer diagnosis, compared with cancer incidence rates in unexposed individuals. RESULTS: 60,674 cancers were recorded, including 3150 in 680,211 people exposed to a CT scan at least one year before any cancer diagnosis. The mean duration of follow-up after exposure was 9.5 years. Overall cancer incidence was 24% greater for exposed than for unexposed people, after accounting for age, sex, and year of birth (incidence rate ratio (IRR) 1.24 (95% confidence interval 1.20 to 1.29); P<0.001). We saw a dose-response relation, and the IRR increased by 0.16 (0.13 to 0.19) for each additional CT scan. The IRR was greater after exposure at younger ages (P<0.001 for trend). At 1-4, 5-9, 10-14, and 15 or more years since first exposure, IRRs were 1.35 (1.25 to 1.45), 1.25 (1.17 to 1.34), 1.14 (1.06 to 1.22), and 1.24 (1.14 to 1.34), respectively. The IRR increased significantly for many types of solid cancer (digestive organs, melanoma, soft tissue, female genital, urinary tract, brain, and thyroid); leukaemia, myelodysplasia, and some other lymphoid cancers. There was an excess of 608 cancers in people exposed to CT scans (147 brain, 356 other solid, 48 leukaemia or myelodysplasia, and 57 other lymphoid). The absolute excess incidence rate for all cancers combined was 9.38 per 100,000 person years at risk, as of 31 December 2007. The average effective radiation dose per scan was estimated as 4.5 mSv. CONCLUSIONS: The increased incidence of cancer after CT scan exposure in this cohort was mostly due to irradiation. Because the cancer excess was still continuing at the end of follow-up, the eventual lifetime risk from CT scans cannot yet be determined. Radiation doses from contemporary CT scans are likely to be lower than those in 1985-2005, but some increase in cancer risk is still likely from current scans. Future CT scans should be limited to situations where there is a definite clinical indication, with every scan optimised to provide a diagnostic CT image at the lowest possible radiation dose.

INTRODUCTION: Systematic reviews provide a rigorous synthesis of the best available evidence regarding a certain question. Where high-quality evidence is lacking, systematic reviewers may choose to rely on case series studies to provide information in relation to their question. However, to date there has been limited guidance on how to incorporate case series studies within systematic reviews assessing the effectiveness of an intervention, particularly with reference to assessing the methodological quality or risk of bias of these studies. METHODS: An international working group was formed to review the methodological literature regarding case series as a form of evidence for inclusion in systematic reviews. The group then developed a critical appraisal tool based on the epidemiological literature relating to bias within these studies. This was then piloted, reviewed, and approved by JBI's international Scientific Committee. RESULTS: The JBI critical appraisal tool for case series studies includes 10 questions addressing the internal validity and risk of bias of case series designs, particularly confounding, selection, and information bias, in addition to the importance of clear reporting. CONCLUSION: In certain situations, case series designs may represent the best available evidence to inform clinical practice. The JBI critical appraisal tool for case series offers systematic reviewers an approved method to assess the methodological quality of these studies.

Reviewed by Don Hindle, Visiting Professor, School of Health Services Management,University of New South Wales

There are a number of problems and challenges in relating the science of epidemiology to mental retardation (MR). These relate to how MR is defined and classified and how these definitions may change over time. These as well as other differences in ascertainment sources and methods need to be considered when comparing MR prevalence over time and place. On the other hand, advances in technology also provide new and efficient methods of data collection both by data linkage and by use of web-based methods to study rare diseases. While prevalence studies have not been individually reviewed, we have examined the range of data including recent studies relating to how prevalence differs according to age, gender, social class and ethnicity. Some problems with available etiological classification systems have been identified. Recent etiological studies, most of which use different classification systems, have been reviewed and explanations have been postulated to account for differences in results. Individual risk factors for MR are considered whilst the option of considering a population as opposed to a high risk strategy to MR prevention is raised. This might well involve improving the social milieu surrounding the occurrence of individual risk factors. The impact of biotechnological advances such as antenatal and neonatal screening and assisted reproduction on MR are discussed. The issue of how inequalities in access to technology may impact on case identification and even have the potential to further widen inequalities is raised. The importance of extending the use of epidemiological tools to study the social, health and economic burden of MR is also emphasized. However, in order to apply to MR the "prevention-intervention-research" cycle, which surely underpins all epidemiology, it is vital to ensure that the methodological challenges we raise are adequately addressed.

BACKGROUND: 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. METHODS: 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). FINDINGS: =83·5%, p<0·0001). Despite the heterogeneity in environmental conditions and population dynamics among the reviewed studies, results showed that a 1°C increase in temperature was positively associated with cardiovascular disease-related mortality across all considered diagnoses. The overall risk of cardiovascular disease-related mortality increased by 2·1% (RR 1·021 [95%CI 1·020-1·023]), with the highest specific disease risk being for stroke and coronary heart disease. A 1°C temperature rise was also associated with a significant increase in morbidity due to arrhythmias and cardiac arrest and coronary heart disease. Our findings suggest heat exposure leads to elevated risk of morbidity and mortality for women, people 65 years and older, individuals living in tropical climates, and those in countries of lower-middle income. Heatwaves were also significantly associated with a 17% increase in risk of mortality (RR 1·117 [95% CI 1·093-1·141]), and increasing heatwave intensity with an increasing risk (RR 1·067 [95% CI 1·056-1·078] for low intensity, 1·088 [1·058-1·119] for middle intensity, and 1·189 [1·109-1·269] for high intensity settings). INTERPRETATION: This 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. FUNDING: Australian Research Council Discovery Program.

Studies of the mortality among nuclear industry workforces have been carried out, and nationally combined analyses performed, in the U.S., the UK and Canada. This paper presents the results of internationally combined analyses of mortality data on 95,673 workers (85.4% men) monitored for external exposure to ionizing radiation and employed for 6 months or longer in the nuclear industry of one of the three countries. These analyses were undertaken to obtain a more precise direct assessment of the carcinogenic effects of protracted low-level exposure to external, predominantly gamma, radiation. The combination of the data from the various studies increases the power to study associations between radiation and specific cancers. The combined analyses covered a total of 2,124,526 person-years (PY) at risk and 15,825 deaths, 3,976 of which were due to cancer. There was no evidence of an association between radiation dose and mortality from all causes or from all cancers. Mortality from leukemia, excluding chronic lymphocytic leukemia (CLL)--the cause of death most strongly and consistently related to radiation dose in studies of atomic bomb survivors and other populations exposed at high dose rates--was significantly associated with cumulative external radiation dose (one-sided P value = 0.046; 119 deaths). Among the 31 other specific types of cancer studied, a significant association was observed only for multiple myeloma (one-sided P value = 0.037; 44 deaths), and this was attributable primarily to the associations reported previously between this disease and radiation dose in the Hanford (U.S.) and Sellafield (UK) cohorts. The excess relative risk (ERR) estimates for all cancers excluding leukemia, and leukemia excluding CLL, the two main groupings of causes of death for which risk estimates have been derived from studies of atomic bomb survivors, were -0.07 per Sv [90% confidence interval (CI): -0.4, 0.3] and 2.18 per Sv (90% CI: 0.1, 5.7), respectively. These values correspond to a relative risk of 0.99 for all cancers excluding leukemia and 1.22 for leukemia excluding CLL for a cumulative protracted dose of 100 mSv compared to 0 mSv. These estimates, which did not differ significantly across cohorts or between men and women, are the most comprehensive and precise direct estimates of cancer risk associated with low-dose protracted exposures obtained to date. Although they are lower than the linear estimates obtained from studies of atomic bomb survivors, they are compatible with a range of possibilities, from a reduction of risk at low doses, to risks twice those on which current radiation protection recommendations are based.(ABSTRACT TRUNCATED AT 400 WORDS)

Design and objectives Every organisation has a unique culture. There is a widely held view that a positive organisational culture is related to positive patient outcomes. Following the Preferred Reporting Items for Systematic Review and Meta-Analyses statement, we systematically reviewed and synthesised the evidence on the extent to which organisational and workplace cultures are associated with patient outcomes. Setting A variety of healthcare facilities, including hospitals, general practices, pharmacies, military hospitals, aged care facilities, mental health and other healthcare contexts. Participants The articles included were heterogeneous in terms of participants. This was expected as we allowed scope for wide-ranging health contexts to be included in the review. Primary and secondary outcome measures Patient outcomes, inclusive of specific outcomes such as pain level, as well as broader outcomes such as patient experience. Results The search strategy identified 2049 relevant articles. A review of abstracts using the inclusion criteria yielded 204 articles eligible for full-text review. Sixty-two articles were included in the final analysis. We assessed studies for risk of bias and quality of evidence. The majority of studies (84%) were from North America or Europe, and conducted in hospital settings (89%). They were largely quantitative (94%) and cross-sectional (81%). The review identified four interventional studies, and no randomised controlled trials, but many good quality social science studies. We found that overall, positive organisational and workplace cultures were consistently associated with a wide range of patient outcomes such as reduced mortality rates, falls, hospital acquired infections and increased patient satisfaction. Conclusions Synthesised, although there was no level 1 evidence, our review found a consistently positive association held between culture and outcomes across multiple studies, settings and countries. This supports the argument in favour of activities that promote positive cultures in order to enhance outcomes in healthcare organisations.

AIM: To compare alternative survey methods for estimating (a) levels of at risk alcohol consumption and (b) total volume of alcohol consumed per capita in comparison with estimates from sales data and to investigate reasons for under-reporting. SETTING: The homes of respondents who were eligible and willing to participate. PARTICIPANTS: A total of 21,674 Australians aged 14 years and older. DESIGN: A 2001 national household survey of drug use, experiences and attitudes with weights applied for age, sex, geographic location and day of week of interview. MEASURES: Self-completion questionnaire using quantity-frequency (QF) and graduated-frequency (GF) methods plus two questions about consumption 'yesterday': one in standard drinks, another with empirically based estimates of drink size and strength. RESULTS: The highest estimate of age 14 + per capita consumption of 7.00 l of alcohol derived from recall of consumption 'yesterday' or 76.8% of the official estimate. The lowest was QF with 49.8%. When amount consumed 'yesterday' was recalled in standard drinks this estimate was 5.27 l. GF questions yielded higher estimates than did QF questions both for total volume (5.25 versus 4.54 l) and also for the proportion of the population at risk of long-term alcohol-related harm (10.6%versus 8.1%). With the detailed 'yesterday' method 61% of all consumption was on high risk drinking days. CONCLUSIONS: Questions about typical quantities of alcohol consumed can lead to underestimates, as do questions about drinking 'standard drinks' of alcohol. Recent recall methods encourage fuller reporting of volumes plus more accurate estimates of unrecorded consumption and the proportion of total alcohol consumption that places drinkers at risk of harm. However, they do not capture longer-term drinking patterns. It is recommended that both recent recall and measures of longer-term drinking patterns are included in national surveys.

Our report deals with the relationship of pattern and timing of sun exposure to basal cell carcinoma (BCC) in a population-based case-control study conducted in Western Australia in 1988. The main measure of intermittent exposure was based on the amount of exposure on non-working days relative to that over the whole week. Outdoor recreational activities, holidays and sunburn were also considered to be markers of intermittent exposure. We observed a statistically significant increase in risk of BCC with increasing proportion of weekly sun exposure obtained at the weekend, especially in late teenage (OR = 3.9, 95% CI 1.9-7.8 for maximum intermittency of exposure), exposure of the site of skin cancer during holidays (OR = 1.9, 95% CI 1.1-3.1 for the highest exposure quarter) and sunburn to the site (ORs of 1.8 for 3-10 and 1.5 for 11+ sunburns in a lifetime). Risk of BCC increased substantially with increasing intermittency in poor tanners but not at all in good tanners. Our data suggest that a particular amount of sun exposure delivered in infrequent, probably intense increments will increase risk of BCC more than a similar dose delivered more continuously over the same total period of time.

Abstract The objective of much epidemiological research is to relate exposure to external agents to the occurrence of particular diseases. The achievement of this objective depends critically on accurate measurement of exposure. This book brings together for the first time in a single volume the principles and techniques of exposure measurement as they relate specifically to causes of non-infectious diseases. In doing so, it draws on experience and results from a number of disciplines including psychology, survey research, sociology, environmental hygiene, epidemiology, and biostatistics, and synthesizes them for direct practical application in epidemiological and related research. The book covers questionnaire design, conducting personal interviews, abstracting information from medical records, use of proxy respondents, and use of biological and environmental measurements. It gives a comprehensive account of measurement effects, and the design, analysis, and interpretation of validity and reliability studies. Emphasis is given to the ways in which the validity of measurements can be increased. Techniques to maximize participation of subjects in epidemiological studies are discussed, and ethical issues relevant to exposure measurement are outlined. The book will be useful as a handbook for anyone wishing to design or conduct an epidemiological study and can also be used as the text for a graduate course in exposure measurement in epidemiology.

Key points Three weeks of intensified training and mild energy deficit in elite race walkers increases peak aerobic capacity independent of dietary support. Adaptation to a ketogenic low carbohydrate, high fat (LCHF) diet markedly increases rates of whole‐body fat oxidation during exercise in race walkers over a range of exercise intensities. The increased rates of fat oxidation result in reduced economy (increased oxygen demand for a given speed) at velocities that translate to real‐life race performance in elite race walkers. In contrast to training with diets providing chronic or periodised high carbohydrate availability, adaptation to an LCHF diet impairs performance in elite endurance athletes despite a significant improvement in peak aerobic capacity. Abstract We investigated the effects of adaptation to a ketogenic low carbohydrate (CHO), high fat diet (LCHF) during 3 weeks of intensified training on metabolism and performance of world‐class endurance athletes. We controlled three isoenergetic diets in elite race walkers: high CHO availability (g kg −1 day −1 : 8.6 CHO, 2.1 protein, 1.2 fat) consumed before, during and after training (HCHO, n = 9); identical macronutrient intake, periodised within or between days to alternate between low and high CHO availability (PCHO, n = 10); LCHF (&lt; 50 g day −1 CHO; 78% energy as fat; 2.1 g kg −1 day −1 protein; LCHF, n = 10). Post‐intervention, during race walking increased in all groups ( P &lt; 0.001, 90% CI: 2.55, 5.20%). LCHF was associated with markedly increased rates of whole‐body fat oxidation, attaining peak rates of 1.57 ± 0.32 g min −1 during 2 h of walking at ∼80% . However, LCHF also increased the oxygen (O 2 ) cost of race walking at velocities relevant to real‐life race performance: O 2 uptake (expressed as a percentage of new ) at a speed approximating 20 km race pace was reduced in HCHO and PCHO (90% CI: −7.047, −2.55 and −5.18, −0.86, respectively), but was maintained at pre‐intervention levels in LCHF. HCHO and PCHO groups improved times for 10 km race walk: 6.6% (90% CI: 4.1, 9.1%) and 5.3% (3.4, 7.2%), with no improvement (−1.6% (−8.5, 5.3%)) for the LCHF group. In contrast to training with diets providing chronic or periodised high‐CHO availability, and despite a significant improvement in , adaptation to the topical LCHF diet negated performance benefits in elite endurance athletes, in part due to reduced exercise economy.

BACKGROUND: Mental health is an important public health issue globally. A potential link between heat exposure and mental health outcomes has been recognised in the scientific literature; however, the associations between heat exposure (both high ambient temperatures and heatwaves) and mental health-related mortality and morbidity vary between studies and locations. OBJECTIVE: To fill gaps in knowledge, this systematic review aims to summarize the epidemiological evidence and investigate the quantitative effects of high ambient temperatures and heatwaves on mental health-related mortality and morbidity outcomes, while exploring sources of heterogeneity. METHODS: A systematic search of peer-reviewed epidemiological studies on heat exposure and mental health outcomes published between January 1990 and November 2020 was conducted using five databases (PubMed, Embase, Scopus, Web of Science and PsycINFO). We included studies that examined the association between high ambient temperatures and/or heatwaves and mental health-related mortality and morbidity (e.g. hospital admissions and emergency department visits) in the general population. A range of mental health conditions were defined using ICD-10 classifications. We performed random effects meta-analysis to summarize the relative risks (RRs) in mental health outcomes per 1 °C increase in temperature, and under different heatwaves definitions. We further evaluated whether variables such as age, sex, socioeconomic status, and climate zone may explain the observed heterogeneity. RESULTS: The keyword search yielded 4560 citations from which we identified 53 high temperatures/heatwaves studies that comprised over 1.7 million mental health-related mortality and 1.9 million morbidity cases in total. Our findings suggest associations between heat exposures and a range of mental health-related outcomes. Regarding high temperatures, our meta-analysis of study findings showed that for each 1 °C increase in temperature, the mental health-related mortality and morbidity increased with a RR of 1.022 (95%CI: 1.015-1.029) and 1.009 (95%CI: 1.007-1.015), respectively. The greatest mortality risk was attributed to substance-related mental disorders (RR, 1.046; 95%CI: 0.991-1.101), followed by organic mental disorders (RR, 1.033; 95%CI: 1.020-1.046). A 1 °C temperature rise was also associated with a significant increase in morbidity such as mood disorders, organic mental disorders, schizophrenia, neurotic and anxiety disorders. Findings suggest evidence of vulnerability for populations living in tropical and subtropical climate zones, and for people aged more than 65 years. There were significant moderate and high heterogeneities between effect estimates in overall mortality and morbidity categories, respectively. Lower heterogeneity was noted in some subgroups. The magnitude of the effect estimates for heatwaves varied depending on definitions used. The highest effect estimates for mental health-related morbidity was observed when heatwaves were defined as "mean temperature ≥90th percentile for ≥3 days" (RR, 1.753; 95%CI: 0.567-5.421), and a significant effect was also observed when the definition was "mean temperature ≥95th percentile for ≥3 days", with a RR of 1.064 (95%CI: 1.006-1.123). CONCLUSIONS: Our findings support the hypothesis of a positive association between elevated ambient temperatures and/or heatwaves and adverse mental health outcomes. This problem will likely increase with a warming climate, especially in the context of climate change. Further high-quality studies are needed to identify modifying factors of heat impacts.

An overview of the results of the Australian Burden of Disease (ABD) study is presented. The ABD study was the first to use methodology developed for the Global Burden of Disease study to measure the burden of disease and injury in a developed country. In 1996, mental disorders were the main causes of disability burden, responsible for nearly 30% of total years of life lost to disability (YLD), with depression accounting for 8% of the total YLD. Ischaemic heart disease and stroke were the main contributors to the disease burden disability-adjusted life years (DALYs), together causing nearly 18% of the total disease burden. Risk factors such as smoking, alcohol consumption, physical inactivity, hypertension, high blood cholesterol, obesity and inadequate fruit and vegetable consumption were responsible for much of the overall disease burden in Australia. The lessons learnt from the ABD study are discussed, together with methodological issues that require further attention.

This is an overview of the first burden of disease and injury studies carried out in Australia. Methods developed for the World Bank and World Health Organization Global Burden of Disease Study were adapted and applied to Australian population health data. Depression was found to be the top-ranking cause of non-fatal disease burden in Australia, causing 8% of the total years lost due to disability in 1996. Mental disorders overall were responsible for nearly 30% of the non-fatal disease burden. The leading causes of total disease burden (disability-adjusted life years [DALYs]) were ischaemic heart disease and stroke, together causing nearly 18% of the total disease burden. Depression was the fourth leading cause of disease burden, accounting for 3.7% of the total burden. Of the 10 major risk factors to which the disease burden can be attributed, tobacco smoking causes an estimated 10% of the total disease burden in Australia, followed by physical inactivity (7%).

This study estimates fatal and nonfatal disease burden among Indigenous Australians in 2011 and compares it with non-Indigenous Australians. The study found that there were 284 years lost per 1000 people because of premature death or living with ill health. Most of the disease burden was from chronic diseases (64%), particularly mental and substance-use disorders, injuries, cardiovascular diseases, cancer and respiratory diseases. The burden of disease was higher among males (54%) than females (46%) and higher for fatal (53%) than for nonfatal burden (47%). The disease groups with the highest burden varied by age group, with mental and substance-use disorders and injuries being the largest disease groups among those aged 5-44 years, and cardiovascular disease and cancer becoming more prominent among those aged 45 and older. Large disparities existed between Indigenous and non-Indigenous Australians, with the total burden being 2.3 times the non-Indigenous rates, fatal burden being 2.7 times and nonfatal burden being 2 times.

Mathers and Schofield, from the Australian Institute of Health and Welfare, review recent studies, including Australian research, on the health effects of unemployment and the mechanisms by which unemployment causes adverse health outcomes. The relationship is complex: ill-health also causes unemployment, and confounding factors include socioeconomic status and lifestyle. However, longitudinal studies with a range of designs provide reasonably good evidence that unemployment itself is detrimental to health and has an impact on health outcomes--increasing mortality rates, causing physical and mental ill-health and greater use of health services.

OBJECTIVE: To develop national birthweight percentiles by gestational age for male and female singleton infants born in Australia, and to compare the birthweight percentiles of Indigenous and non-Indigenous infants. DESIGN AND SETTING: Cross-sectional study of singleton live births to Australian-born mothers from 1991 to 1994. MAIN OUTCOME MEASURES: Birthweight percentiles by gestational age. RESULTS: During 1991-1994 Australian-born women gave birth to 769,077 live singleton infants. Of these, 28,230 (3.7%) were reported as births to Aboriginal or Torres Strait Islander women. Birthweight was missing for 581 (0.1%) births and gestational age was missing for 3014 (0.4%). An additional 3283 (0.4%) births were excluded because the recorded birthweights were extreme outliers for their recorded gestational ages. Indigenous women were more likely to be recorded as giving birth preterm (< 37 weeks' gestation) than non-Indigenous women (11.6% v. 5.4%) and were more likely to give birth to small-for-gestational-age infants at term. After 34 weeks' gestation, the median birthweights of Indigenous infants were consistently lower than those of non-Indigenous infants. At 40 weeks' gestation the difference in the median birthweights between these two groups was 160 g for males and 130 g for females. CONCLUSIONS: We present recent birthweight percentiles by gestational age based on national data in Australia. These percentiles provide current Australian norms for clinicians and researchers, and can provide a baseline for monitoring Indigenous perinatal outcomes.

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BACKGROUND: Australia was one of the first countries to introduce a publicly funded national human papillomavirus (HPV) vaccination program that commenced in April 2007, using the quadrivalent HPV vaccine targeting 12- to 13-year-old girls on an ongoing basis. Two-year catch-up programs were offered to 14- to 17- year-old girls in schools and 18- to 26-year-old women in community-based settings. We present data from the school-based program on population-level vaccine effectiveness against cervical abnormalities in Victoria, Australia. METHODS: Data for women age-eligible for the HPV vaccination program were linked between the Victorian Cervical Cytology Registry and the National HPV Vaccination Program Register to create a cohort of screening women who were either vaccinated or unvaccinated. Entry into the cohort was 1 April 2007 or at first Pap test for women not already screening. Vaccine effectiveness (VE) and hazard ratios (HR) for cervical abnormalities by vaccination status between 1 April 2007 and 31 December 2011 were calculated using proportional hazards regression. RESULTS: The study included 14,085 unvaccinated and 24,871 vaccinated women attending screening who were eligible for vaccination at school, 85.0% of whom had received three doses. Detection rates of histologically confirmed high-grade (HG) cervical abnormalities and high-grade cytology (HGC) were significantly lower for vaccinated women (any dose) (HG 4.8 per 1,000 person-years, HGC 11.9 per 1,000 person-years) compared with unvaccinated women (HG 6.4 per 1,000 person-years, HGC 15.3 per 1,000 person-years) HR 0.72 (95% CI 0.58 to 0.91) and HR 0.75 (95% CI 0.65 to 0.87), respectively. The HR for low-grade (LG) cytological abnormalities was 0.76 (95% CI 0.72 to 0.80). VE adjusted a priori for age at first screening, socioeconomic status and remoteness index, for women who were completely vaccinated, was greatest for CIN3+/AIS at 47.5% (95% CI 22.7 to 64.4) and 36.4% (95% CI 9.8 to 55.1) for women who received any dose of vaccine, and was negatively associated with age. For women who received only one or two doses of vaccine, HRs for HG histology were not significantly different from 1.0, although the number of outcomes was small. CONCLUSION: A population-based HPV vaccination program in schools significantly reduced cervical abnormalities for vaccinated women within five years of implementation, with the greatest vaccine effectiveness observed for the youngest women.

Using individual subject data from 10 case-control studies, comprising over 3000 cases and almost 4000 controls, we have estimated the relative risk of melanoma associated with aspects of complexion, namely, hair, eye and skin colour and freckling in adulthood, and have examined the relationships between these factors and naevus count in terms of melanoma risk. Compared with individuals with black or dark brown hair, the relative risks for developing melanoma in those with light brown, blonde and red hair were 1.49 (95% CI 1.31, 1.70), 1.84 (95% CI 1.54, 2.21) and 2.38 (95% CI 1.90, 2.97), respectively. Individuals with blue eyes had a risk 1.55 (95% CI 1.35, 1.78) times that for those with brown eyes, or 1.15 (95% CI 0.94, 1.40) after adjusting for hair colour and freckling in adulthood. The relative risks associated with hair and eye colour were independent of those for naevus count and skin colour. Light skin colour and high freckle density were also highly significant risk factors, independent of each other and of naevus count and hair and eye colour. The risks associated with these factors, while individually modest, are largely independent, and thus pigmentation characteristics and freckling tendency should be useful in identifying high risk groups to be targeted for prevention.