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Objective To systematically compare midlife mortality patterns in the United States across racial and ethnic groups during 1999-2016, documenting causes of death and their relative contribution to excess deaths. Design Trend analysis of US vital statistics among racial and ethnic groups. Setting United States, 1999-2016. Population US adults aged 25-64 years (midlife). Main outcome measures Absolute changes in mortality measured as average year-to-year change during 1999-2016 and 2012-16; excess deaths attributable to increasing mortality; and relative changes in mortality measured as relative difference between mortality in 1999 versus 2016 and the nadir year versus 2016, and the slope of modeled mortality trends for 1999-2016 and for intervals between joinpoints. Results During 1999-2016, all cause mortality in midlife increased not only among non-Hispanic (NH) whites but also among NH American Indians and Alaskan Natives. Although all cause mortality initially decreased among NH blacks, Hispanics, and NH Asians and Pacific Islanders, this trend ended in 2009-11. Drug overdoses were the leading cause of increased mortality in midlife in each population, but mortality also increased for alcohol related conditions, suicides, and organ diseases involving multiple body systems. Although midlife mortality among NH whites increased across a multitude of conditions, a similar trend affected non-white populations. Absolute (year-to-year) increases in midlife mortality among non-white populationsoften matched or exceeded those of NH whites, especially in 2012-16, when the rate of increase intensified for many causes of death. During 1999-2016, NH American Indians and Alaskan Natives experienced large increases in midlife mortality from 12 causes, not only drug overdoses (411.4%) but also hypertensive diseases (269.3%), liver cancer (115.1%), viral hepatitis (112.1%), and diseases of the nervous system (99.8%). NH blacks experienced increased midlife mortality from 17 causes, including drug overdoses (149.6%), homicides (21.4%), hypertensive diseases (15.5%), obesity (120.7%), and liver cancer (49.5%). NH blacks also experienced retrogression: after a period of stable or declining midlife mortality early in 1999-2016, death rates increased for alcohol related liver disease, chronic lower respiratory tract disease, suicides, diabetes, and pancreatic cancer. Among Hispanics, midlife mortality increased across 12 causes, including drug overdoses (80.0%), hypertensive diseases (40.6%), liver cancer (41.8%), suicides (21.9%), obesity (106.6%), and metabolic disorders (60.0%). Retrogression also occurred in this population; after a period of declining mortality, death rates increased for alcohol related liver disease, mental and behavioral disorders involving psychoactive substances, and homicides. NH Asians and Pacific Islanders were least affected by this trend but also experienced increases in midlife mortality from drug overdoses (300.6%), alcohol related liver disease (62.9%), hypertensive diseases (28.3%), and brain cancer (56.6%). The suicide rate in this group increased by 29.7% after 2001. The relative increase in US midlife mortality differed by sex and geography. For example, the relative increase in fatal drug overdoses was greater among women than among men. Although the relative increase in midlife mortality was generally greater in non-metropolitan (ie, rural) areas, the relative increase in drug overdoses among NH whites and Hispanics was greatest in suburban fringe areas of large cities, and among NH blacks was greatest in small cities. Conclusions Mortality in midlife in the US has increased across racial-ethnic populations for a variety of conditions, especially in recent years, offsetting years of progress in lowering mortality rates. This reversal carries added consequences for racial groups with high baseline mortality rates, such as for NH blacks and NH American Indians and Alaskan Natives. That death rates are increasing throughout the US population for dozens of conditions signals a systemic cause and warrants prompt action by policy makers to tackle the factors responsible for declining health in the US.

Objectives A multinational occupational epidemiological study of workers exposed to tungsten carbide with a cobalt binder (WCCo) is underway in the US and Europe. The epidemiological component will investigate total and cause-specific mortality risks and exposure-response relationships with focus on lung cancer. We designed the study to overcome certain limitations of earlier epidemiology studies. Method The epidemiological and exposure assessment components of the study are coordinated by the University of Pittsburgh and the University of Illinois at Chicago, respectively. Our cohort comprises 12 manufacturing sites in the US and nine sites in Europe, and represents three companies, five countries (US, Austria, Germany, Sweden and UK) and multiple manufacturing processes and exposures. Statistical analyses will adjust external and internal mortality rate comparisons for potential co-exposures, including smoking histories obtained via a nested case-control study. The study will include separate and pooled analyses. Results Our data collection effort identified two additional US study sites and additional subjects in the German and Swedish sites. Accordingly, our originally projected cohort size of 21 000 subjects has increased to 35 508 (US-7005; Europe-33 508). Vital status tracing, cause of death determination and identification of subjects for the nested case-control study are ongoing. Conclusions Our study will enable country-specific and pooled analyses of mortality rates and exposure-response relationships among workers from 21 study sites and the opportunity to compare and contrast findings across countries, sites, companies and/or manufacturing processes and exposures involved in this global industry. We will detail progress to date on the US and combined epidemiological component of the study.

Objectives A multinational occupational epidemiological study is underway to investigate the total and cause-specific mortality of workers exposed to tungsten carbide with a cobalt binder (WCCo). The study includes 12 US and 9 European plants. The objective of the exposure assessment component, coordinated by the University of Illinois at Chicago, is to reconstruct agent-specific exposure estimates for use in the epidemiological analyses. Method Quantitative occupational exposures are being generated through a process of modelling and validation using industrial hygiene data from study plants. Innovative semi-quantitative methods are being developed to extrapolate data for years in which it is missing, and are based on exposure changes due to manufacturing process changes over time (e.g., moving from manual to automated methods). Company work history information is being used to construct a job dictionary. The resulting exposure estimates and job dictionary will form the job-exposure matrix. Results The agents of interest are WCCo, tungsten carbide, tungsten, cobalt, and carbon black. Current and past working environments are being characterised according to products manufactured and operations performed and in relation to potential exposures using sampling data, job descriptions, plant and process histories, and information provided by knowledgeable plant personnel. Conclusions Exposure estimates will be generated for the study plants. The multinational aspect of the study provides the opportunity to pool data and produce exposure estimates for all 21 facilities with potential insight into similarities or differences among countries and/or plants involved in the same global industry. This presentation will detail the progress to date on the exposure assessment effort.