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Suicide remains a leading cause of death in the United States, and recent data suggest suicide deaths involving opioids are increasing. Given unprecedented increases in drug-poisoning deaths, suicidality, and suicide deaths in recent years, an updated examination of the trends in suicide deaths involving opioids is warranted. In this descriptive epidemiologic analysis, we leverage final and provisional mortality data from the US Centers for Disease Control and Prevention's WONDER database to examine trends in suicide deaths involving opioid poisoning from 1999 to 2021 by biological sex. Results reveal complex changes over time: the number and age-adjusted rate of suicide deaths involving opioid poisoning among male and female residents tended to track together, and both increased through 2010, but then diverged, with the number and rate of suicide deaths involving opioid poisoning among female residents outpacing that of male residents. However, the number and rate of suicide deaths involving opioid poisoning among male residents then began to stabilize, while that of female residents declined, closing the sex-based gap. Across all years of data, the proportion of suicide deaths that involved opioid poisoning was consistently higher among female decedents (5.8%-11.0%) compared with male decedents (1.4%-2.8%). Findings have implications for improved suicide prevention and harm reduction efforts. This article is part of a Special Collection on Mental Health. [ABSTRACT FROM AUTHOR]

High and low daily ambient temperatures are associated with higher mortality in the general population. People experiencing homelessness (PEH) are thought to be particularly vulnerable, but there is almost no direct evidence available. We examined the temperature-mortality association among PEH in 2 populous, urban counties in hot-climate regions of the United States, focusing on heat effects. Study setting was Los Angeles County, CA, and Clark County, NV, which encompass the cities of Los Angeles and Las Vegas, respectively. Outcomes were 2015-2022 deaths among decedents categorized as homeless in county administrative records. We used quasi-Poisson distributed lag nonlinear models to estimate the association of mortality with daily temperatures and with 7-day lagged temperatures, adjusting for day of week, seasonality, and long-term trends. We estimated the minimum mortality temperature and fraction of mortality attributable to temperatures above and below minimum mortality temperature. The association between daily temperature and PEH mortality was skewed towards greater risk at higher temperatures, especially in Clark County. Temperature-attributable mortality equaled 50.1% of deaths in Clark County (95% CI, 29.0-62.8) and 7.0% in Los Angeles County (95% CI, 1.4-12.1). In both counties, most temperature-attributable deaths were attributable to heat rather than cold. In these hot-climate urban counties, our estimates of heat-attributable mortality among PEH were orders of magnitude greater than those reported in prior research on the general population. These results indicate that temperature vulnerability, particularly heat vulnerability, requires stronger public health and policy responses. This article is part of a Special Collection on Environmental Epidemiology. [ABSTRACT FROM AUTHOR]

Polysocial risk scores were recently proposed as a strategy for improving the clinical relevance of knowledge about social determinants of health. Our objective in this study was to assess whether the polysocial risk score model improves prediction of cognition and all-cause mortality in middle-aged and older adults beyond simpler models including a smaller set of key social determinants of health. We used a sample of 13 773 individuals aged ≥50 years at baseline from the 2006-2018 waves of the Health and Retirement Study, a US population-based longitudinal cohort study. Four linear mixed models were compared: 2 simple models including a priori–selected covariates and 2 polysocial risk score models which used least absolute shrinkage and selection operator (LASSO) regularization to select covariates among 9 or 21 candidate social predictors. All models included age. Predictive accuracy was assessed via R 2 and root mean-squared prediction error (RMSPE) using training/test split validation and cross-validation. For predicting cognition, the simple model including age, race, sex, and education had an R 2 value of 0.31 and an RMSPE of 0.880. Compared with this, the most complex polysocial risk score selected 12 predictors (R 2 = 0.35 and RMSPE = 0.858; 2.2% improvement). For all-cause mortality, the simple model including age, race, sex, and education had an area under the receiver operating characteristic curve (AUROC) of 0.747, while the most complex polysocial risk score did not demonstrate improved performance (AUROC = 0.745). Models built on a smaller set of key social determinants performed comparably to models built on a more complex set of social "risk factors." [ABSTRACT FROM AUTHOR]

Many ecological studies examine health outcomes and disparities using administrative boundaries such as census tracts, counties, or states. These boundaries help us to understand the patterning of health by place, along with impacts of policies implemented at these levels. However, additional geopolitical units (units with both geographic and political meaning), such as congressional districts (CDs), present further opportunities to connect research with public policy. Here we provide a step-by-step guide on how to conduct disparities-focused analysis at the CD level. As an applied case study, we use geocoded vital statistics data from 2010-2015 to examine levels of and disparities in infant mortality and deaths of despair in the 19 US CDs of Pennsylvania for the 111th-112th (2009-2012) Congresses and 18 CDs for the 113th-114th (2013-2016) Congresses. We also provide recommendations for extending CD-level analysis to other outcomes, states, and geopolitical boundaries, such as state legislative districts. Increased surveillance of health outcomes at the CD level can help prompt policy action and advocacy and, hopefully, reduce rates of and disparities in adverse health outcomes. [ABSTRACT FROM AUTHOR]

Few reliable estimates have been available for assessing the impact of the COVID-19 pandemic on mortality among Native Americans. Using deidentified publicly available data on deaths and populations by age, we estimated life expectancy for the years 2019-2022 for single-race non-Hispanic Native Americans. Life expectancy in 2022 was 67.8 years, 2.3 years higher than in 2021 but a huge 4-year loss from 2019. Although our life expectancy estimates for 2022 varied under different assumptions about racial/ethnic classification and age misreporting errors, all estimates were lower than the average for middle-income countries. Estimates of losses and gains in life expectancy were consistent across assumptions. Large reductions in COVID-19 death rates between 2021 and 2022 were largely offset by increases in rates of death from unintentional injuries (particularly drug overdoses), chronic liver disease, diabetes, and heart disease, underscoring the difficulties facing Native Americans in achieving reductions in mortality, let alone returning to levels of mortality prior to the pandemic. Serious data problems have persisted for many years, but the scarcity and inadequacy of estimates during the pandemic have underscored the urgent need for timely and accurate demographic data on the Native American population. [ABSTRACT FROM AUTHOR]

We aimed to compare rates and characteristics of suicide mortality in formerly incarcerated people with those of the general population in North Carolina. We conducted a retrospective cohort study of 266,400 people released from North Carolina state prisons between January 1, 2000, and March 1, 2020. Using direct and indirect standardization by age, sex, and calendar year, we calculated standardized suicide mortality rates and standardized mortality ratios comparing formerly incarcerated people with the North Carolina general population. We evaluated effect modification by race/ethnicity, sex, age, and firearm involvement. Formerly incarcerated people had approximately twice the overall suicide mortality of the general population for 3 years after release, with the highest rate of suicide mortality being observed in the 2-week period after release. In contrast to patterns in the general population, formerly incarcerated people had higher rates of non–firearm-involved suicide mortality than firearm-involved suicide mortality. Formerly incarcerated female, White and Hispanic/Latino, and emerging adult people had a greater elevation of suicide mortality than their general-population peers compared with other groups. These findings suggest a need for long-term support for formerly incarcerated people as they return to community living and a need to identify opportunities for interventions that reduce the harms of incarceration for especially vulnerable groups. This article is part of a Special Collection on Mental Health. [ABSTRACT FROM AUTHOR]

Monitoring morbidity and mortality in resurgences of respiratory infections poses significant challenges, as shown by coronavirus disease 2019 (COVID-19). For example, case fatality rates and deaths attributed to specific respiratory pathogens are known to suffer from significant biases undermining their comparability through time and space. As a result, it is difficult to evaluate the protective effect of public health interventions or quantify the impact of a resurgence on the general population through direct recording of COVID-19 related deaths. To overcome these limitations, more robust, less-biased metrics, such as all-cause deaths, have been proposed for monitoring the effect of an epidemic over a population and over time. More specifically, metrics of excess mortality over time, which have been used for influenza surveillance in the past, are increasingly considered important for COVID-19 surveillance. Here, we discuss excess mortality surveillance focusing on standardized single-point and standardized cumulative metrics that allow comparability of excess mortality through space and time. We explain why z score allows for comparison of excess mortality between countries and different periods, while cumulative z score allows assessment of excess mortality over long periods. Our commentary reiterates the importance of standardized statistics of excess mortality for COVID-19 surveillance as we move toward a coexistence with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that will allow drawing conclusions from best practices in different health systems and different periods. [ABSTRACT FROM AUTHOR]

Estimates of excess mortality can provide insight into direct and indirect impacts of the coronavirus disease 2019 (COVID-19) pandemic beyond deaths specifically attributed to COVID-19. We analyzed death certificate data from Baltimore City, Maryland, from March 1, 2020, to March 31, 2021, and found that 1,725 individuals (95% confidence interval: 1,495, 1,954) died in excess of what was expected from all-cause mortality trends in 2016–2019; 1,050 (61%) excess deaths were attributed to COVID-19. Observed mortality was 23%–32% higher than expected among individuals aged 50 years and older. Non-White residents of Baltimore City also experienced 2 to 3 times higher rates of excess mortality than White residents (e.g. 37.4 vs. 10.7 excess deaths per 10,000 population among Black residents vs. White residents). There was little to no observed excess mortality among residents of hospice, long-term care, and nursing home facilities, despite accounting for nearly 30% (312/1,050) of recorded COVID-19 deaths. There was significant geographic variation in excess mortality within the city, largely following racial population distributions. These results demonstrate the substantial and unequal impact of the COVID-19 pandemic on Baltimore City residents and the importance of building robust, timely surveillance systems to track disparities and inform targeted strategies to remediate the impact of future epidemics. [ABSTRACT FROM AUTHOR]

Understanding consequences of the COVID-19 pandemic requires information on the excess mortality resulting from it. Multiple studies have examined excess deaths during the pandemic's initial stages, but how these have changed over time is unclear. National- and state-level death counts and population data from 2009 to 2022 were used in this analysis to evaluate excess fatalities from March 2020 to February 2021 and March 2021 to February 2022, with deaths from earlier years used to project baseline counts. The outcomes were total, group-specific, cause-specific, and age-by-cause excess fatalities, and numbers and percentages directly involving COVID-19. Excess deaths declined from 655,735 (95% confidence interval: 619,028, 691,980) during the first pandemic year to 586,505 (95% confidence interval: 532,823, 639,205) in the second. The reductions were particularly large for Hispanics, Blacks, Asians, seniors, and residents of states with high vaccination rates. Excess deaths increased from the first to second year for persons younger than 65 years and in low-vaccination states. Excess mortality from some diseases declined, but those from alcohol, drug, vehicle, and homicide causes likely increased between the first and second pandemic year, especially for prime-age and younger individuals. The share of excess fatalities involving COVID-19 decreased modestly over time, with little change in its role as an underlying versus contributing cause of death. [ABSTRACT FROM AUTHOR]

The Aspirin in Reducing Events in the Elderly (ASPREE) Trial recruited 19,114 participants across Australia and the United States during 2010–2014. Participants were randomized to receive either 100 mg of aspirin daily or matching placebo, with disability-free survival as the primary outcome. During a median 4.7 years of follow-up, 37% of participants in the aspirin group permanently ceased taking their study medication and 10% commenced open-label aspirin use. In the placebo group, 35% and 11% ceased using study medication and commenced open-label aspirin use, respectively. In order to estimate compliance-adjusted effects of aspirin, we applied rank-preserving structural failure time models. The results for disability-free survival and most secondary endpoints were similar in intention-to-treat and compliance-adjusted analyses. For major hemorrhage, cancer mortality, and all-cause mortality, compliance-adjusted effects of aspirin indicated greater risks than were seen in intention-to-treat analyses. These findings were robust in a range of sensitivity analyses. In accordance with the original trial analyses, compliance-adjusted results showed an absence of benefit with aspirin for primary prevention in older people, along with an elevated risk of clinically significant bleeding. [ABSTRACT FROM AUTHOR]

In first-line antiretroviral therapy (ART) for human immunodeficiency virus (HIV) treatment, some subgroups of patients may respond better to an efavirenz-based regimen than an integrase strand transfer inhibitor (InSTI)-based regimen, or vice versa, due to patient characteristics modifying treatment effects. Using data based on nearly 16,000 patients from the North American AIDS Cohort Collaboration on Research and Design from 2009–2016, statistical methods for precision medicine were employed to estimate an optimal treatment rule that minimizes the 5-year risk of the composite outcome of acquired immune deficiency syndrome (AIDS)-defining illnesses, serious non-AIDS events, and all-cause mortality. The treatment rules considered were functions that recommend either an efavirenz- or InSTI-based regimen conditional on baseline patient characteristics such as demographic information, laboratory results, and health history. The estimated 5-year risk under the estimated optimal treatment rule was 10.0% (95% confidence interval (CI): 8.6, 11.3), corresponding to an absolute risk reduction of 2.3% (95% CI: 0.9, 3.8) when compared with recommending an efavirenz-based regimen for all patients and 2.6% (95% CI: 1.0, 4.2) when compared with recommending an InSTI-based regimen for all. Tailoring ART to individual patient characteristics may reduce 5-year risk of the composite outcome compared with assigning all patients the same drug regimen. [ABSTRACT FROM AUTHOR]

Since about 2010, life expectancy at birth in the United States has stagnated and begun to decline, with concurrent increases in the socioeconomic divide in life expectancy. The Simulation of Alcohol Control Policies for Health Equity (SIMAH) Project uses a novel microsimulation approach to investigate the extent to which alcohol use, socioeconomic status (SES), and race/ethnicity contribute to unequal developments in US life expectancy and how alcohol control interventions could reduce such inequalities. Representative, secondary data from several sources will be integrated into one coherent, dynamic microsimulation to model life-course changes in SES and alcohol use and cause-specific mortality attributable to alcohol use by SES, race/ethnicity, age, and sex. Markov models will be used to inform transition intensities between levels of SES and drinking patterns. The model will be used to compare a baseline scenario with multiple counterfactual intervention scenarios. The preliminary results indicate that the crucial microsimulation component provides a good fit to observed demographic changes in the population, providing a robust baseline model for further simulation work. By demonstrating the feasibility of this novel approach, the SIMAH Project promises to offer superior integration of relevant empirical evidence to inform public health policy for a more equitable future. [ABSTRACT FROM AUTHOR]

Knowledge regarding deaths due to suicide or alcohol- or drug-related causes may be limited by inconsistent and/or restrictive case definitions, resulting in concerns regarding validity of findings and underestimates of burden. In this proof-of-concept study, we assessed varying case definitions (suicide, alcohol-related, and drug-related mortality using underlying-cause-of-death (UCOD) versus multiple-cause-of-death (MCOD) International Classification of Diseases, Tenth Revision (ICD-10) codes) on the basis of counts and rates among Colorado veterans who died (2009–2020). Suicide, alcohol-related, or drug-related ICD-10 codes were identified, and 2 case definitions were compared: UCOD (qualifying ICD-10 code listed as the UCOD) and MCOD (qualifying ICD-10 code in any cause-of-death field). Of 109,314 decedents, the number of deaths and the age-adjusted mortality rate (per 100,000 persons) significantly increased when MCOD codes were included: n  = 4,930 (110.3 deaths/100,000 persons) for UCOD versus n  = 6,954 (138.4 deaths/100,000 persons) for MCOD. While rates of suicide mortality did not change, rates of alcohol-related mortality doubled with the more inclusive case definition: 1,752 (27.3 deaths/100,000 persons) for UCOD versus 3,847 (59.8 deaths/100,000 persons) for MCOD. Alcohol-use disorder codes accounted for 71% of additional alcohol-related deaths captured with the MCOD definition. Studies that rely on UCOD codes may be underestimating the burden of deaths, especially alcohol-related deaths. Increased effort is required to reevaluate current classifications of deaths associated with suicide, alcohol use, or drug use. [ABSTRACT FROM AUTHOR]

Using 5 diet quality indexes, we estimated the mortality and life expectancy lost, at the national level, attributable to poor dietary patterns, which had previously been largely unknown. We used the Canadian Community Health Survey 2004, linked to vital statistics (n  = 16,212 adults; representing n  = 22,898,880). After a median follow-up of 7.5 years, 1,722 deaths were recorded. Population attributable fractions were calculated to estimate the mortality burden of poor dietary patterns (Dietary Guidelines for Americans Adherence Index 2015, Dietary Approaches to Stop Hypertension, Healthy Eating Index, Alternative Healthy Eating Index, and Mediterranean Style Dietary Pattern Score). Better diet quality was associated with a 32%–51% and 21%–43% reduction in all-cause mortality among adults aged 45–80 years and ≥20 years, respectively. Projected life expectancy at 45 years was longer for Canadians adhering to a healthy dietary pattern (average of 5.2–8.0 years (men) and 1.6–4.1 (women)). At the population level, 26.5%–38.9% (men) and 8.9%–22.9% (women) of deaths were attributable to poor dietary patterns. Survival benefit was greater for individuals with higher scores on all diet indexes, even with relatively small intake differences. The large attributable burden was likely from assessing overall dietary patterns instead of a limited range of foods and nutrients. [ABSTRACT FROM AUTHOR]

Multimorbidity (≥2 chronic conditions) is a common and important marker of aging. To better understand racial differences in multimorbidity burden and associations with important health-related outcomes, we assessed differences in the contribution of chronic conditions to hospitalization, skilled nursing facility admission, and mortality among non-Hispanic Black and non-Hispanic White older adults in the United States. We used data from a nationally representative study, the National Health and Aging Trends Study, linked to Medicare claims from 2011–2015 (n  = 4,871 respondents). This analysis improved upon prior research by identifying the absolute contributions of chronic conditions using a longitudinal extension of the average attributable fraction for Black and White Medicare beneficiaries. We found that cardiovascular conditions were the greatest contributors to outcomes among White respondents, while the greatest contributor to outcomes for Black respondents was renal morbidity. This study provides important insights into racial differences in the contributions of chronic conditions to costly health-care utilization and mortality, and it prompts policy-makers to champion delivery reforms that will expand access to preventive and ongoing care for diverse Medicare beneficiaries. [ABSTRACT FROM AUTHOR]

Suicide is one of the leading causes of death in young adults in many Western countries. We examined the short-term association of temperature with cause-specific mortality, comparing suicide with other causes of death and describing possible attenuation of associations with temperature across decades. We considered all deaths that occurred in France between 1968 and 2016. For each cause of death, we conducted a 2-stage meta-analysis of associations with daily temperature. We stratified the association across time periods. A total of 502 , 017 deaths by suicide were recorded over 49 years. Temperature was monotonically associated with suicide mortality. The strongest association was found at lag 0 days. The relative risk of suicide mortality at the 99th (compared with the 1st) temperature percentile was 1.54 (95% confidence interval, 1.46, 1.63). Among all causes of death, suicide was the only cause displaying a monotonic trend with temperature and ranked seventh for heat-related mortality; 2 other causes of death implying the nervous system ranked third and fourth. Associations with temperature attenuated between the 1968–1984 and 1985–2000 periods for all-cause mortality and suicide mortality, without clear further attenuation in the 2001–2016 period. The robust short-term monotonic association between temperature and suicide risk could be considered in heat effects– and suicide-related prevention campaigns. [ABSTRACT FROM AUTHOR]

Whether monthly excess mortality in the United States during 2020 varied by age and cause of death is investigated in this analysis. Based on national-level death counts and population estimates for 1999–2020, sex-specific negative binomial regression models were used to estimate monthly cause-specific excess mortality by age group during 2020. Among men, 71% non-COVID excess deaths occurred at working ages (25–64 years), but those ages accounted for only 36% of non-COVID excess deaths among women. Many excess deaths resulted from external causes (particularly among men), heart disease, diabetes, Alzheimer disease (particularly among women), and cerebrovascular disease. For men, the largest share of non-COVID excess deaths resulted from external causes, nearly 80% of which occurred at working ages. Although incorrectly classified COVID-19 deaths may explain some excess non-COVID mortality, misclassification is unlikely to explain the increase in external causes of death. Auxiliary analyses suggested that drug-related deaths may be driving the increase in external mortality, but drug overdoses were already increasing for a full year before the pandemic. The oldest Americans bore the brunt of COVID-19 deaths, but working-age Americans, particularly men, suffered substantial numbers of excess non-COVID deaths, most commonly from external causes and heart disease. [ABSTRACT FROM AUTHOR]

Official statistics in Australia and the United States show large recent increases in dementia mortality rates. In this study, we assessed whether these trends are biased by an increasing tendency of medical certifiers (predominantly physicians) to report on the death certificate that dementia was a direct cause of death. Regression models of multiple-cause-of-death data in Australia (2006–2016) and the United States (2006–2017) were constructed to adjust dementia mortality rates for changes in death certification practices. Compared with official statistics, the recent increase in adjusted age-standardized dementia death rates was less than half as large in Australia and about two-thirds as large in the United States. Further adjustment for changes in reporting of dementia anywhere on the death certificate implied even lower increases in dementia mortality. Declines in reporting of cardiovascular diseases as comorbid conditions also contributed to rises in dementia mortality rates. The increasing likelihood of dementia's being reported as directly leading to death largely explains recent increases in dementia mortality rates in both countries. However, studies have found that reported dementia on death certificates remains low compared with clinical evaluations of its prevalence. Improved guidance and training for certifiers in reporting of dementia on death certificates will help standardize mortality statistics within and between countries. [ABSTRACT FROM AUTHOR]

Consumption of ultra-processed foods (UPF) has increased worldwide during the last decades because they are hyperpalatable, cheap, and ready-to-consume products. However, uncertainty exists about their impact on health. We conducted a systematic review and meta-analysis evaluating the association of UPF consumption with all-cause mortality risk. Five bibliographic databases were searched for relevant studies. Random effects models were used to calculate pooled relative risks (RRs) and 95% confidence intervals (CIs). Of 6,951 unique citations, 40 unique prospective cohort studies comprising 5,750,133 individuals were included; publication dates ranged from 1984 to 2021. Compared with low consumption, highest consumption of UPF (RR = 1.29, 95% CI: 1.17, 1.42), sugar-sweetened beverages (RR = 1.11, 95% CI, 1.04, 1.18), artificially sweetened beverages (RR = 1.14, 95% CI, 1.05, 1.22), and processed meat/red meat (RR = 1.15, 95% CI, 1.10, 1.21) were significantly associated with increased risk of mortality. However, breakfast cereals were associated with a lower mortality risk (RR = 0.85, 95% CI, 0.79, 0.92). This meta-analysis suggests that high consumption of UPF, sugar-sweetened beverages, artificially sweetened beverages, processed meat, and processed red meat might increase all-cause mortality, while breakfast cereals might decrease it. Future studies are needed to address lack of standardized methods in UPF categorization. [ABSTRACT FROM AUTHOR]

Pregnancy loss is a common reproductive complication, but its association with long-term mortality and whether this varies by maternal race/ethnicity is not well understood. Data from a racially diverse cohort of pregnant women enrolled in the Collaborative Perinatal Project (CPP) from 1959 to 1966 were used for this study. CPP records were linked to the National Death Index and the Social Security Death Master File to identify deaths and underlying cause (until 2016). Pregnancy loss comprised self-reported losses, including abortions, stillbirths, and ectopic pregnancies. Among 48,188 women (46.0% White, 45.8% Black, 8.2% other race/ethnicity), 25.6% reported at least 1 pregnancy loss and 39% died. Pregnancy loss was associated with a higher absolute risk of all-cause mortality (risk difference, 4.0 per 100 women, 95% confidence interval: 1.4, 6.5) and cardiovascular mortality (risk difference, 2.2 per 100 women, 95% confidence interval: 0.8, 3.5). Stratified by race/ethnicity, a higher risk of mortality persisted in White, but not Black, women. Women with recurrent losses are at increased risk of death, both overall and across all race/ethnicity groups. Pregnancy loss is associated with death; however, it does not confer an excess risk above the observed baseline risk in Black women. These findings support the need to assess reproductive history as part of routine screening in women. [ABSTRACT FROM AUTHOR]

Increasing numbers of adults in the United States use more than 1 tobacco product. Most use cigarettes in combination with other tobacco products. However, little is known about the all-cause and cancer-specific mortality risks of dual– and poly–tobacco-product use. We examined these associations by pooling nationally representative data from the 1991, 1992, 1998, 2000, 2005, and 2010 National Health Interview Surveys (n = 118,144). Mortality information was obtained through linkage to the National Death Index. Cigarette smokers who additionally used other tobacco products smoked as many if not more cigarettes per day than exclusive cigarette smokers. Furthermore, cigarette smokers who additionally used other tobacco products had mortality risks that were as high as and sometimes higher than those of exclusive cigarette smokers. As tobacco use patterns continue to change and diversify, investigators in future studies need to carefully assess the impact of noncigarette tobacco products on cigarette use and determine associated disease risks. [ABSTRACT FROM AUTHOR]

Potential health benefits of melatonin have been suggested. Although melatonin is present in various foods, little is known about the health effects of dietary melatonin intake. We estimated habitual dietary melatonin intake and examined its association with total and cause-specific mortality in a population-based cohort study in Japan. Study subjects included 13,355 men and 15,724 women aged ≥35 years who responded to a self-administered questionnaire in 1992. Their diets were assessed via a food frequency questionnaire at baseline. The melatonin content in various foods on the questionnaire was measured to estimate melatonin intake. Mortality was ascertained during 16 years of follow-up (1992–2008). Hazard ratios (HRs) and 95% confidence intervals (CIs) for total and cause-specific mortality were calculated according to melatonin quartiles. A total of 5,339 deaths occurred during follow-up. Melatonin intake was significantly associated with decreased risks of total mortality, cardiovascular mortality, and noncancer, noncardiovascular mortality after controlling for covariates; HRs for the highest quartile of melatonin intake versus the lowest were 0.90 (95% CI: 0.82, 0.98; P for trend = 0.05), 0.85 (95% CI: 0.72, 0.99; P for trend = 0.10), and 0.77 (95% CI: 0.67, 0.90; P for trend = 0.003), respectively. The data suggest a potential benefit of dietary melatonin with regard to mortality rates. [ABSTRACT FROM AUTHOR]

With unprecedented increases, mortality trends in the United States have received significant attention in recent years. To date, research on this topic has emphasized specific causes of death and proximal behavioral or physiological determinants. In this commentary, I consider novel contributions of Zheng and Echave (Am J Epidemiol. 2021;190(11):2242–2255) in examining trends in mental health, health behaviors, and physiological dysregulation. I then discuss broader developments in related research and make a case for: 1) not allowing recent health trends among Whites to overshadow the urgent work that needs to be done to mitigate persistent racial inequities, 2) further investigation of what accounts for increases in income inequality and its life-span health consequences, and 3) broadening the scope of mechanisms considered to include underdiscussed topics such as the role of increases in social media use or environmental toxicant exposures. Underlying several potential explanations for observed trends in health and mortality is the fact that substantial change has occurred on multiple fronts in US society and that policy responses to these changes have been insufficient. An enhanced emphasis on innovative population health research will be essential to provide the evidence base needed for policy makers to rise to these urgent challenges. [ABSTRACT FROM AUTHOR]

Unemployment insurance is hypothesized to play an important role in mitigating the adverse health consequences of job loss. In this prospective cohort study, we examined whether receiving unemployment benefits is associated with lower mortality among the long-term unemployed. Census records from the 2006 Canadian Census Health and Environment Cohort (n  = 2,105,595) were linked to mortality data from 2006–2016. Flexible parametric survival analysis and propensity score matching were used to model time-varying relationships between long-term unemployment (≥20 weeks), unemployment-benefit recipiency, and all-cause mortality. Mortality was consistently lower among unemployed individuals who reported receiving unemployment benefits, relative to matched nonrecipients. For example, mortality at 2 years of follow-up was 18% lower (95% confidence interval (CI): 9, 26) among men receiving benefits and 30% lower (95% CI: 18, 40) among women receiving benefits. After 10 years of follow-up, unemployment-benefit recipiency was associated with 890 (95% CI: 560, 1,230) fewer deaths per 100,000 men and 1,070 (95% CI: 810, 1,320) fewer deaths per 100,000 women. Our findings indicate that receiving unemployment benefits is associated with lower mortality among the long-term unemployed. Expanding access to unemployment insurance may improve population health and reduce health inequalities associated with job loss. [ABSTRACT FROM AUTHOR]

Life expectancy for US White men and women declined between 2013 and 2017. Initial explanations for the decline focused on increases in "deaths of despair" (i.e. deaths from suicide, drug use, and alcohol use), which have been interpreted as a cohort-based phenomenon afflicting middle-aged White Americans. There has been less attention on Black mortality trends from these same causes, and whether the trends are similar or different by cohort and period. We complement existing research and contend that recent mortality trends in both the US Black and White populations most likely reflect period-based exposures to 1) the US opioid epidemic and 2) the Great Recession. We analyzed cause-specific mortality trends in the United States for deaths from suicide, drug use, and alcohol use among non-Hispanic Black and non-Hispanic White Americans, aged 20–64 years, over 1990–2017. We employed sex-, race-, and cause-of-death–stratified Poisson rate models and age-period-cohort models to compare mortality trends. Results indicate that rising "deaths of despair" for both Black and White Americans are overwhelmingly driven by period-based increases in drug-related deaths since the late 1990s. Further, deaths related to alcohol use and suicide among both White and Black Americans changed during the Great Recession, despite some racial differences across cohorts. [ABSTRACT FROM AUTHOR]

Two frequently encountered but underrecognized challenges for causal inference in studying the long-term health effects of disasters among survivors include 1) time-varying effects of disasters on a time-to-event outcome and 2) selection bias due to selective attrition. In this paper, we review approaches for overcoming these challenges and demonstrate application of the approaches to a real-world longitudinal data set of older adults who were directly affected by the 2011 Great East Japan Earthquake and Tsunami (n  = 4,857). To illustrate the problem of time-varying effects of disasters, we examined the association between degree of damage due to the tsunami and all-cause mortality. We compared results from Cox regression analysis assuming proportional hazards with those derived using adjusted parametric survival curves allowing for time-varying hazard ratios. To illustrate the problem of selection bias, we examined the association between proximity to the coast (a proxy for housing damage from the tsunami) and depressive symptoms. We corrected for selection bias due to attrition in the 2 postdisaster follow-up surveys (conducted in 2013 and 2016) using multivariable adjustment, inverse probability of censoring weighting, and survivor average causal effect estimation. Our results demonstrate that analytical approaches which ignore time-varying effects on mortality and selection bias due to selective attrition may underestimate the long-term health effects of disasters. [ABSTRACT FROM AUTHOR]

Preliminary evidence points to higher morbidity and mortality from coronavirus disease 2019 (COVID-19) in certain racial and ethnic groups, but population-based studies using microlevel data are lacking so far. We used register-based cohort data including all adults living in Stockholm, Sweden, between January 31, 2020 (the date of the first confirmed case of COVID-19) and May 4, 2020 (n  = 1,778,670) to conduct Poisson regression analyses with region/country of birth as the exposure and underlying cause of COVID-19 death as the outcome, estimating relative risks and 95% confidence intervals. Migrants from Middle Eastern countries (relative risk (RR) = 3.2, 95% confidence interval (CI): 2.6, 3.8), Africa (RR = 3.0, 95% CI: 2.2, 4.3), and non-Sweden Nordic countries (RR = 1.5, 95% CI: 1.2, 1.8) had higher mortality from COVID-19 than persons born in Sweden. Especially high mortality risks from COVID-19 were found among persons born in Somalia, Lebanon, Syria, Turkey, Iran, and Iraq. Socioeconomic status, number of working-age household members, and neighborhood population density attenuated up to half of the increased COVID-19 mortality risks among the foreign-born. Disadvantaged socioeconomic and living conditions may increase infection rates in migrants and contribute to their higher risk of COVID-19 mortality. [ABSTRACT FROM AUTHOR]

Increasing hospitalizations for COVID-19 in the United States and elsewhere have ignited debate over whether to reinstate shelter-in-place policies adopted early in the pandemic to slow the spread of infection. The debate includes claims that sheltering in place influences deaths unrelated to infection or other natural causes. Testing this claim should improve the benefit/cost accounting that informs choice on reimposing sheltering in place. We used time-series methods to compare weekly nonnatural deaths in California with those in Florida. California was the first state to begin, and among the last to end, sheltering in place, while sheltering began later and ended earlier in Florida. During weeks when California had shelter-in-place orders in effect, but Florida did not, the odds that a nonnatural death occurred in California rather than Florida were 14.4% below expected levels. Sheltering-in-place policies likely reduce mortality from mechanisms unrelated to infection or other natural causes of death. [ABSTRACT FROM AUTHOR]

In this study, we aimed to estimate the causal effect of normalized protein catabolic rate (nPCR) on mortality among end-stage renal disease (ESRD) patients in the presence of time-varying confounding affected by prior exposure using g-estimation. Information about 553 ESRD patients was retrospectively collected over an 8-year period (2011–2019) from hemodialysis facilities in Kerman, Iran. nPCR was dichotomized as <1.2 g/kg/day versus ≥1.2 g/kg/day. Then a standard time-varying accelerated failure time (AFT) Weibull model was built, and results were compared with those generated by g-estimation. After appropriate adjustment for time-varying confounders, weighted g-estimation yielded 78% shorter survival time (95% confidence interval (95% CI): −81, −73) among patients with a continuous nPCR <1.2 g/kg/day than among those who had nPCR ≥1.2 g/kg/day during follow-up, though it was 18% (95% CI: −57, 54) in the Weibull model. Moreover, hazard ratio estimates of 4.56 (95% CI: 3.69, 5.37) and 1.20 (95% CI: 0.66, 2.17) were obtained via weighted g-estimation and the Weibull model, respectively. G-estimation indicated that inadequate dietary protein intake characterized by nPCR increases all-cause mortality among ESRD patients, but the Weibull model provided an effect estimate that was substantially biased toward the null. [ABSTRACT FROM AUTHOR]

Air pollution epidemiology studies have primarily investigated long- and short-term exposures separately, have used multiplicative models, and have been associational studies. Implementing a generalized propensity score adjustment approach with 3.8 billion person-days of follow-up, we simultaneously assessed causal associations of long-term (1-year moving average) and short-term (2-day moving average) exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5), ozone, and nitrogen dioxide with all-cause mortality on an additive scale among Medicare beneficiaries in Massachusetts (2000–2012). We found that long- and short-term PM2.5, ozone, and nitrogen dioxide exposures were all associated with increased mortality risk. Specifically, per 10 million person-days, each 1-μg/m3 increase in long- and short-term PM2.5 exposure was associated with 35.4 (95% confidence interval (CI): 33.4, 37.6) and 3.04 (95% CI: 2.17, 3.94) excess deaths, respectively; each 1–part per billion (ppb) increase in long- and short-term ozone exposure was associated with 2.35 (95% CI: 1.08, 3.61) and 2.41 (95% CI: 1.81, 2.91) excess deaths, respectively; and each 1-ppb increase in long- and short-term nitrogen dioxide exposure was associated with 3.24 (95% CI: 2.75, 3.77) and 5.60 (95% CI: 5.24, 5.98) excess deaths, respectively. Mortality associated with long-term PM2.5 and ozone exposure increased substantially at low levels. The findings suggested that air pollution was causally associated with mortality, even at levels below national standards. [ABSTRACT FROM AUTHOR]

Whether genetic and familial factors influence the association between cardiorespiratory fitness (CRF) and cardiovascular disease (CVD) is unknown. Two cohorts were formed based on data from 1,212,295 men aged 18 years who were conscripted for military service in Sweden during 1972–1996. The first comprised 4,260 twin pairs in which the twins in each pair had different CRF (≥1 watt). The second comprised 90,331 nonsibling pairs with different CRF and matched on birth year and year of conscription. Incident CVD and all-cause mortality were identified using national registers. During follow-up (median 32 years), there was no difference in CVD and mortality between fitter twins and less fit twins (246 vs. 251 events; hazard ratio (HR) = 1.00, 95% confidence interval (CI): 0.83, 1.20). The risks were similar in twin pairs with ≥60-watt difference in CRF (HR = 0.96, 95% CI: 0.57, 1.64). In contrast, in the nonsibling cohort, fitter men had a lower risk of the outcomes than less fit men (4,444 vs. 5,298 events; HR = 0.83, 95% CI: 0.79, 0.86). The association was stronger in pairs with ≥60-watt difference in CRF (HR = 0.65, 95% CI: 0.59, 0.71). These findings indicate that genetic and familial factors influence the association of CRF with CVD and mortality. [ABSTRACT FROM AUTHOR]

Tuberculosis (TB) has been a leading infectious cause of death worldwide for much of human history, with 1.6 million deaths estimated in 2017. The Department of Epidemiology at the Johns Hopkins Bloomberg School of Public Health has played an important role in understanding and responding to TB, and it has made particularly substantial contributions to prevention of TB with chemoprophylaxis. TB preventive therapy is highly efficacious in the prevention of TB disease, yet it remains underutilized by TB programs worldwide despite strong evidence to support its use in high-risk groups, such as people living with HIV and household contacts, including those under 5 years of age. We review the evidence for TB preventive therapy and discuss the future of TB prevention. [ABSTRACT FROM AUTHOR]

Studies have documented that age at immigration and generational status are important predictors of socioeconomic outcomes among children of immigrants. Whether these characteristics are related to long-term risk of death is unknown. Leveraging variation within sibships, we evaluated the association of age at immigration and generational status (i.e. first or second generation) with death among children of immigrant mothers to Sweden. Data included 272,429 individuals (126,701 sibships) aged 15 or more years from the total Swedish population followed between 1990 and 2009. Population-average and sibling fixed-effect regressions were estimated, with the latter controlling for unobserved factors shared by siblings. The foreign-born children of immigrants experienced a 17% higher risk of death than the Swedish-born children of immigrants. This excess risk was evident for external and nonexternal causes of death. In general, a graded association was not detected between age at immigration and death among the foreign-born individuals; however, those arriving during primary school ages appeared especially vulnerable. This study provides robust evidence that among children of immigrants, being foreign born was associated with a long-term death penalty compared with being born in the host country. [ABSTRACT FROM AUTHOR]

Since the turn of the 21st century, during which White mortality has been rising, there has been a sharp increase in only 3 causes of death: drug use, alcohol use, and suicide. Because all 3 of these causes conjure notions of anguish and hopelessness, they have been conceptualized as a collective "deaths of despair" phenomenon. Simon and Masters (Am J Epidemiol. 2021;190(6)1169-1171) challenge this conceptualization by asking whether these 3 causes are empirically associated with each other. Their analyses produce small correlations, which lead them to call into question that the 3 causes are part of a unified phenomenon. We contest their work on several grounds. Their analyses suffer from several technical problems, including the fact that, for any given year and cause of death, 65.8%–97.6% of counties examined have death counts under 10. More fundamentally, it is unclear that we should expect these causes of death to rise and fall together, even if they are connected to a singular phenomenon. Instead, "despair" might manifest differently in different places (i.e. these causes might be substitutes for each other). We argue that the best answer to the authors' important question comes from assessing whether there is a common, despair-based causal mechanism underlying all 3 of them. [ABSTRACT FROM AUTHOR]

In the article, the authors present a study on the relationship of deaths of despair (DOD) and the levels and trends in age-standardized mortality rates of drug-related deaths, alcohol-related deaths and suicides among White men and women in the U.S. It discusses how death rates from alcohol and drug use and suicide move together across time and place.

In the present article, I aimed to test the hypothesis that possible fatal immunological reactions to the A/H1N1 virus of the 1918 "Spanish" influenza pandemic were the result of previous exposure to the A/H3N8 virus of the 1890–1892 "Russian" influenza pandemic. Using newspapers and official death records to reconstruct mortality peaks from influenza and excess pneumonia deaths in New Zealand before 1918 enabled comparisons with peaks of influenza mortality by age in 1918 from individual death records. For males, mortality peaks in the 1885, 1890–1892, 1894, and 1898 influenza outbreaks appeared to match those from the 1918 pandemic. For females, peaks of deaths in 1918 corresponded to those from the influenza outbreaks of 1887 and 1890–1892. The highest mortality rates for both sexes were among those 28–32 years of age. Although they lend strong support to the hypothesis of fatal immunological reactions derived from early exposure to a different influenza virus, the results from this study also raise more questions: Given that the A/H1N1 virus of 1918 was exceptionally virulent, why did so few children 5–15 years of age die from it? Influenza normally kills only the very young and the very old. In addition, why did twice as many European males as females die in the young-adult age groups, whereas Māori males and females died at almost identical rates? [ABSTRACT FROM AUTHOR]

Earlier studies report inconsistent associations between education and cognitive aging. We assessed the association, accounting for selective dropout due to death or dementia, and, in a subsample, accounting for confounding by early-life intelligence. Data from the Danish component of the Survey of Health, Ageing and Retirement in Europe (n = 3,400) were linked to registry data (education records, dementia diagnoses, and mortality) and the Danish Conscription Database (youth intelligence measurements for 854 men). Word recall and verbal fluency were assessed up to 4 times over 10 years (2004–2013) and combined by averaging the z scores. We fitted a joint model linking a time-to-event model for dementia or death to a linear mixed-effects model for cognitive change. Rate of cognitive decline was slower among people with high education compared with low education (β = 0.112, 95% confidence interval (CI): 0.056, 0.170). Adjusting for youth intelligence did not attenuate the association between education and cognitive decline (crude β = 0.136, 95% CI: 0.028, 0.244 vs. adjusted β = 0.145, 95% CI: 0.022, 0.269). The results suggest that higher education may slow cognitive decline in later life. In this sample, results changed little when accounting for selective attrition and confounding by intelligence. [ABSTRACT FROM AUTHOR]

Although previous studies examining leukocyte telomere length (LTL) and all-cause mortality controlled for several confounders, the observed association could be biased due to unmeasured confounders, including familial factors. We aimed to examine the association of LTL with all-cause mortality in a Swedish twin sample while adjusting for familial factors and allowing for time-dependent effects. A total of 366 participants (174 twin pairs and 18 individuals) were recruited from the Swedish Twin Registry. LTL was assessed using the Southern blot method. All-cause mortality data were obtained through linkage with the Swedish Population Registry, updated through November 15, 2017. To control for familial factors within twin pairs, we applied a between-within shared frailty model based on generalized survival models. Overall, 115 (31.4%) participants were men and 251 (68.6%) were women. The average age of the study participants when blood was drawn was 79.1 years, and follow-up duration ranged from 10 days to 25.7 years (mean = 10.2 years). During the follow-up period, 341 (93.2%) participants died. Shorter LTL was associated with higher mortality rates when controlling for familial factors in the between-within shared frailty model. We found significant time-dependent effects of LTL on all-cause mortality, where the mortality rate ratios were attenuated with increasing age. [ABSTRACT FROM AUTHOR]

Tobacco use, hypertension, hyperglycemia, overweight, and inactivity are leading causes of overall and cardiovascular disease (CVD) mortality worldwide, yet the relevant metabolic alterations responsible are largely unknown. We conducted a serum metabolomic analysis of 620 men in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (1985–2013). During 28 years of follow-up, there were 435 deaths (197 CVD and 107 cancer). The analysis included 406 known metabolites measured with ultra-high-performance liquid chromatography/mass spectrometry–gas chromatography/mass spectrometry. We used Cox regression to estimate mortality hazard ratios for a 1-standard-deviation difference in metabolite signals. The strongest associations with overall mortality were N -acetylvaline (hazard ratio (HR) = 1.28; P < 4.1 × 10−5, below Bonferroni statistical threshold) and dimethylglycine, 7-methylguanine, C -glycosyltryptophan, taurocholate, and N -acetyltryptophan (1.23 ≤ HR ≤ 1.32; 5 × 10−5 ≤ P ≤ 1 × 10−4). C -Glycosyltryptophan, 7-methylguanine, and 4-androsten-3β,17β-diol disulfate were statistically significantly associated with CVD mortality (1.49 ≤ HR ≤ 1.62, P < 4.1 × 10−5). No metabolite was associated with cancer mortality, at a false discovery rate of <0.1. Individuals with a 1-standard-deviation higher metabolite risk score had increased all-cause and CVD mortality in the test set (HR = 1.4, P = 0.05; HR = 1.8, P = 0.003, respectively). The several serum metabolites and their composite risk score independently associated with all-cause and CVD mortality may provide potential leads regarding the molecular basis of mortality. [ABSTRACT FROM AUTHOR]

Cause-specific mortality is an important outcome in studies of interventions to improve survival, yet causes of death can be misclassified. Here, we present an approach to performing sensitivity analyses for misclassification of cause of death in the parametric g-formula. The g-formula is a useful method to estimate effects of interventions in epidemiologic research because it appropriately accounts for time-varying confounding affected by prior treatment and can estimate risk under dynamic treatment plans. We illustrate our approach using an example comparing acquired immune deficiency syndrome (AIDS)-related mortality under immediate and delayed treatment strategies in a cohort of therapy-naive adults entering care for human immunodeficiency virus infection in the United States. In the standard g-formula approach, 10-year risk of AIDS-related mortality under delayed treatment was 1.73 (95% CI: 1.17, 2.54) times the risk under immediate treatment. In a sensitivity analysis assuming that AIDS-related death was measured with sensitivity of 95% and specificity of 90%, the 10-year risk ratio comparing AIDS-related mortality between treatment plans was 1.89 (95% CI: 1.13, 3.14). When sensitivity and specificity are unknown, this approach can be used to estimate the effects of dynamic treatment plans under a range of plausible values of sensitivity and specificity of the recorded event type. [ABSTRACT FROM AUTHOR]

Measures of biological age based on blood DNA methylation, referred to as age acceleration (AA), have been developed. We examined whether AA was associated with health risk factors and overall and cause-specific mortality. At baseline (1990-1994), blood samples were drawn from 2,818 participants in the Melbourne Collaborative Cohort Study (Melbourne, Victoria, Australia). DNA methylation was determined using the Infinium Human Methylation 450 BeadChip array (Illumina Inc., San Diego, California). Mixed-effects models were used to examine the association of AA with health risk factors. Cox models were used to assess the association of AA with mortality. A total of 831 deaths were observed during a median 10.7 years of follow-up. Associations of AA were observed with male sex, Greek nationality (country of birth), smoking, obesity, diabetes, lower education, and meat intake. AA measures were associated with increased mortality, and this was only partly accounted for by known determinants of health (hazard ratios were attenuated by 20%-40%). Weak evidence of heterogeneity in the association was observed by sex (P = 0.06) and cause of death (P = 0.07) but not by other factors. DNA-methylation-based AA measures are associated with several major health risk factors, but these do not fully explain the association between AA and mortality. Future research should investigate what genetic and environmental factors determine AA. [ABSTRACT FROM AUTHOR]

Influenza viruses are associated with a substantial global burden of morbidity and mortality every year. Estimates of influenza-associated mortality often vary between studies due to differences in study settings, methods, and measurement of outcomes. We reviewed 103 published articles assessing population-based influenza-associated mortality through searches of PubMed and Embase, and we identified considerable variation in the statisticalmethods used across studies. Studies using regression models with an influenza activity proxy applied 4 approaches to estimate influenza-associated mortality. The estimates increased with age and ranged widely, from -0.3-1.3 and 0.6-8.3 respiratory deaths per 100, 000 population for children and adults, respectively, to 4-119 respiratory deaths per 100, 000 population for older adults. Meta-regression analysis identified that study design features were associated with the observed variation in estimates. The estimates increased with broader cause-of-death classification and were higher for older adults than for children. The multiplier methods tended to produce lower estimates, while Serfling-type models were associated with higher estimates than other methods. No "average" estimate of excess mortality could reliably be made due to the substantial variability of the estimates, partially attributable to methodological differences in the studies. Standardization of methodology in estimation of influenza-associated mortality would permit improved comparisons in the future. [ABSTRACT FROM AUTHOR]

The cause-of-death (COD) statement on the standard US death certificate is a valuable tool for public health practice, but its utility is impaired by reporting inaccuracies. To assess the quality of CODs reported in New York City, we developed and applied a quality measure to 3 leading CODs: cancer, pneumonia, and diabetes. The COD quality measure characterized 5 common issues with COD completion: nonspecific conditions as the underlying COD (UCOD); UCOD discrepancies; the presence of only 1 informative cause on the entire certificate; competing causes listed together on 1 line; and clinically improbable sequences. COD statements with more than 1 quality issue were defined as statements of "limited" quality. Of 82,116 deaths with cancer, diabetes, or pneumonia assigned as the UCOD in New York City from 2010 to 2014, 66.8% of pneumonia certificates were classified as "limited" quality as compared with 45.6% of cancer certificates and 32.3% of diabetes certificates. Forty percent of cancer certificates listed only 1 informative condition on the death certificate. Almost half of pneumonia certificates (45.9%) contained only enough information to assign International Classification of Diseases, Tenth Revision, code J18.9 ("unspecified pneumonia") as the UCOD, whereas most diabetes certificates contained UCOD discrepancies (25.2%). These limitations affect the quality of mortality data but may be reduced through quality improvement efforts. [ABSTRACT FROM AUTHOR]

The impact of chronic exposure to fine particulate matter (particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5)) on respiratory disease and lung cancer mortality is poorly understood. In a cohort of 18.9 million Medicare beneficiaries (4.2 million deaths) living across the conterminous United States between 2000 and 2008, we examined the association between chronic PM2.5 exposure and cause-specific mortality. We evaluated confounding through adjustment for neighborhood behavioral covariates and decomposition of PM2.5 into 2 spatiotemporal scales. We found significantly positive associations of 12-month moving average PM2.5 exposures (per 10-μg/m3 increase) with respiratory, chronic obstructive pulmonary disease, and pneumonia mortality, with risk ratios ranging from 1.10 to 1.24. We also found significant PM2.5-associated elevated risks for cardiovascular and lung cancer mortality. Risk ratios generally increased with longer moving averages; for example, an elevation in 60-month moving average PM2.5 exposures was linked to 1.33 times the lung cancer mortality risk (95% confidence interval: 1.24, 1.40), as compared with 1.13 (95% confidence interval: 1.11, 1.15) for 12-month moving average exposures. Observed associations were robust in multivariable models, although evidence of unmeasured confounding remained. In this large cohort of US elderly, we provide important new evidence that long-term PM2.5 exposure is significantly related to increased mortality from respiratory disease, lung cancer, and cardiovascular disease. [ABSTRACT FROM AUTHOR]

The association between low-level crystalline silica (silica) exposure and mortality risk is not well understood. We investigated a cohort of 44,807 Chinese workers who had worked in metal mines or pottery factories for at least 1 year from January 1, 1960, to December 31, 1974, and were followed through 2003. Low-level silica exposure was defined as having a lifetime highest annual mean silica exposure at or under a permissible exposure limit (PEL). We considered 3 widely used PELs, including 0.05 mg/m³, 0.10 mg/m³, and 0.35 mg/m³. Cumulative silica exposure was estimated by linking a job exposure matrix with each participant's work history. For the 0.10-mg/m³ exposure level, Cox proportional hazards models showed significantly increased risk of mortality from all diseases (for each 1-ln mg/m³-years increase in logged cumulative silica exposure, hazard ratio (HR) = 1.05, 95% confidence interval (CI): 1.03, 1.07), malignant neoplasms (HR = 1.06, 95% CI: 1.03, 1.09), lung cancer (HR = 1.08, 95% CI: 1.02,1.14), ischemic heart disease (HR = 1.09, 95% CI: 1.02,1.16), pulmonary heart disease (HR = 1.08, 95% CI: 1.00,1.16), and respiratory disease (HR = 1.20, 95% CI: 1.14,1.26). The 0.05-mg/m³ and 0.35-mg/m³ exposure levels yielded similar associations. Long-term exposure to low levels (PELs ≤0.05 mg/m³, ≤0.10 mg/m³, or ≤0.35 mg/m³) of silica is associated with increased total and certain cause-specific mortality risk. Control of ambient silica levels and use of personal protective equipment should be emphasized in practice. [ABSTRACT FROM AUTHOR]

Although there is some evidence of an association between loss of a sibling in adulthood and subsequent mortality, there have been no previous studies in which investigators have examined whether the death of a sibling in childhood is associated with adult mortality using total population data. Data on a national cohort born in Sweden in 1973-1982 (n = 717,723) were prospectively collected from the Cause of Death Register until 2013 (i.e., from the ages of 18 years to 31-40 years). Cox proportional hazards models were used to analyze the association between sibling loss during childhood and death in young adulthood. After adjustment for sociodemographic confounders and parental psychosocial covariates, the hazard ratio for all-cause mortality in bereaved siblings versus nonbereaved siblings was 1.39 (95% confidence interval: 1.14, 1.69). Risks were more pronounced for those who lost a noninfant sibling (i.e., >1 year of age) (hazard ratio = 1.53, 95% confidence interval: 1.18,1.95) and those who lost a sibling in adolescence (i.e., between the ages of 12 and 18 years) (hazard ratio = 1.71, 95% confidence interval: 1.24, 2.35). Excess mortality risk was found for concordant causes of death (i.e., siblings dying from the same causes) but not for discordant causes. [ABSTRACT FROM AUTHOR]