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BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.

Background Previous studies with large data have been widely reported that exposure to fine particulate matter (PM2.5) is associated with all-cause mortality; however, most of these studies adopted ecological time-series designs or have included limited study areas or individuals residing in well-monitored urban areas. However, nationwide cohort studies including cause-specific mortalities with different age groups were sparse. Therefore, this study examined the association between PM2.5 and cause-specific mortality in South Korea using the nationwide cohort. Methods A longitudinal cohort with 187 917 National Health Insurance Service-National Sample Cohort participants aged 50–79 years in enrolment between 2002 and 2019 was used. Annual average PM2.5 was collected from a machine learning-based ensemble model (a test R 2 = 0.87) as an exposure. We performed a time-varying Cox regression model to examine the association between long-term PM2.5 exposure and mortality. To reduce the potential estimation bias, we adopted generalized propensity score weighting method. Results The association with long-term PM2.5 (2-year moving average) was prominent in mortalities related to diabetes mellitus [hazard ratio (HR): 1.03 (95% CI: 1.01, 1.06)], circulatory diseases [HR: 1.02 (95% CI: 1.00, 1.03)] and cancer [HR: 1.01 (95% CI: 1.00, 1.02)]. Meanwhile, circulatory-related mortalities were associated with a longer PM2.5 exposure period (1 or 2-year lags), whereas respiratory-related mortalities were associated with current-year PM2.5 exposure. In addition, the association with PM2.5 was more evident in people aged 50–64 years than in people aged 65–79 years, especially in heart failure-related deaths. Conclusions This study identified the hypothesis that long-term exposure to PM2.5 is associated with mortality, and the association might be different by causes of death. Our result highlights a novel vulnerable population: the middle-aged population with risk factors related to heart failure. [ABSTRACT FROM AUTHOR]

Background Estimates of excess deaths provide critical intelligence on the impact of population health threats including seasonal respiratory infections, pandemics and environmental hazards. Timely estimates of excess deaths can inform the response to COVID-19. However, access to timely mortality data is challenging due to the time interval between the death occurring and the date the death is registered and available for analysis ('registration interval'). Development Using data from the New South Wales, Australia, Births Deaths and Marriages Registry, we developed a Poisson regression model that estimated near-complete weekly counts, for a given week of death, from partially-complete death registration counts. A 10-weeks lag was considered, and a 2-year baseline of historical registration intervals was used to correct lag weeks. Application Validation of estimated counts found that the root-mean-square error (as a percentage of mean observed near-complete registrations) was less than 7% for lag week 3, and <5% for lag weeks 4–9. We incorporated this method utilizing an existing rapid weekly mortality surveillance system. Counts corrected for registration interval replaced observed values for the most recent weeks. Excess death estimates, based on corrected counts, were within 1.2% of near-complete counts available 9 weeks from the end of the analysis period. Conclusions This study demonstrates a method for estimating recent death counts to correct for registration intervals. Estimates obtained at a 3-week lag were acceptable, while those at greater than 3 weeks were optimal. [ABSTRACT FROM AUTHOR]

Background Before the COVID-19 pandemic, stagnating life expectancy trends were reported in some high-income countries (HICs). Despite previous evidence from country-specific studies, there is a lack of comparative research that provides a broader perspective and challenges existing assumptions. This study aims to examine longevity trends and patterns in six English-speaking countries (Australia, Canada, Ireland, New Zealand, United Kingdom, United States) by combining period and cohort perspectives and to compare them with other HICs. Methods Using data from the Human Mortality and World Health Organization Mortality Databases, we estimated partial life expectancy, lifespan inequality and cohort survival differences for 1970–2021, as well as the contribution of causes of death to the gap in life expectancy between English-speaking countries and the average for other HICs in 2017–19. Results In the pre-pandemic period, the increase in life expectancy slowed in all English-speaking countries, except Ireland, mainly due to stagnating or rising mortality at young-middle ages. Relative to other HICs, those born in Anglophone countries since the 1970s experienced relative survival disadvantage, largely attributable to injuries (mainly suicides) and substance-related mortality (mainly poisonings). In contrast, older cohorts enjoyed advantages for females in Australia and Canada and for males in all English-speaking countries except the United States. Conclusions Although future gains in life expectancy in wealthy societies will increasingly depend on reducing mortality at older ages, adverse health trends at younger ages are a cause for concern. This emerging and avoidable threat to health equity in English-speaking countries should be the focus of further research and policy action. [ABSTRACT FROM AUTHOR]

Background Our aim was to evaluate the prevalence, mortality, regional and sex distribution of neural tube defects (NTDs) in Finland. Methods Data for this population-based study were collected from 1987 to 2018 from the national health and social welfare registers. Results There were in total 1634 cases of NTDs, of which 511 were live births, 72 pregnancies ended in stillbirth and 1051 were terminations of pregnancy due to fetal anomaly (TOPFA). The total prevalence of NTDs was 8.6 per 10 000 births and it increased slightly annually (OR 1.008; 95% CI: 1.002, 1.013) during the 32-year study period. The birth prevalence of NTDs decreased (OR 0.979; 95% CI: 0.970, 0.987), but the prevalence of TOPFA increased annually (OR 1.024; 95% CI 1.017, 1.031). The perinatal mortality of NTD children was 260.7 per 1000 births and the infant mortality was 184.0 per 1000 live births, whereas these measures in the general population were 4.6 per 1000 births and 3.3 per 1000 live births, respectively. There was no difference in the NTD prevalence between males and females (P- value 0.77). The total prevalence of NTDs varied from 7.1 to 9.4 per 10 000 births in Finland by region. Conclusions Although the majority of NTDs are preventable with an adequate folic acid supplementation, the total prevalence increased in Finland during the study period when folic acid supplementation was mainly recommended to high-risk families and to women with folic acid deficiency. NTDs remain an important cause of infant morbidity and mortality in Finland. [ABSTRACT FROM AUTHOR]

Background This study aimed to estimate population-level and state-level lead-attributable mortality burdens stratified by socioeconomic status (SES) class in the USA. Methods Based on the National Health and Nutrition Examination Survey (NHANES), we constructed individual-level SES scores from income, employment, education and insurance data. We assessed the association between the blood lead levels (BLL) and all-cause mortality by Cox regression in the NHANES cohort (n  = 31 311, 4467 deaths). With estimated hazard ratios (HR) and prevalences of medium (2–5 μg/dL) and high (≥ 5 μg/dL) BLL, we computed SES-stratified population-attributable fractions (PAFs) of all-cause mortality from lead exposure across 1999–2019. We additionally conducted a systematic review to estimate the lead-attributable mortality burden at state-level. Results The HR for every 2-fold increase in the BLL decreased from 1.23 (1.10–1.38) for the lowest SES class to 1.05 (0.90–1.23) for the highest SES class. Across all SES quintiles, medium BLL exhibited a greater mortality burden. Individuals with lower SES had higher lead-attributable burdens, and such disparities haver persisted over the past two decades. In 2017–19, annually 67 000 (32 000–112 000) deaths in the USA were attributable to lead exposure, with 18 000 (2000–41 000) of these deaths occurring in the lowest SES class. Substantial disparities in the state-level mortality burden attributable to lead exposure were also highlighted. Conclusions These findings suggested that disparities in lead-attributable mortality burden persisted within US adults, due to heterogeneities in the effect sizes of lead exposure as well as in the BLL among different SES classes. [ABSTRACT FROM AUTHOR]

Background Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. Methods In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). Results Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032–1.053) vs OR = 1.009 (95% CI, 0.996–1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019–1.047), RERI = 0.039 (95% CI, 0.025–0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. Conclusions The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users. [ABSTRACT FROM AUTHOR]

Background Model-estimated air pollution exposure products have been widely used in epidemiological studies to assess the health risks of particulate matter with diameters of ≤2.5 µm (PM2.5). However, few studies have assessed the disparities in health effects between model-estimated and station-observed PM2.5 exposures. Methods We collected daily all-cause, respiratory and cardiovascular mortality data in 347 cities across 15 countries and regions worldwide based on the Multi-City Multi-Country collaborative research network. The station-observed PM2.5 data were obtained from official monitoring stations. The model-estimated global PM2.5 product was developed using a machine-learning approach. The associations between daily exposure to PM2.5 and mortality were evaluated using a two-stage analytical approach. Results We included 15.8 million all-cause, 1.5 million respiratory and 4.5 million cardiovascular deaths from 2000 to 2018. Short-term exposure to PM2.5 was associated with a relative risk increase (RRI) of mortality from both station-observed and model-estimated exposures. Every 10-μg/m3 increase in the 2-day moving average PM2.5 was associated with overall RRIs of 0.67% (95% CI: 0.49 to 0.85), 0.68% (95% CI: –0.03 to 1.39) and 0.45% (95% CI: 0.08 to 0.82) for all-cause, respiratory, and cardiovascular mortality based on station-observed PM2.5 and RRIs of 0.87% (95% CI: 0.68 to 1.06), 0.81% (95% CI: 0.08 to 1.55) and 0.71% (95% CI: 0.32 to 1.09) based on model-estimated exposure, respectively. Conclusions Mortality risks associated with daily PM2.5 exposure were consistent for both station-observed and model-estimated exposures, suggesting the reliability and potential applicability of the global PM2.5 product in epidemiological studies. [ABSTRACT FROM AUTHOR]

Background While previous studies indicate muscle-strengthening exercises may reduce mortality risk, further research is needed to increase certainty of the evidence. We investigated overall and dose-response associations between weight training and the risks of all-cause, cardiovascular disease (CVD) and cancer mortality in a large cohort of older adults with long follow-up time and a large number of deaths. We also investigated the joint associations of weight training and aerobic exercise with mortality risk. Methods Weight training was assessed via self-report in 2004–05 in the National Institutes of Health-American Association of Retired Persons (NIH-AARP) Diet and Health Study (USA; n  = 216 339), with follow-up to 2019. Cox regression estimated the hazard ratios (HR) and 95% confidence intervals (CI) for the associations between weight training and mortality, after adjusting for confounders including aerobic exercise. Results Around 25% of participants [mean age = 69.9 years (standard deviation = 5.4), 58% men] reported engaging in weight training over the past year, and there were 79 107 (37%) deaths. Engaging in any weight training (vs none) was associated with lower risks of all-cause (HR = 0.94; 95% CI = 0.93–0.96), CVD (HR = 0.92; 95% CI = 0.90–0.95) and cancer mortality (HR = 0.95; 95% CI = 0.92–0.98). More time spent in weight training was associated with only marginally greater risk reductions. Larger risk reductions were observed among women than men. Performing both aerobic exercise and weight training conferred the greatest mortality risk reduction; weight training was not associated with mortality risk among participants who did no aerobic exercise. Conclusion Performing any amount of weight training lowered mortality risk. [ABSTRACT FROM AUTHOR]

Background Many observational studies support light-to-moderate alcohol intake as potentially protective against premature death. We used a genetic approach to evaluate the linear and nonlinear relationships between alcohol consumption and mortality from different underlying causes. Methods We used data from 278 093 white-British UK Biobank participants, aged 37–73 years at recruitment and with data on alcohol intake, genetic variants, and mortality. Habitual alcohol consumption was instrumented by 94 variants. Linear Mendelian randomization (MR) analyses were conducted using five complementary approaches, and nonlinear MR analyses by the doubly-ranked method. Results There were 20 834 deaths during the follow-up (median 12.6 years). In conventional analysis, the association between alcohol consumption and mortality outcomes was 'J-shaped'. In contrast, MR analyses supported a positive linear association with premature mortality, with no evidence for curvature (P nonlinearity ≥ 0.21 for all outcomes). The odds ratio [OR] for each standard unit increase in alcohol intake was 1.27 (95% confidence interval [CI] 1.16–1.39) for all-cause mortality, 1.30 (95% CI 1.10–1.53) for cardiovascular disease, 1.20 (95% CI 1.08–1.33) for cancer, and 2.06 (95% CI 1.36–3.12) for digestive disease mortality. These results were consistent across pleiotropy-robust methods. There was no clear evidence for an association between alcohol consumption and mortality from respiratory diseases or COVID-19 (1.32, 95% CI 0.96–1.83 and 1.46, 95% CI 0.99–2.16, respectively; P nonlinearity ≥ 0.21). Conclusion Higher levels of genetically predicted alcohol consumption had a strong linear association with an increased risk of premature mortality with no evidence for any protective benefit at modest intake levels. [ABSTRACT FROM AUTHOR]

Background Women carry a substantial burden of psychiatric, somatic and lifestyle-related morbidity in the prison context. By describing causes of death and estimating the risk and burden of mortality compared with the general population, this study investigates how mortality operates in this highly marginalized and under-researched population. Methods In this registry-based study of all women incarcerated in Norwegian prisons from 2000 to 2019 (N  = 11 313), we calculated crude mortality rates, years of lost life and, by using mortality in age-matched women from the general population as a reference, age-standardized mortality ratios and years of lost life rates. Results Over a mean follow-up time of 10.7 years, at a median age of 50 years, 9% of the population had died (n  = 1005). Most deaths (80%) were premature deaths from an avoidable cause. Drug-induced causes and deaths from major non-communicable diseases (NCDs) were most frequent (both 32%). Compared with women in the general population, women with a history of incarceration were more likely to die from any cause. Trends in annual age-standardized years of lost life rates suggest that the mortality burden associated with major NCDs has gradually replaced drug-induced causes. Conclusions Women with a history of incarceration die at a greater rate than their peers and largely from avoidable causes. The profile of causes contributing to the substantial burden of mortality placed on this population has changed over time and has important implications for future efforts to reduce morbidity and the risk of premature death following release from prison. [ABSTRACT FROM AUTHOR]

Background Studying the causes of death among deceased spouses and surviving partners may provide insights into the underlying mechanisms of the association between widowhood and mortality. This study investigated the mortality risk of widowhood in Taiwan, examined the association of the cause of death between widowed individuals and their deceased spouses and explored potential modifying effects by age, gender and duration after widowhood. Methods This matched cohort study utilized Taiwan's National Health Insurance claims database and National Death Registry. In total, 204 010 widowed men and 596 136 widowed women were identified with a mean follow-up period of 6.9 and 7.9 years, respectively, and 816 040 comparison men and 2 384 544 comparison women were selected. Results Widowhood was associated with an increased mortality risk, with widowed men having a 1.32 increased risk and widowed women having a 1.27 increased risk. Age at spousal death and duration modified the associations after widowhood. The widowed individuals are more likely to die by the same cause as the deceased spouse if they died by suicide, accident, endocrine, gastrointestinal disorders or infection. Conclusions The study suggests that healthcare policies and interventions should be developed to improve widowed individuals' health and overall welfare. [ABSTRACT FROM AUTHOR]

The Dale-Wonsho health and demographic surveillance system is a population cohort in rural southern Ethiopia that collects data on births, deaths, migrations, and immunizations. It consists of 12 administrative units with a population of 69,021 people. The cohort provides valuable data for researchers and policymakers to guide public health initiatives in rural Ethiopia. The document also provides demographic characteristics of the Dale-Wonsho HDSS, including household size, sex ratio, and dependency ratio. It highlights the lower total dependency ratio compared to other sites in Ethiopia, potentially due to lower fertility rates. The document acknowledges the support and funding received from various organizations. [Extracted from the article]

The Public Health Data Asset (PHDA) 2011 cohort is a population-based cohort in England that combines data from the 2011 Census with Hospital Episodes Statistics and death registration records. It aims to investigate inequalities in mortality and morbidity and understand the social determinants of health. The cohort includes detailed information on sociodemographic characteristics and health outcomes for nearly the entire population of England. However, there are limitations to the PHDA, including non-inclusion of all people living in England and a decline in coverage over time. The data can be accessed through the ONS Secure Research Service. [Extracted from the article]

Background Diabetes has been increasing worldwide and is now among the 10 leading causes of death globally. Diabetic kidney disease (DKD), a complication of poorly managed diabetes, is related to high mortality risk. To better understand the situation in the Americas region, we evaluated diabetes and DKD mortality trends over the past 20 years. Methods We analysed diabetes and DKD mortality for 33 countries in the Americas from 2000 to 2019. Data were extracted from the World Health Organization (WHO) Global Health Estimates and the World Population Prospects, 2019 Revision, estimating annual age-standardized mortality rates (ASMR) and gaps in the distribution of diabetes and DKD mortality by sex and country. Trend analyses were based on the annual average percentage of change (AAPC). Results From 2000 to 2019, the overall mortality trend from diabetes in the Americas remained stable [AAPC: -0.2% (95% CI: -0.4%–0.0%]; however, it showed important differences by sex and by country over time. By contrast, DKD mortality increased 1.5% (1.3%–1.6%) per year, rising faster in men than women, with differences between countries. Central America, Mexico and the Latin Caribbean showed significant increases in mortality for both diseases, especially DKD. In contrast in North America, diabetes mortality decreased whereas DKD mortality increased. Conclusions The increase in DKD mortality is evidence of poorly controlled diabetes in the region. The lack of programmes on prevention of complications, self-care management and gaps in quality health care may explain this trend and highlight the urgent need to build more robust health systems based on primary care, prioritizing diabetes prevention and control. [ABSTRACT FROM AUTHOR]

Background Sustainable dietary patterns that incorporate multiple dimensions may have benefits for both human health and the environment. We examined the association between sustainable dietary patterns assessed by using the Sustainable Diet Index-US (SDI-US) and mortality in US adults. Methods This study used data from the National Health and Nutrition Examination Survey 2007–18 (N  = 22 414 aged ≥20 years). The SDI-US (range: 4–20) was composed of four sub-indices representing nutritional, environmental, economic and sociocultural dimensions, and was computed using 24-h dietary recalls, food expenditures and food preparation habits. A higher score indicates a more sustainable dietary pattern. All-cause mortality from baseline until 31 December 2019 was obtained through linkage to the National Death Index. Hazard ratios (HRs) with 95% CIs were estimated using Cox proportional-hazards models, adjusting for covariates. Results During 150 386 person-years of follow-up, 2100 total deaths occurred and the median SDI-US was 9.8 in Quintile 1 (Q1) and 16.3 in Quintile 5 (Q5). In a multivariable-adjusted model, the highest SDI-US quintile was associated with a 36% reduction in mortality risk (Q5 vs Q1, HR 0.64, 95% CI 0.49–0.84, P  =   0.002) compared with the lowest quintile. When stratified by age (P interaction = 0.002), an inverse association between SDI-US and mortality was observed in younger adults (<65 years, HR 0.41, 95% CI 0.25–0.68, P  =   0.001) but not in older adults (≥65 years, HR 0.91, 95% CI 0.71–1.16, P  =   0.15). Conclusions A higher SDI-US score was associated with lower mortality risk among US adults, particularly in younger adults. [ABSTRACT FROM AUTHOR]

Background To date, the excess mortality experienced by residential aged care facility (RACF) residents related to COVID-19 has not been estimated in Australia. This study examined (i) the historical mortality trends (2008–09 to 2021–22) and (ii) the excess mortality (2019–20 to 2021–22) of Australian RACF residents. Methods A retrospective population-based study was conducted using the Australian Institute of Health and Welfare's GEN website data (publicly available aged care services information). Non-Aboriginal, older (≥65 years old) RACF residents between 2008–09 and 2021–22 were evaluated. The observed mortality rate was estimated from RACF exits compared with the RACF cohort yearly. Direct standardization was employed to estimate age-standardized mortality rates and 95% CIs. Excess mortality and 95% prediction intervals (PIs) for 2019–20 to 2021–22 were estimated using four negative binomial (NB) and NB generalized additive models and compared. Results The age-standardized mortality rate in 2018–19 was 23 061/100 000 residents (95% CI, 22 711–23 412). This rate remained similar in 2019–20 (23 023/100 000; 95% CI, 22 674–23 372), decreased in 2020–21 (22 559/100 000; 95% CI, 22 210–22 909) and increased in 2021–22 (24 885/100 000; 95% CI, 24 543–25 227). The mortality rate increase between 2020–21 and 2021–22 was observed in all age and sex groups. All models yielded excess mortality in 2021–22. Using the best-performing model (NB), the excess mortality for 2019–20 was –160 (95% PI, –418 to 98), –958 (95% PI, –1279 to –637) for 2020–21 and 4896 (95% PI, 4503–5288) for 2021–22. Conclusions In 2021–22, RACF residents, who represented <1% of the population, experienced 21% of the Australian national excess mortality (4896/22 886). As Australia adjusts to COVID-19, RACF residents remain a population vulnerable to COVID-19. [ABSTRACT FROM AUTHOR]

Background Low socioeconomic status and underlying health increase the risk of fatal outcomes from COVID-19, resulting in more years of life lost (YLL) among the poor. However, using standard life expectancy overestimates YLL to COVID-19. We aimed to quantify YLL associated with COVID-19 deaths by sex and income quartile, while accounting for the impact of individual-level pre-existing health on remaining life expectancy for all Dutch adults aged 50+. Methods Extensive administrative data were used to model probability of dying within the year for the entire 50+ population in 2019, considering age, sex, disposable income and health care use (n  = 6 885 958). The model is used to predict mortality probabilities for those who died of COVID-19 (had they not died) in 2020. Combining these probabilities in life tables, we estimated YLL by sex and income quartile. The estimates are compared with YLL based on standard life expectancy and income-stratified life expectancy. Results Using standard life expectancy results in 167 315 YLL (8.4 YLL per death) which is comparable to estimates using income-stratified life tables (167 916 YLL with 8.2 YLL per death). Considering pre-existing health and income, YLL decreased to 100 743, with 40% of years lost in the poorest income quartile (5.0 YLL per death). Despite individuals in the poorest quartile dying at younger ages, there were minimal differences in average YLL per COVID-19 death compared with the richest quartile. Conclusions Accounting for prior health significantly affects estimates of YLL due to COVID-19. However, inequality in YLL at the population level is primarily driven by higher COVID-19 deaths among the poor. To reduce income inequality in the health burden of future pandemics, policies should focus on limiting structural differences in underlying health and exposure of lower income groups. [ABSTRACT FROM AUTHOR]

Background Only little is known about trends in temperature–mortality associations among the most vulnerable subgroups, especially in the areas of central and eastern Europe, which are considered major climatic hotspots in terms of heatwave exposure. Thus, we aimed to assess trends in temperature-related mortality in the Czech Republic by sex, age and cause of death, and to quantify the temporal evolution of possible inequalities. Methods We collected daily time series of all-cause (1987–2019) and cause-specific (1994–2019) mortality by sex and age category, and population-weighted daily mean 2-metre temperatures for each region of the Czech Republic. We applied a quasi-Poisson regression model to estimate the trends in region-specific temperature–mortality associations, with distributed lag non-linear models and multivariate random-effects meta-analysis to derive average associations across the country. We then calculated mortality attributable to non-optimal temperatures and implemented the indicator of sex- and age-dependent inequalities. Results We observed a similar risk of mortality due to cold temperatures for men and women. Conversely, for warm temperatures, a higher risk was observed for women. Results by age showed a clear pattern of increasing risk due to non-optimum temperatures with increasing age category. The relative risk (RR) related to cold was considerably attenuated in most of the studied subgroups during the study period, whereas an increase in the RR associated with heat was seen in the overall population, in women, in the age category 90+ years and with respect to respiratory causes. Moreover, underlying sex- and age-dependent inequalities experienced substantial growth. Conclusions Our findings suggest ongoing adaptation to cold temperatures. Mal/adaptation to hot temperatures occurred unequally among population subgroups and resulted in growing inequalities between the sexes and among age categories. [ABSTRACT FROM AUTHOR]

Background Despite an increasing proportion of smokers who use non-cigarette products, the harmfulness of these is inconsistent. This study aimed to evaluate the impact of waterpipe tobacco (WTP) smoking on all-cause mortality. Methods A prospective cohort study followed up on 35 646 participants from 2007 to 2019 in Northern Viet Nam. Data for each type of cigarette and WTP smoking were collected based on demographic lifestyle and semi-quantitative food frequency questionnaires. Smokers were categorized as current smokers and former smokers who were lifetime ever smokers but stopped smoking >6 months before the interview. Data on all-cause mortality (2449 deaths) were obtained from medical records at the state health facilities. The hazard ratios (HRs) and 95% CIs for mortality were estimated using a Cox proportional-hazards model. Results Compared with non-smokers, ever smokers had a higher all-cause mortality risk (HR = 1.29, 95% CI = 1.16–1.43). Current WTP (HR = 1.37, 95% CI = 1.19–1.57), current cigarette (HR = 1.40, 95% CI = 1.22–1.60) and former WTP smokers (HR = 1.39, 95% CI = 1.10–1.76) showed an elevated risk of dying. The mortality risk was significantly elevated in dual smokers using WTP and cigarettes (HR = 1.55, 95% CI = 1.35–1.79) and exclusive WTP smokers (HR = 1.38, 95% CI = 1.21–1.57). Elevated risk was observed for the main targeted attractions of cancer, diabetes and heart diseases. Smoking cessation of >10 years decreased the risk of all-cause mortality (HR = 0.61, 95% CI = 0.44–0.85) and cancer (HR = 0.24, 95% CI = 0.11–0.52). Conclusions WTP smoking increases the risk of all-cause mortality. A unique programme to control exposure to WTP should be a high priority in Viet Nam and other countries. [ABSTRACT FROM AUTHOR]

Background The effect of exposure to extreme temperature events (ETEs) on dementia mortality remains largely unknown. We aimed to quantify the association of ETE exposure with dementia mortality. Methods We conducted a population-based, case-crossover study among 57 791 dementia deaths in Jiangsu province, China, during 2015–20. Daily mean temperatures were extracted from a validated grid dataset at each subject's residential address, and grid-specific exposures to heat wave and cold spell were assessed with a combination of their intensity and duration. We applied conditional logistic regression models to investigate cumulative and lag effects for ETE exposures. Results Exposure to ETE with each of all 24 definitions was associated with an increased odds of dementia mortality, which was higher when exposed to heat wave. Exposure to heat wave (daily mean temperature ≥95th percentile, duration ≥3 days (d); P95_3d) and cold spell (≤5th percentile, duration ≥3 d; P5_3d) was associated with a 75% (95% CI: 61%, 90%) and 30% (19%, 43%) increase in odds of dementia mortality, respectively. Definitions with higher intensity were generally associated with a higher odds of dementia mortality. We estimated that 6.14% of dementia deaths were attributable to exposure to heat wave (P90_2d) and cold spell (P10_2d). No effect modifications were observed by sex or age, except that the association for heat wave was stronger among women. Conclusions Exposure to both heat wave and cold spell was associated with an increased odds of dementia mortality. Our findings highlight that reducing individual ETE exposures may be helpful in preventing deaths from dementia, especially among women in summer. [ABSTRACT FROM AUTHOR]

This article compares two methods of counting COVID-19 deaths in England during the pandemic. The Office for National Statistics (ONS) uses death registrations and distinguishes between deaths 'involving' COVID-19 and deaths 'due to' COVID-19, while Public Health England (PHE) counts people who died following a positive COVID-19 test. The study found that there was a high overlap between the two measures, but they diverged during certain periods, particularly in the early part of the pandemic and from January 2022 onwards. Factors such as limited testing capacity and the emergence of the Omicron variant were attributed to this divergence. The article discusses changes in testing policy and the measurement of COVID-19 deaths in the UK, highlighting the importance of consistent definitions and monitoring of COVID-19 mortality. [Extracted from the article]

Background We aimed to identify patterns within the rate of kidney function decline, determinants of these patterns and their association with all-cause mortality risk in the general population. Methods Participants aged ≥ 45 years with at least one assessment of creatinine-based estimated glomerular filtration rate (eGFR) taken between 1997 and 2018 were selected from a population-based cohort study. Analyses were performed using several distinct latent class trajectory modelling methods. Cumulative incidences were calculated with 45 years of age as the starting point. Results In 12 062 participants (85 922 eGFR assessments, mean age 67.0 years, 58.7% women, median follow-up 9.6 years), four trajectories of eGFR change with age were identified: slow eGFR decline [rate of change in mL/min/1.73 m2 per year (RC), –0.9; 95% CI, –0.9 to –0.9; reference group], intermediate eGFR decline (RC, –2.5; 95% CI, –2.7 to –2.5) and fast eGFR decline (RC, –4.3; 95% CI, –4.4 to –4.1), and an increase/stable eGFR (RC, 0.3; 95% CI, 0.3 to 0.4). Women were more likely to have an increase/stable eGFR [odds ratio (OR), 1.94; 95% CI, 1.53 to 2.46] whereas men were more likely to have a fast eGFR decline (OR, 1.86; 95% CI, 1.33 to 2.60). Participants with diabetes, cardiovascular disease (CVD) or hypertension were more likely to have an intermediate or fast eGFR decline. All-cause mortality risks (cumulative incidence at age of 70 years) were 32.3% (95% CI, 21.4 to 47.9, slow eGFR decline), 6.7% (95% CI, 3.5 to 12.4, intermediate eGFR decline), 68.8% (95% CI, 44.4 to 87.8, fast eGFR decline) and 9.5% (95% CI, 5.5 to 15.7, increase/stable eGFR). Conclusion Sex, hypertension, diabetes and CVD were identified as trajectory membership determinants. Having fast eGFR decline was associated with the highest risk of all-cause mortality, highlighting the need for extensive monitoring and prevention of kidney function decline in individuals at risk of having fast eGFR decline. [ABSTRACT FROM AUTHOR]

Background Most analyses of excess mortality during the COVID-19 pandemic have employed aggregate data. Individual-level data from the largest integrated healthcare system in the US may enhance understanding of excess mortality. Methods We performed an observational cohort study following patients receiving care from the Department of Veterans Affairs (VA) between 1 March 2018 and 28 February 2022. We estimated excess mortality on an absolute scale (i.e. excess mortality rates, number of excess deaths) and a relative scale by measuring the hazard ratio (HR) for mortality comparing pandemic and pre-pandemic periods, overall and within demographic and clinical subgroups. Comorbidity burden and frailty were measured using the Charlson Comorbidity Index and Veterans Aging Cohort Study Index, respectively. Results Of 5 905 747 patients, the median age was 65.8 years and 91% were men. Overall, the excess mortality rate was 10.0 deaths/1000 person-years (PY), with a total of 103 164 excess deaths and pandemic HR of 1.25 (95% CI 1.25–1.26). Excess mortality rates were highest among the most frail patients (52.0/1000 PY) and those with the highest comorbidity burden (16.3/1000 PY). However, the largest relative mortality increases were observed among the least frail (HR 1.31, 95% CI 1.30–1.32) and those with the lowest comorbidity burden (HR 1.44, 95% CI 1.43–1.46). Conclusions Individual-level data offered crucial clinical and operational insights into US excess mortality patterns during the COVID-19 pandemic. Notable differences emerged among clinical risk groups, emphasizing the need for reporting excess mortality in both absolute and relative terms to inform resource allocation in future outbreaks. [ABSTRACT FROM AUTHOR]

Background Estimating the number of childhood cancer survivors is crucial for cancer control, including clinical guidelines. To compare estimates across countries despite data sharing restrictions, we propose a new method of computing limited-duration prevalence of childhood cancer survivors (POCCS) using aggregated data. Methods We developed a Markov model that simulates, for each calendar year and birth cohort in a population, the proportion of individuals in the following health states: healthy, newly diagnosed with cancer, surviving with cancer, and deceased. Transitions between health states were informed using annual sex- and age-specific incidence rates, conditional 1-year net survival probabilities from the Netherlands Cancer Registry (1989–2011), and annual mortality probability by sex and age group for The Netherlands from the Human Mortality Database. Applying a Markov model, we computed 20-year prevalence of childhood cancer survivors. The resulting POCCS estimates, stratified by sex, were compared with SEER*Stat estimates derived from individual cancer records from the same registry. Results In 2011, POCCS predicted 654 males [95% confidence interval (95% CI): 637–672] and 539 females (95% CI: 523–555) per million persons living in The Netherlands after childhood cancer diagnosed within the previous 20 years. Using SEER*Stat, the 20-year prevalence was 665 males (95% CI: 647–683) and 544 females (95% CI: 529–560) per million persons on 1 July 2011. Conclusions Using the POCCS model and aggregated cancer data, our estimates of childhood cancer survivors limited-duration prevalence were consistent with those computed by a standard method requiring individual cancer records. The POCCS method provides relevant information for planning follow-up and care for childhood cancer survivors. [ABSTRACT FROM AUTHOR]

Background Australia provides a valuable international case study of life expectancy during the pandemic. In contrast to many other countries, it experienced relatively stringent restrictions and low COVID-19 mortality during 2020–21, followed by relaxation of these restrictions when high vaccination rates were achieved. This study measures Australia's life expectancy trends and the contributions of age group and causes of death, during the pandemic. Methods Trends in life expectancy at birth in Australia and its states and territories were measured from 2020 to 2022. The contributions of age group and cause of death to these trends were measured using decomposition methods. Life expectancy was compared with other high-income countries. Results Australia's life expectancy fell by more than half a year in 2022, following a sharp increase in 2020 and moderate decline in 2021. For the 3 years 2020 to 2022, life expectancy was 0.13 years (95% confidence interval 0.07-0.19) higher for males and 0.09 years (0.03-0.14) higher for females versus 2017–19. Australia's life expectancy increase in 2020 was larger than that in the vast majority of other high-income countries, but its decline in 2022 was greater than in other countries whose life expectancy rose in the first year of the pandemic. The small negative contribution of COVID-19 deaths to life expectancy in Australia was more than offset by lower non-communicable disease mortality. There were only small differences in life expectancy change between the states with the most stringent restrictions (Victoria and New South Wales) and the rest of Australia. Conclusions Australia's life expectancy trends during 2020–22 were relatively favourable compared with other high-income countries, with the exception of its sharp decline in 2022 once restrictions were loosened. [ABSTRACT FROM AUTHOR]

ObjectiveIt is unclear whether relatively low glycated haemoglobin (HbA1c) levels are beneficial or harmful for the long-term health outcomes among people without diabetes. We aimed to investigate the association between low HbA1c levels and mortality among the US general population.MethodsThis study includes a nationally representative sample of 39 453 US adults from the National Health and Nutrition Examination Surveys 1999-2014, linked to mortality data through 2015. We employed the parametric g-formula with pooled logistic regression models and the ensemble machine learning algorithms to estimate the time-varying risk of all-cause and cardiovascular mortality by HbA1c categories (low, 4.0 to

Background Previous Mendelian randomization (MR) studies using population samples (population MR) have provided evidence for beneficial effects of educational attainment on health outcomes in adulthood. However, estimates from these studies may have been susceptible to bias from population stratification, assortative mating and indirect genetic effects due to unadjusted parental genotypes. MR using genetic association estimates derived from within-sibship models (within-sibship MR) can avoid these potential biases because genetic differences between siblings are due to random segregation at meiosis. Methods Applying both population and within-sibship MR, we estimated the effects of genetic liability to educational attainment on body mass index (BMI), cigarette smoking, systolic blood pressure (SBP) and all-cause mortality. MR analyses used individual-level data on 72 932 siblings from UK Biobank and the Norwegian HUNT study, and summary-level data from a within-sibship Genome-wide Association Study including >140 000 individuals. Results Both population and within-sibship MR estimates provided evidence that educational attainment decreased BMI, cigarette smoking and SBP. Genetic variant–outcome associations attenuated in the within-sibship model, but genetic variant–educational attainment associations also attenuated to a similar extent. Thus, within-sibship and population MR estimates were largely consistent. The within-sibship MR estimate of education on mortality was imprecise but consistent with a putative effect. Conclusions These results provide evidence of beneficial individual-level effects of education (or liability to education) on adulthood health, independently of potential demographic and family-level confounders. [ABSTRACT FROM AUTHOR]

Background Studies found a J-shaped association between body mass index (BMI) and mortality. However, it is unclear whether the association is driven by biases, particularly confounding by fat-free mass. Methods We conducted an individual-level pooled analysis of three cohorts of Korean adults (aged ≥ 40 years; n  = 153 248). Mortality was followed up through December 2019. Anthropometric data were directly measured at baseline. Fat and fat-free mass were predicted using validated prediction models. Using Cox proportional hazards models, we estimated the associations of BMI and waist circumference (WC) with all-cause and cause-specific mortality. To account for biases, we excluded participants aged ≥ 70 years, deaths that occurred within 5 years of follow-up and ever smokers, and adjusted for fat-free mass index (FFMI). Results During the follow-up of up to 18 years, 6061 deaths were identified. We observed J-shaped association of BMI (nadir at 22–26) and monotonically positive association of WC with all-cause, cardiovascular, and cancer mortality among Korean adults without a history of cancer or cardiovascular disease. In the BMI analysis, excluding ever smokers and adjusting for FFMI attenuated the excess mortality in underweight participants and transformed the J-shaped association into a monotonically positive shape, suggesting an increased mortality at BMI > 22.0. Excluding participants aged ≥ 70 years and deaths that occurred within 5 years of follow-up did not change the results. In the WC analysis, the monotonic positive associations did not change after the control. Similar results were observed among participants with a history of cancer or cardiovascular disease. Conclusions Our data suggest that both overall and abdominal body fat are associated with increased mortality in Korean adults. [ABSTRACT FROM AUTHOR]

Background We investigated whether military personnel involved in chemical warfare agent research at Porton Down had increased rates of mortality or cancer incidence. Methods This was a historical cohort study comprising male UK veterans who participated in the 'Service Volunteer Programme', 1941–89, identified from Porton Down experiment books, and a comparison group of similar 'non-Porton Down' veterans identified from military personnel files. Of 19 233 records retrieved for each group, 18 133 (94%) Porton Down and 17 591 (92%) non-Porton Down were included in our analytical sample. Mortality and cancer incidence data were obtained from national registries up to December 2019. Results Over a median follow-up of 48.1 years, 10 935 Porton Down veterans (60.3%) and 10 658 non-Porton Down veterans (60.6%) had died. After adjustment for age, year of birth and military service characteristics, overall, Porton Down veterans had a 6% higher rate of all-cause mortality compared with non-Porton Down veterans [hazard ratio (HR) = 1.06, 95% confidence interval (CI) 1.03–1.09]. For cause-specific mortality, Porton Down veterans had higher rates of death from genitourinary diseases (HR = 1.34, 95% CI 1.05–1.70) and deaths attributable to alcohol (HR = 1.44, 95% CI 1.07–1.94), with weaker associations observed for deaths from infectious and parasitic diseases (HR = 1.32, 95% CI 0.99–1.78), lung cancer (HR = 1.10, 95% CI 1.01–1.20) and external causes (HR = 1.15, 95% CI 1.00–1.32). Associations with all-cause mortality were stronger for veterans who attended Porton Down between 1960 and 1964 (HR = 1.34, 95% CI 1.19–1.50); likelihood-ratio test, P  = 0.006. There was no association between attendance at Porton Down and overall cancer incidence (HR = 1.00, 95% CI 0.95–1.03). Conclusions Overall, mortality rates were slightly higher in Porton Down veterans, but there was no difference in cancer incidence. Associations for mortality were stronger in Porton Down veterans who attended in the early 1960s. [ABSTRACT FROM AUTHOR]

Background Benefits of elevated high-density lipoprotein cholesterol (HDL-C) levels are challenged by reports demonstrating U-shaped relations between HDL-C levels and all-cause mortality; the association with cause-specific mortality is less studied. Methods A total of 344 556 individuals (20–79 years, 52 % women) recruited from population-based health screening during 1985 – 2003 were followed until the end of 2018 for all-cause and cause-specific mortality by serum HDL-C level at inclusion of <30, 30–39, 40–49, 50–59, 60–69, 70–79, 80–89, 90–99 and >99 mg/dl (< 0.78, 0.78–1.01, 1.04–1.27, 1.30–1.53, 1.55–1.79, 1.81–2.04, 2.07–2.31, 2.33–2.56, >2.56 mmol/L). Hazard ratios (HRs) were adjusted for sex, age, calendar period, smoking, total cholesterol, triglycerides, systolic blood pressure, physical activity, educational length, body mass index and ill health. Results During a mean follow-up of 22 years, 69 505 individuals died. There were U-shaped associations between HDL-C levels and all-cause, cancer and non-cardiovascular disease/non-cancer mortality (non-CVD/non-cancer), whereas for CVD there was increased risk of death only at lower levels. With HDL-C stratum 50 – 59 mg/dl (1.30–1.53 mmol/L) as reference, HRs [95% confidence intervals (CIs)] for levels >99 mg/dl (>2.56 mmol/L) were 1.32 (1.21–1.43), 1.05 (0.89–1.24), 1.26 (1.09–1.46) and 1.68 (1.48–1.90) for all–cause, CVD, cancer and non–CVD/non–cancer mortality, respectively. For HDL-C levels <30 mg/dl (0.78 mmol/L), the corresponding HRs (95% CIs) were 1.30 (1.24–1.36), 1.55 (1.44–1.67), 1.14 (1.05–1.23) and 1.19 (1.10–1.29). The mortality from alcoholic liver disease, cancers of mouth-oesophagus-liver, chronic liver diseases, chronic obstructive pulmonary disease, accidents and diabetes increased distinctly with increasing HDL-C above the reference level. HDL-C levels lower than the reference level were mainly associated with increased mortality of ischaemic heart disease (IHD), other CVDs, stomach cancer and diabetes. Conclusions Higher HDL-C levels were associated with increased mortality risk of several diseases which also have been associated with heavy drinking, and lower HDL-C levels were associated with increased mortality from IHD, other CVDs, gastric cancer and diabetes. [ABSTRACT FROM AUTHOR]

Background: Whether changes in stroke mortality are affected by age distribution and birth cohorts, and if the decline in stroke mortality exhibits heterogeneity by stroke type, remains uncertain.Methods: We undertook a sequential time series analysis to examine stroke mortality trends in the USA among people aged 18-84 years between 1975 and 2019 (n = 4 332 220). Trends were examined for overall stroke and by ischaemic and haemorrhagic subtypes. Mortality data were extracted from the US death files, and age-sex population data were extracted from US census. Age-standardized stroke mortality rates and incidence rate ratio (IRR) with 95% confidence interval [CI] were derived from Poisson regression models.Results: Age-standardized stroke mortality declined for females from 87.5 in 1975 to 30.9 per 100 000 in 2019 (IRR 0.27, 95% CI 0.26, 0.27; average annual decline -2.78%, 95% CI -2.79, -2.78). Among males, age-standardized mortality rate declined from 112.1 in 1975 to 38.7 per 100 000 in 2019 (RR 0.26, 95% CI 0.26, 0.27; average annual decline -2.80%, 95% CI -2.81, -2.79). Stroke mortality increased sharply with advancing age. Decline in stroke mortality was steeper for ischaemic than haemorrhagic strokes.Conclusions: Stroke mortality rates have substantially declined, more so for ischaemic than haemorrhagic strokes. [ABSTRACT FROM AUTHOR]

Background To understand the impact of the COVID-19 pandemic on mortality, this study investigates overall, sex- and age-specific excess all-cause mortality in 20 countries, during 2020. Methods Total, sex- and age-specific weekly all-cause mortality for 2015–2020 was collected from national vital statistics databases. Excess mortality for 2020 was calculated by comparing weekly 2020 observed mortality against expected mortality, estimated from historical data (2015–2019) accounting for seasonality, long- and short-term trends. Crude and age-standardized rates were analysed for total and sex-specific mortality. Results Austria, Brazil, Cyprus, England and Wales, France, Georgia, Israel, Italy, Northern Ireland, Peru, Scotland, Slovenia, Sweden, and the USA displayed substantial excess age-standardized mortality of varying duration during 2020, while Australia, Denmark, Estonia, Mauritius, Norway, and Ukraine did not. In sex-specific analyses, excess mortality was higher in males than females, except for Slovenia (higher in females) and Cyprus (similar in both sexes). Lastly, for most countries substantial excess mortality was only detectable (Austria, Cyprus, Israel, and Slovenia) or was higher (Brazil, England and Wales, France, Georgia, Italy, Northern Ireland, Sweden, Peru and the USA) in the oldest age group investigated. Peru demonstrated substantial excess mortality even in the <45 age group. Conclusions This study highlights that excess all-cause mortality during 2020 is context dependent, with specific countries, sex- and age-groups being most affected. As the pandemic continues, tracking excess mortality is important to accurately estimate the true toll of COVID-19, while at the same time investigating the effects of changing contexts, different variants, testing, quarantine, and vaccination strategies. [ABSTRACT FROM AUTHOR]

BackgroundAmbient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere.MethodsWe investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI).ResultsEach increase of 10  μg/m3 PM2.5 (overall range, 2.9-28.0  μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure

Background People experiencing homelessness have an increased risk of mortality. The association between being at risk of homelessness and premature mortality is unclear. We aimed to determine all-cause and cause-specific mortality in patients who were homeless, at risk of homelessness (marginally housed), or housed. Methods This retrospective longitudinal cohort study compared mortality patterns in adult patients identified in 2003/04 by linking data from an Australian metropolitan emergency department to national mortality data. We used Cox proportional hazards models to estimate associations between housing status and mortality. To address competing risks, cause-specific hazards were modelled and transformed into stacked cumulative incidence functions. Findings Data from 6290 patients (homeless deceased = 382/1050, marginally housed deceased = 259/518, housed deceased = 1204/4722) found increased risk of mortality in homeless [hazard ratio (HR) = 4.0, 95% confidence interval (CI) = 2.0–3.3) and marginally housed (HR = 2.6, 95% CI = 3.4–4.8) patients. Homeless patients had an excess risk from external causes (HR = 6.1, 95% CI = 4.47–8.35), cardiovascular disease (HR = 4.9, 95% CI = 2.78–8.70) and cancer (HR = 1.5, 95% CI = 1.15–2.09). Marginally housed patients had increased risk from external causes (HR = 3.6, 95% CI = 2.36–5.40) and respiratory diseases (HR = 4.7, 95% CI = 1.82–12.05). Taking account of competing risk, marked inequality was observed, with homeless, marginally housed and housed patients having probabilities of death by 55 years of 0.2, 0.1 and 0.02, respectively. Conclusions Mortality rates were elevated in patients who were homeless or at risk of homelessness. Increasing numbers of people are at risk of homelessness, and the effect of this on mortality is relatively unrecognized. Marginal housing may assuage some risk of premature mortality associated with homelessness; however, it is not equivalent to stable housing. [ABSTRACT FROM AUTHOR]

Background An increasing proportion of people have a body mass index (BMI) classified as overweight or obese and published studies disagree whether this will be beneficial or detrimental to health. We applied and evaluated two intergenerational instrumental variable methods to estimate the average causal effect of BMI on mortality in a cohort with many deaths: the parents of UK Biobank participants. Methods In Cox regression models, parental BMI was instrumented by offspring BMI using an 'offspring as instrument' (OAI) estimation and by offspring BMI-related genetic variants in a 'proxy-genotype Mendelian randomization' (PGMR) estimation. Results Complete-case analyses were performed in parents of 233 361 UK Biobank participants with full phenotypic, genotypic and covariate data. The PGMR method suggested that higher BMI increased mortality with hazard ratios per kg/m2 of 1.02 (95% CI: 1.01, 1.04) for mothers and 1.04 (95% CI: 1.02, 1.05) for fathers. The OAI method gave considerably higher estimates, which varied according to the parent–offspring pairing between 1.08 (95% CI: 1.06, 1.10; mother–son) and 1.23 (95% CI: 1.16, 1.29; father–daughter). Conclusion Both methods supported a causal role of higher BMI increasing mortality, although caution is required regarding the immediate causal interpretation of these exact values. Evidence of instrument invalidity from measured covariates was limited for the OAI method and minimal for the PGMR method. The methods are complementary for interrogating the average putative causal effects because the biases are expected to differ between them. [ABSTRACT FROM AUTHOR]

Background Although the death of a child, sibling or spouse has been associated with elevated risk of mortality, less is known about the survival of twin siblings exposed to a co-twin loss. Methods In a Swedish population-based sibling-matched cohort, we compared the mortality of 5548 twin individuals who lost their co-twin between 1932 and 2011 with that of 27 740 age-matched and sex-matched twin individuals without such a loss and 6772 full siblings of these exposed twin individuals. Cox regression models were used to estimate the hazard ratios (HRs) of all-cause and cause-specific mortality. Results We found increased risk of all-cause mortality among twin individuals exposed to a co-twin loss compared with matched unexposed twin individuals (HR = 1.30, 95% CI: 1.18–1.43) and their full siblings (HR = 1.10, 95% CI: 0.96–1.27) after adjusting for multiple covariates. The all-cause mortality risk was greater for loss of a co-twin due to unnatural deaths (HR = 1.54, 95% CI: 1.17–2.03) than natural deaths (HR = 1.26, 95% CI: 1.14–1.40). For cause-specific mortality, co-twin loss was associated with a higher risk of unnatural deaths both among twin individuals who lost their co-twin due to unnatural deaths (HR = 1.98, 95% CI: 1.27–3.10) and those whose loss was due to natural deaths (HR = 1.48, 95% CI: 1.07–2.06). The risk elevations were generally stronger for loss of a monozygotic co-twin than loss of a dizygotic co-twin. Conclusion Loss of a co-twin, especially a monozygotic co-twin, was associated with increased mortality, particularly of unnatural causes, among the surviving twin individuals. The excess mortality is likely attributable to both shared disease susceptibility within the twin pair and the adverse health sequelae of bereavement. [ABSTRACT FROM AUTHOR]

Background Mortality statistics using a single underlying cause of death (UC) are key health indicators. Rising multimorbidity and chronic disease mean that deaths increasingly involve multiple conditions. However, additional causes reported on death certificates are rarely integrated into mortality indicators, partly due to complexities in data and methods. This study aimed to assess trends and patterns in cause-related mortality in Australia, integrating multiple causes (MC) of death. Methods Deaths (n  = 1 773 399) in Australia (2006–17) were mapped to 136 ICD-10-based groups and MC indicators applied. Age-standardized cause-related rates (deaths/100 000) based on the UC (ASRUC) were compared with rates based on any mention of the cause (ASRAM) using rate ratios (RR = ASRAM/ASRUC) and to rates based on weighting multiple contributing causes (ASRW). Results Deaths involved on average 3.4 causes in 2017; the percentage with >4 causes increased from 20.9 (2006) to 24.4 (2017). Ischaemic heart disease (ASRUC = 73.3, ASRAM = 135.8, ASRW = 63.5), dementia (ASRUC = 51.1, ASRAM = 98.1, ASRW = 52.1) and cerebrovascular diseases (ASRUC = 39.9, ASRAM = 76.7, ASRW = 33.5) ranked as leading causes by all methods. Causes with high RR included hypertension (ASRUC = 2.2, RR = 35.5), atrial fibrillation (ASRUC = 8.0, RR = 6.5) and diabetes (ASRUC = 18.5, RR = 3.5); the corresponding ASRW were 12.5, 12.6 and 24.0, respectively. Renal failure, atrial fibrillation and hypertension ranked among the 10 leading causes by ASRAM and ASRW but not by ASRUC. Practical considerations in working with MC data are discussed. Conclusions Despite the similarities in leading causes under the three methods, with integration of MC several preventable diseases emerged as leading causes. MC analyses offer a richer additional perspective for population health monitoring and policy development. [ABSTRACT FROM AUTHOR]

Background Previous research has suggested that individuals with Type 2 diabetes and initiated on metformin monotherapy present with a survival advantage compared with the general population without diabetes. This finding has generated considerable interest in the prophylactic use of metformin against age-related morbidity. Methods Utilizing Danish National Health Registers, we assessed differences in survival associated with metformin monotherapy for Type 2 diabetes compared with no diagnosis of diabetes in both singleton and discordant twin populations between 1996 and 2012. Data were analysed in both nested case–control and matched cohort study designs, with incidence rate ratios (IRRs) and hazard ratios estimated using conditional logistic regression and Cox proportional hazards regression, respectively. Results In case–control pairs matched on birth year and sex or co-twin (sex, birth year and familial factors), incident Type 2 diabetes with treatment by metformin monotherapy initiation compared with no diagnosis of diabetes was associated with increased mortality in both singletons (IRR = 1.52, 95% CI: 1.37, 1.68) and discordant twin pairs (IRR = 1.90, 95% CI: 1.35, 2.67). After adjusting for co-morbidities and social indicators, these associations were attenuated to 1.32 (95% CI: 1.16, 1.50) and 1.64 (95% CI: 1.10, 2.46), respectively. Increased mortality was observed across all levels of cumulative use and invariant to a range of study designs and sensitivity analyses. Conclusions Treatment initiation by metformin monotherapy in Type 2 diabetes was not associated with survival equal or superior to that of the general population without diabetes. Our contrasting findings compared with previous research are unlikely to be the result of differences in epidemiological or methodological parameters. [ABSTRACT FROM AUTHOR]

Background: Excess mortality during the COVID-19 pandemic is of major scientific and political interest.Methods: We critically reviewed different estimates of all-cause excess mortality for the five Nordic countries (Denmark, Finland, Iceland, Norway and Sweden), which have been much studied during the COVID-19 pandemic, using the latest register data to discuss uncertainties and implications.Results: We show using back-calculation of expected deaths from Nordic all-cause deaths that the Institute for Health Metrics and Evaluation model is a clear outlier in the compared estimates and likely substantially overestimates excess mortality of Finland and Denmark, and probably Sweden. Our review suggests a range of total Nordic excess deaths of perhaps 15 000-20 000, but results are sensitive to assumptions in the models as shown.Conclusions: We document substantial heterogeneity and uncertainty in estimates of excess mortality. All estimates should be taken with caution in their interpretation as they miss detailed account of demographics, such as changes in the age group populations over the study period. [ABSTRACT FROM AUTHOR]

Background Cardiovascular disease (CVD) has a disproportionate effect on mortality among the poorest people. We assessed the impact on CVD and all-cause mortality of the world's largest conditional cash transfer, Brazil's Bolsa Família Programme (BFP). Methods We linked administrative data from the 100 Million Brazilian Cohort with BFP receipt and national mortality data. We followed individuals who applied for BFP between 1 January 2011 and 31 December 2015, until 31 December 2015. We used marginal structural models to estimate the effect of BFP on all-age and premature (30–69 years) CVD and all-cause mortality. We conducted stratified analyses by levels of material deprivation and access to healthcare. We checked the robustness of our findings by restricting the analysis to municipalities with better mortality data and by using alternative statistical methods. Results We studied 17 981 582 individuals, of whom 4 855 324 were aged 30–69 years. Three-quarters (76.2%) received BFP, with a mean follow-up post-award of 2.6 years. We detected 106 807 deaths by all causes, of which 60 893 were premature; and 23 389 CVD deaths, of which 15 292 were premature. BFP was associated with reductions in premature all-cause mortality [hazard ratio (HR) = 0.96, 95% CI = 0.94–0.98], premature CVD (HR = 0.96, 95% CI = 0.92–1.00) and all-age CVD (HR = 0.96, 95% CI = 0.93–1.00) but not all-age all-cause mortality (HR = 1.00, 95% CI = 0.98–1.02). In stratified and robustness analyses, BFP was consistently associated with mortality reductions for individuals living in the two most deprived quintiles. Conclusions BFP appears to have a small to null effect on premature CVD and all-cause mortality in the short term; the long-term impact remains unknown. [ABSTRACT FROM AUTHOR]

Background Biannual azithromycin distribution to children 1–59 months old reduced all-cause mortality by 18% [incidence rate ratio (IRR) 0.82, 95% confidence interval (CI): 0.74, 0.90] in an intention-to-treat analysis of a randomized controlled trial in Niger. Estimation of the effect in compliance-related subgroups can support decision making around implementation of this intervention in programmatic settings. Methods The cluster-randomized, placebo-controlled design of the original trial enabled unbiased estimation of the effect of azithromycin on mortality rates in two subgroups: (i) treated children (complier average causal effect analysis); and (ii) untreated children (spillover effect analysis), using negative binomial regression. Results In Niger, 594 eligible communities were randomized to biannual azithromycin or placebo distribution and were followed from December 2014 to August 2017, with a mean treatment coverage of 90% [standard deviation (SD) 10%] in both arms. Subgroup analyses included 2581 deaths among treated children and 245 deaths among untreated children. Among treated children, the incidence rate ratio comparing mortality in azithromycin communities to placebo communities was 0.80 (95% CI: 0.72, 0.88), with mortality rates (deaths per 1000 person-years at risk) of 16.6 in azithromycin communities and 20.9 in placebo communities. Among untreated children, the incidence rate ratio was 0.91 (95% CI: 0.69, 1.21), with rates of 33.6 in azithromycin communities and 34.4 in placebo communities. Conclusions As expected, this analysis suggested similar efficacy among treated children compared with the intention-to-treat analysis. Though the results were consistent with a small spillover benefit to untreated children, this trial was underpowered to detect spillovers. [ABSTRACT FROM AUTHOR]

Background: This study assesses the national distribution of ambient fine particulate matter (PM2.5) exposure across socioeconomic status (SES) and its confounding on long-term PM2.5 mortality in Korea, aiming to minimize SES influence., Methods: A nationwide cohort of 5% of Koreans, aged 30 or older, from 2007 to 2019, from the National Health Information Database, was analysed. PM2.5 exposure levels were estimated at the city level using the Community Multiscale Air Quality system. Mortality data were obtained from Statistics Korea. The study examined annual PM2.5 exposure by SES indicators and its confounding on mortality risks associated with PM2.5, using time-varying Cox proportional hazards models., Results: The study followed 1 453 036 individuals from 2007 to 2019, totalling 17 760 227 person-years (PYs). The non-accidental (A00-R99), cardiovascular (I00-I99) and respiratory (J00-J99) mortality rates per 1000 PY were 7.6, 1.9 and 0.8, respectively. We observed a trend of decreasing PM2.5 exposure levels but increased mortality among medical aid beneficiaries, those with lower household incomes and those residing in neighbourhoods with a higher area deprivation index. When adjusting for these SES covariates, the long-term mortality effects of PM2.5 shifted in the direction of increased risk [hazard ratio (HR) for cardiovascular mortality in the unadjusted model = 0.968 (95% CI: 0.909-0.959); HR in the fully adjusted model = 1.053 (95% CI: 1.004-1.105)]., Conclusion: In regions where SES and PM2.5 concentrations are positively correlated, as in Korea, it is crucial to rigorously control for SES confounding to avoid underestimating the mortality effects associated with PM2.5., (© The Author(s) 2025; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Background: Deaths in Australia and other high-income countries increasingly involve multiple conditions. However, key burden of disease measures typically only use the underlying cause of death (UC). We quantified sex and cause-specific years of life lost (YLL) based on UC compared with a method integrating multiple causes of death., Methods: Causes of death for all deaths in Australia (2015-17), mapped to 136 groups based on International Classification of Diseases 10th revision (ICD-10), were ascribed using (1) the UC only and (2) a multiple cause weighting (WT) strategy. Applying the Global Burden of Disease 2010 life table, YLLUC and YLLWT rates were calculated for each sex and cause of death and compared using relative and absolute measures., Results: All-cause YLL rates were 113.4/1000 for males and 79.9/1000 for females. Cancers, cardiovascular diseases, external causes, respiratory diseases and nervous system diseases were the five biggest contributors to YLL for each method. For the top 20 causes combined, YLLWT rates were 10% lower for males (YLLWT = 74.93/1000 vs YLLUC = 67.38/1000) and 7% lower for females (YLLWT = 51.34/1000; YLLUC = 47.90/1000); YLLWT rates were lower for ischaemic heart disease and all cancers, but higher for diabetes and dementia, and for chronic obstructive pulmonary disease in males. With multiple cause weighting, renal failure emerged among the top 20 causes of YLL, as did atrial fibrillation and hypertension among females. YLLWT rates for substance abuse, mood disorders, hypertension and schizophrenia were relatively high compared with YLLUC., Conclusion: The YLLWT metric highlights epidemiologically important conditions that are less often selected as the UC., (© The Author(s) 2025. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Background Unlike other countries, South Korea did not implement a large-scale lockdown or closure of businesses to manage the coronavirus disease 2019 (COVID-19) pandemic, but relied on changes in population behaviours and early isolation and treatment of patients. It is important to evaluate the effectiveness of such alternative strategies on the mortality of the general population. Methods Mortality and monthly population data from 2013 to 2020 were obtained. A quasi-Poisson regression model adjusting for age structure, seasonality and time was used to evaluate whether underlying trends for monthly mortality rate have changed with the pandemic. Stratification analyses based on sex and location of deaths (inside vs outside of medical facilities) were conducted. Results The risk estimates showed no changes in non-accidental mortality during the COVID-19 pandemic [relative risk (RR) (95% confidence interval, 95% CI), slope change: 1.00 (1.00, 1.01), step change: 0.99 (0.97, 1.01)] compared with those before the pandemic. In cause-specific analysis, there was an abrupt and sustained decrease in the mortality rate of respiratory diseases [RR (95% CI), step change: 0.81 (0.77, 0.84)]. In the analysis of deaths by location, an increase in non-accidental mortality [RR (95% CI), slope change: 1.01 (1.01, 1.02), step change: 1.16 (1.11, 1.22)] and several cause-specific mortalities was observed outside of medical facilities. Conclusions The non-accidental mortality rate in South Korea for the first year of the pandemic followed the historical trends. However, there was a decrease in mortality associated with respiratory diseases, and an increase in mortality occurring outside of medical facilities. The findings may be attributed to changes in public behaviours, and availability of medical resources during the pandemic. [ABSTRACT FROM AUTHOR]

Several methods have been used to assess the seasonality of health outcomes in epidemiological studies. However, little information is available on the methods to study the changes in seasonality before and after adjusting for environmental or other known seasonally varying factors. Such investigations will help us understand the role of these factors in seasonal variation in health outcomes and further identify currently unknown or unmeasured risk factors. This tutorial illustrates a statistical procedure for examining the seasonality of health outcomes and their changes, after adjusting for potential environmental drivers by assessing and comparing shape, timings and size. We recommend a three-step procedure, each carried out and compared before and after adjustment: (i) inspecting the fitted seasonal curve to determine the broad shape of seasonality; (ii) identifying the peak and trough of seasonality to determine the timings of seasonality; and (iii) estimating the peak-to-trough ratio and attributable fraction to measure the size of seasonality. Reporting changes in these features on adjusting for potential drivers allows readers to understand their role in seasonality and the nature of any residual seasonal pattern. Furthermore, the proposed approach can be extended to other health outcomes and environmental drivers. [ABSTRACT FROM AUTHOR]

Background: Estimates of the relative contribution of different pathogens to all-cause diarrhoea mortality are needed to inform global diarrhoea burden models and prioritize interventions. We aimed to investigate and estimate heterogeneity in the case fatality risk (CFR) of different diarrhoeal pathogens.Methods: We conducted a systematic review and meta-analysis of studies that reported cases and deaths for 15 enteric pathogens published between 1990 and 2019. The primary outcome was the pathogen-specific CFR stratified by age group, country-specific under-5 mortality rate, setting, study year and rotavirus vaccine introduction status. We developed fixed-effects and multilevel mixed-effects logistic regression models to estimate the pooled CFR overall and for each pathogen, controlling for potential predictors of heterogeneity.Results: A total of 416 studies met review criteria and were included in the analysis. The overall crude CFR for all pathogens was 0.65%, but there was considerable heterogeneity between and within studies. The overall CFR estimated from a random-effects model was 0.04% (95% CI: 0.026%-0.062%), whereas the pathogen-specific CFR estimates ranged from 0% to 2.7%. When pathogens were included as predictors of the CFR in the overall model, the highest and lowest odds ratios were found for enteropathogenic Escherichia coli (EPEC) [odds ratio (OR) = 3.0, 95% CI: 1.28-7.07] and rotavirus (OR = 0.23, 95% CI: 0.13-0.39), respectively.Conclusion: We provide comprehensive estimates of the CFR across different diarrhoeal pathogens and highlight pathogens for which more studies are needed. The results motivate the need for diarrhoeal interventions and could help prioritize pathogens for vaccine development. [ABSTRACT FROM AUTHOR]