Search

Background In the United States, lung cancer death rates have been declining for decades, primarily as a result of pronounced decreases in cigarette smoking. It is unclear, however, whether there have been similar declines in mortality rates of lung cancer unrelated to smoking. We estimated trends in US lung cancer death rates attributable and not attributable to smoking from 1991 to 2018. Methods The study included 30- to 79-year-olds in the National Health Interview Survey who were linked to the National Death Index, 1991-2014. Adjusted hazard ratios for smoking status and lung cancer death were estimated, and age-specific population attributable fractions were calculated. Annual population attributable fractions were multiplied by annual US national lung cancer mortality, partitioning rates into smoking-attributable and smoking-unrelated lung cancer deaths. All statistical tests were 2-sided. Results During 1991-2018, the proportion of never smokers increased among both men (35.1%-54.6%) and women (54.0%-65.4%). Compared with those who had ever smoked, those who had never smoked had 86% lower risk (hazard ratio = 0.14; 95% confidence interval [CI] = 0.12 to 0.16) of lung cancer death. The fraction of lung cancer deaths attributable to smoking decreased from 81.4% (95% CI = 78.9 to 81.4) to 74.7% (95% CI = 78.1 to 71.4). Smoking-attributable lung cancer death rates declined 2.7% per year (95% CI = ‒2.9% to ‒2.5%) and smoking-unrelated lung cancer death rates declined 1.8% per year (95% CI = ‒2.0% to ‒1.5%); these declines have accelerated in recent years. Conclusions An increasing proportion of lung cancer deaths are unrelated to smoking based on declines in smoking prevalence. Smoking-unrelated lung cancer death rates have declined, however, perhaps because of decreases in secondhand smoke and air pollution exposure as well as treatment improvements. [ABSTRACT FROM AUTHOR]

Background Starting in 2018, national death certificates included a new racial classification system that accounts for multiple-race decedents and separates Native Hawaiian and Pacific Islander (NHPI) individuals from Asian individuals. We estimated cancer death rates across updated racial and ethnic categories, sex, and age. Methods Age-standardized US cancer mortality rates and rate ratios from 2018 to 2020 among individuals aged 20 years and older were estimated with national death certificate data by race and ethnicity, sex, age, and cancer site. Results In 2018, there were approximately 597 000 cancer deaths, 598 000 in 2019, and 601 000 in 2020. Among men, cancer death rates were highest in Black men (298.2 per 100 000; n = 105 632), followed by White (250.8; n = 736 319), American Indian/Alaska Native (AI/AN; 249.2; n = 3376), NHPI (205.6; n = 1080), Latino (177.2; n = 66 167), and Asian (147.9; n = 26 591) men. Among women, Black women had the highest cancer death rates (206.5 per 100 000; n = 104 437), followed by NHPI (192.1; n = 1141), AI/AN (189.9; n = 3239), White (183.0; n = 646 865), Latina (128.4; n = 61 579), and Asian (111.4; n = 26 396) women. The highest death rates by age group occurred among NHPI individuals aged 20-49 years and Black individuals aged 50-69 and 70 years and older. Asian individuals had the lowest cancer death rates across age groups. Compared with Asian individuals, total cancer death rates were 39% higher in NHPI men and 73% higher in NHPI women. Conclusions There were striking racial and ethnic disparities in cancer death rates during 2018-2020. Separating NHPI and Asian individuals revealed large differences in cancer mortality between 2 groups that were previously combined in vital statistics data. [ABSTRACT FROM AUTHOR]

Seroprevalence studies provide useful information about the proportion of the population either vaccinated against SARS-CoV-2, previously infected with the virus, or both. Numerous studies have been conducted in the United States, but differ substantially by dates of enrollment, target population, geographic location, age distribution, and assays used. This can make it challenging to identify and synthesize available seroprevalence data by geographic region or to compare infection-induced versus combined infection- and vaccination-induced seroprevalence. To facilitate public access and understanding, the National Institutes of Health and the Centers for Disease Control and Prevention developed the COVID-19 Seroprevalence Studies Hub (COVID-19 SeroHub, https://covid19serohub.nih.gov/), a data repository in which seroprevalence studies are systematically identified, extracted using a standard format, and summarized through an interactive interface. Within COVID-19 SeroHub, users can explore and download data from 178 studies as of September 1, 2022. Tools allow users to filter results and visualize trends over time, geography, population, age, and antigen target. Because COVID-19 remains an ongoing pandemic, we will continue to identify and include future studies. Measurement(s) SARS-CoV-2 seroprevalence Technology Type(s) serology assay Factor Type(s) geography • age • sex • race/ethnicity • Collection date Sample Characteristic - Organism Homo sapiens Sample Characteristic - Environment spatiotemporal region Sample Characteristic - Location United States of America [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]

Background: Although racial/ethnic disparities in U.S. COVID-19 death rates are striking, focusing on COVID-19 deaths alone may underestimate the true effect of the pandemic on disparities. Excess death estimates capture deaths both directly and indirectly caused by COVID-19.Objective: To estimate U.S. excess deaths by racial/ethnic group.Design: Surveillance study.Setting: United States.Participants: All decedents.Measurements: Excess deaths and excess deaths per 100 000 persons from March to December 2020 were estimated by race/ethnicity, sex, age group, and cause of death, using provisional death certificate data from the Centers for Disease Control and Prevention (CDC) and U.S. Census Bureau population estimates.Results: An estimated 2.88 million deaths occurred between March and December 2020. Compared with the number of expected deaths based on 2019 data, 477 200 excess deaths occurred during this period, with 74% attributed to COVID-19. Age-standardized excess deaths per 100 000 persons among Black, American Indian/Alaska Native (AI/AN), and Latino males and females were more than double those in White and Asian males and females. Non-COVID-19 excess deaths also disproportionately affected Black, AI/AN, and Latino persons. Compared with White males and females, non-COVID-19 excess deaths per 100 000 persons were 2 to 4 times higher in Black, AI/AN, and Latino males and females, including deaths due to diabetes, heart disease, cerebrovascular disease, and Alzheimer disease. Excess deaths in 2020 resulted in substantial widening of racial/ethnic disparities in all-cause mortality from 2019 to 2020.Limitations: Completeness and availability of provisional CDC data; no estimates of precision around results.Conclusion: There were profound racial/ethnic disparities in excess deaths in the United States in 2020 during the COVID-19 pandemic, resulting in rapid increases in racial/ethnic disparities in all-cause mortality between 2019 and 2020.Primary Funding Source: National Institutes of Health Intramural Research Program. [ABSTRACT FROM AUTHOR]

Background A growing body of literature suggests chronically higher bile acid (BA) concentrations may be associated with multiple health conditions. Diet may affect BA metabolism and signaling; however, evidence from human populations is lacking. Objectives We systematically investigated cross-sectional associations of a priori–selected dietary components (fiber, alcohol, coffee, fat) with circulating BA concentrations. Methods We used targeted, quantitative LC-MS/MS panels to measure 15 circulating BAs in a subset of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC; n  = 2224) and Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO; n  = 986) comprising Finnish male smokers and United States men and women, respectively. We used multivariable linear regression to estimate associations of each dietary component with log-transformed BAs; exponentiated coefficients estimate proportional differences. We included the median of the dietary component quartile in linear regression models to test for trend. Results In ATBC, fiber was inversely associated with multiple circulating BAs. The proportional difference was –10.09% (95% CI: −19.29 to 0.16; P- trend = 0.04) when comparing total BAs among those in the highest relative to the lowest fiber quartile. Alcohol, trans fat, and polyunsaturated fat were positively associated with BAs in ATBC. The proportional difference comparing total BAs among those in the highest relative to the lowest alcohol quartile was 8.76% (95% CI: –3.10 to 22.06; P- trend = 0.03). Coffee and monounsaturated fat were inversely associated with BAs. The proportional difference comparing total BAs among those in the highest relative to the lowest coffee quartile was –24.03% (95% CI: –31.57 to –15.66; P- trend < 0.0001). In PLCO, no dietary components were associated with BAs except fiber, which was inversely associated with tauroursodeoxycholic acid. Conclusions Alcohol, coffee, certain fat subtypes, and fiber were associated with circulating concentrations of multiple BAs among Finnish male smokers. Given the potential role of BAs in disease risk, further investigation of the effects of diet on BAs in humans is warranted. [ABSTRACT FROM AUTHOR]

Background: Coffee consumption has been associated with a reduced risk of some cancers, but the evidence for renal cell carcinoma (RCC) is inconclusive. We investigated the relationship between coffee and RCC within a large cohort.Methods: Coffee intake was assessed at baseline in the National Institutes of Health-American Association of Retired Persons Diet and Health Study. Among 420 118 participants eligible for analysis, 2674 incident cases were identified. We fitted Cox-regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for coffee consumption vs non-drinkers.Results: We observed HRs of 0.94 (95% CI 0.81, 1.09), 0.94 (0.81, 1.09), 0.80 (0.70, 0.92) and 0.77 (0.66, 0.90) for usual coffee intake of <1, 1, 2-3 and ≥4 cups/day, respectively (Ptrend = 0.00003). This relationship was observed among never-smokers (≥4 cups/day: HR 0.62, 95% CI 0.46, 0.83; Ptrend = 0.000003) but not ever-smokers (HR 0.85, 95% CI 0.70, 1.05; Ptrend = 0.35; Pinteraction = 0.0009) and remained in analyses restricted to cases diagnosed >10 years after baseline (HR 0.65, 95% CI 0.51, 0.82; Ptrend = 0.0005). Associations were similar between subgroups who drank predominately caffeinated or decaffeinated coffee (Pinteraction = 0.74).Conclusion: In this investigation of coffee and RCC, to our knowledge the largest to date, we observed a 20% reduced risk for intake of ≥2 cups/day vs not drinking. Our findings add RCC to the growing list of cancers for which coffee consumption may be protective. [ABSTRACT FROM AUTHOR]

Background: Excess death estimates quantify the full impact of the coronavirus disease 2019 (COVID-19) pandemic. Widely reported U.S. excess death estimates have not accounted for recent population changes, especially increases in the population older than 65 years.Objective: To estimate excess deaths in the United States in 2020, after accounting for population changes.Design: Surveillance study.Setting: United States, March to August 2020.Participants: All decedents.Measurements: Age-specific excess deaths in the United States from 1 March to 31 August 2020 compared with 2015 to 2019 were estimated, after changes in population size and age were taken into account, by using Centers for Disease Control and Prevention provisional death data and U.S. Census Bureau population estimates. Cause-specific excess deaths were estimated by month and age.Results: From March through August 2020, 1 671 400 deaths were registered in the United States, including 173 300 COVID-19 deaths. An average of 1 370 000 deaths were reported over the same months during 2015 to 2019, for a crude excess of 301 400 deaths (128 100 non-COVID-19 deaths). However, the 2020 U.S. population includes 5.04 million more persons aged 65 years and older than the average population in 2015 to 2019 (a 10% increase). After population changes were taken into account, an estimated 217 900 excess deaths occurred from March through August 2020 (173 300 COVID-19 and 44 600 non-COVID-19 deaths). Most excess non-COVID-19 deaths occurred in April, July, and August, and 34 900 (78%) were in persons aged 25 to 64 years. Diabetes, Alzheimer disease, and heart disease caused the most non-COVID-19 excess deaths.Limitation: Provisional death data are underestimated because of reporting delays.Conclusion: The COVID-19 pandemic resulted in an estimated 218 000 excess deaths in the United States between March and August 2020, and 80% of those deaths had COVID-19 as the underlying cause. Accounting for population changes substantially reduced the excess non-COVID-19 death estimates, providing important information for guiding future clinical and public health interventions.Primary Funding Source: National Cancer Institute. [ABSTRACT FROM AUTHOR]

Background Whole grains and other foods containing fiber are thought to be inversely related to colorectal cancer (CRC). However, whether these associations reflect fiber or fiber source remains unclear. Objectives We evaluated associations of whole grain and dietary fiber intake with CRC risk in the large NIH-AARP Diet and Health Study. Methods We used Cox proportional hazard models to estimate HRs and 95% CIs for whole grain and dietary fiber intake and risk of CRC among 478,994 US adults, aged 50–71 y. Diet was assessed using a self-administered FFQ at baseline in 1995–1996, and 10,200 incident CRC cases occurred over 16 y and 6,464,527 person-years of follow-up. We used 24-h dietary recall data, collected on a subset of participants, to evaluate the impact of measurement error on risk estimates. Results After multivariable adjustment for potential confounders, including folate, we observed an inverse association for intake of whole grains (HRQ5 vs.Q1 : 0.84; 95% CI: 0.79, 0.90; P -trend < 0.001), but not dietary fiber (HRQ5 vs. Q1: 0.96; 95% CI: 0.88, 1.04; P -trend = 0.40), with CRC incidence. Intake of whole grains was inversely associated with all CRC cancer subsites, particularly rectal cancer (HRQ5 vs. Q1: 0.76; 95% CI: 0.67, 0.87; P -trend < 0.001). Fiber from grains, but not other sources, was associated with lower incidence of CRC (HRQ5 vs. Q1: 0.89; 95% CI: 0.83, 0.96; P -trend < 0.001), particularly distal colon (HRQ5 vs. Q1: 0.84; 95% CI: 0.73, 0.96; P -trend = 0.005) and rectal cancer (HRQ5 vs. Q1: 0.77; 95% CI: 0.66, 0.88; P- trend < 0.001). Conclusions Dietary guidance for CRC prevention should focus on intake of whole grains as a source of fiber. [ABSTRACT FROM AUTHOR]

Disparities in cancer mortality by county-level income have increased. It is unclear whether these widening disparities have affected older and younger adults equally. National death certificate data were utilized to ascertain cancer deaths during 1999-2015. Average annual percent changes in mortality rates and mortality rate ratios (RRs) were estimated by county-level income quintile and age (25-64 vs ≥65 years). Among 25- to 64-year-olds, cancer mortality rates were 30% higher (RR = 1.30, 95% confidence interval [CI] = 1.29 to 1.31) in the lowest-vs the highest-income counties in 1999-2001 and 56% higher (RR = 1.56, 95% CI = 1.55 to 1.57) in 2013-2015; the disparities among those 65 years and older were smaller but also widened over time (RR1999-2001 = 1.04, 95% CI = 1.03 to 1.05; RR2013-2015 = 1.14, 95% CI = 1.13 to 1.14). Widening disparities occurred across cancer sites. If all counties had the mortality rates of the highest-income counties, 21.5% of cancer deaths among 25- to 64-year-olds and 7.3% of cancer deaths in those 65 years and older would have been avoided in 2015. These results highlight an ongoing need for equity-focused interventions, particularly among younger adults. [ABSTRACT FROM AUTHOR]

Background: Previously we showed that adulthood body mass index (BMI) trajectories that result in obesity were associated with elevated risks of fatal prostate cancer (PCA). To further explore this relationship, we conducted a study within the NIH-AARP Diet and Health Study.Methods: Among 153 730 eligible men enrolled in the NIH-AARP cohort from 1995 to 1996 (median follow-up = 15.1 years), we identified 630 fatal PCA cases and 16 896 incident cases. BMI was assessed for ages 18, 35 and 50 and at study entry, enabling examination of latent class-identified BMI trajectories. Hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using Cox proportional hazards regression.Results: BMI at study entry (mean age = 63, HR = 1.12; 95% CI = 1.01, 1.24, per 5-unit increase) and maximum BMI during adulthood (HR = 1.12; 95% CI = 1.02, 1.24, per 5-unit increase) shared modest associations with increased risk of fatal PCA. Smoking status likely modified the relationship between BMI trajectories and fatal PCA (Pinteraction = 0.035 via change-in-estimate variable section, P = 0.065 via full a priori model). Among never-smokers, BMI trajectory of normal weight to obesity was associated with increased risk of fatal disease (HR = 2.37; 95% CI = 1.38, 4.09), compared with the maintained normal weight trajectory, whereas there was no association among former or current-smokers. Total and non-aggressive PCA exhibited modest inverse associations with BMI at all ages, whereas no association was observed for aggressive PCA.Conclusions: Increased BMI was positively associated with fatal PCA, especially among never-smokers. Future studies that examine PCA survival will provide additional insight as to whether these associations are the result of biology or confounding. [ABSTRACT FROM AUTHOR]

Many smokers do not quit but instead reduce the number of cigarettes they smoke per day (CPD) over their lifetime. Yet the associations of such changes in CPD with health risks are unclear. We examined the association of changes in CPD with subsequent death in the period 2004–2011 among 253,947 participants of the National Institutes of Health–AARP Diet and Health Study. Using a questionnaire assessing responders' history of smoking cigarettes, we identified cigarette smokers who quit, decreased, maintained, or increased their CPD between ages 25–29 and 50–59 years. Hazard ratios and 95% confidence intervals were obtained from multivariable adjusted Cox proportional hazards regression models. Relative to never smokers, smokers who maintained a consistent CPD had 2.93 times (95% confidence interval (CI): 2.82, 3.05) higher all-cause mortality risk, and participants who increased their CPD had still higher risk (hazard ratio (HR) = 3.37, 95% CI: 3.23, 3.52). Death risk was lower among participants who decreased their CPD (HR = 2.38, 95% CI: 2.25, 2.52) or quit smoking (for quitting between ages 30 and 39 years, HR = 1.32, 95% CI: 1.25, 1.39). Similar patterns were observed for smoking-related causes of death, with particularly strong associations for lung cancer and respiratory disease. Reductions in CPD over the lifetime meaningfully decreased death risk; however, cessation provided a larger benefit than even large declines in CPD. [ABSTRACT FROM AUTHOR]

Background: Daily aspirin use has been recommended for secondary prevention of cardiovascular disease, but its use for primary prevention remains controversial.Methods: We followed 440,277 men and women from the NIH-AARP Diet and Health Study (ages 50-71) and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (ages 55-74) for mortality for 13 years on average. Frequency of aspirin use was ascertained through self-report, and cause of death by death certificates. We calculated multivariate hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality using Cox proportional hazards models for each cohort and combined by meta-analysis.Results: We found a consistent U-shaped relationship between aspirin use and mortality in both studies, with differential risk patterns for cardiovascular mortality by disease history. Among individuals with a history of cardiovascular disease, daily aspirin use was associated with reduced cardiovascular mortality [HR = 0.78 (95% CI, 0.74, 0.82)]. However, among those without a previous history, we observed no protection for daily aspirin users [HR = 1.06 (1.02, 1.11)], and elevated risk of cardiovascular mortality for those taking aspirin twice daily or more [HR = 1.29 (1.19, 1.39)]. Elevated risk persisted even among participants who lived beyond 5 years of follow-up and used aspirin without other nonsteroidal antiinflammatory drugs [HR = 1.31 (1.17, 1.47)].Conclusions: Results from these 2 large population-based US cohorts confirm the utility of daily aspirin use for secondary prevention of cardiovascular mortality; however, our data suggest that caution should be exercised in more frequent use, particularly among individuals without a history of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background: In 1991, coffee was classified as a group 2B carcinogen, possibly carcinogenic to humans, based on limited epidemiologic evidence of a positive association with bladder cancer. In 2016, the International Agency for Research on Cancer downgraded this classification due to lack of evidence from prospective studies particularly for never smokers.Methods: Baseline coffee drinking was assessed with a food frequency questionnaire in the NIH-AARP prospective cohort study. Among 469,047 US adults, who were cancer free at baseline, 6,012 bladder cancer cases (5,088 men and 924 women) were identified during >6.3 million person-years of follow-up. Multivariable-adjusted Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI), with non-coffee drinkers as the reference group.Results: Coffee drinking was positively associated with bladder cancer in models adjusted for age and sex (HR for ≥4 cups/d relative to coffee nondrinkers = 1.91, 95% CI = 1.70, 2.14; P trend < 0.0001). However, the association was substantially attenuated after adjustment for cigarette smoking and other potential confounders (HR for ≥4 cups/d relative to coffee nondrinkers = 1.18, 95% CI = 1.05, 1.33; P trend = 0.0007). Associations were further attenuated after additional adjustment for lifetime smoking patterns among the majority of the cohort with this available data (P trend = 0.16). There was no evidence of an association among never smokers (P trend = 0.84).Conclusions: Positive associations between coffee drinking and bladder cancer among ever smokers but not never smokers suggest that residual confounding from imperfect measurement of smoking or unmeasured risk factors may be an explanation for our positive findings. [ABSTRACT FROM AUTHOR]

Background: In a European cohort, it was previously reported that 35% of oropharyngeal cancer (OPC) patients were human papillomavirus type-16 (HPV16) seropositive up to 10 years before diagnosis vs 0.6% of cancer-free controls. Here, we describe the kinetics of HPV16-E6 antibodies prior to OPC diagnosis.Methods: We used annual serial prediagnostic blood samples from the PLCO Cancer Screening Trial. Antibodies to HPV were initially assessed in prediagnostic blood drawn at study enrollment from 198 incident head and neck cancer patients (median years to cancer diagnosis = 6.6) and 924 matched control subjects using multiplex serology, and subsequently in serial samples (median = 5/individual). Available tumor samples were identified and tested for HPV16 RNA to define HPV-driven OPC.Results: HPV16-E6 antibodies were present at baseline in 42.3% of 52 OPC patients and 0.5% of 924 control subjects. HPV16-E6 antibody levels were highly elevated and stable across serial blood samples for 21 OPC patients who were seropositive at baseline, as well as for one OPC patient who seroconverted closer to diagnosis. All five subjects with HPV16-driven OPC tumors were HPV16-E6-seropositive, and the four subjects with HPV16-negative OPC tumors were seronegative. The estimated 10-year cumulative risk of OPC was 6.2% (95% confidence interval [CI] = 1.8% to 21.5%) for HPV16-E6-seropositive men, 1.3% (95% CI = 0.1% to 15.3%) for HPV16-E6-seropositive women, and 0.04% (95% CI = 0.03% to 0.06%) among HPV16-E6-seronegative individuals.Conclusions: Forty-two percent of subjects diagnosed with OPC between 1994 and 2009 in a US cohort were HPV16-E6 seropositive, with stable antibody levels during annual follow-up for up to 13 years prior to diagnosis. Tumor analysis indicated that the sensitivity and specificity of HPV16-E6 antibodies were exceptionally high in predicting HPV-driven OPC. [ABSTRACT FROM AUTHOR]

Background: Several studies suggest that cancer is reduced before and after a Parkinson's disease (PD) diagnosis. However, determining relationships among diseases of ageing is challenging due to possible biases in ascertaining disease. This study evaluates the PD and cancer relationship, addressing potential biases.Methods: Using Surveillance, Epidemiology, and End Results-Medicare linked data (1992-2005) of adults ≥ 65 years, we assessed PD risk after cancer comparing PD in 743 779 cancer patients with PD in a non-cancer group (n = 419 432) in prospective cohort analyses. We also conducted a case-control study of 836 947 cancer cases and 142 869 controls to assess cancer following PD. We applied Cox proportional hazards models to estimate hazards ratios (HRs) for PD after cancer and unconditional logistic regression to estimate odds ratios (ORs) for PD preceding cancer, controlling for physician visits and other factors. To explore biases in ascertaining cancer, we examined relationships between cancer and automobile accident injuries, which we expected to be null.Results: No association was observed between cancer and subsequent PD [HR = 0.97; 95% confidence interval (CI) = 0.92-1.01] nor between cancer and subsequent automobile injuries (HR = 1.03; 95% CI = 0.98-1.07). One site, lung cancer, was associated with subsequent reduced PD, which may reflect confounding by smoking. In the case-control analysis, PD was associated with reduced subsequent cancer, overall (OR = 0.77; 95% CI = 0.71-0.82) and for several cancer sites. However, the automobile injury/ subsequent cancer association was similar (OR = 0.83; 95% CI = 0.78-0.88), suggesting a cancer detection bias after serious health outcomes.Conclusions: In totality, our data do not support a biological relationship between PD and cancer. [ABSTRACT FROM AUTHOR]

Alcohol is a carcinogen suspected of increasing lung cancer risk. Therefore, we prospectively evaluated the relationship between alcohol consumption and lung carcinoma in 492,902 persons from the National Institutes of Health-AARP Diet and Health Study. We used Cox models to calculate hazard ratios and 95% confidence intervals, adjusting for tobacco smoking and other potential confounders. Between 1995/1996 and December 31,2006, there were 10,227 incident cases of lung carcinoma, classified as adenocarcinoma (n = 4,036), squamous cell carcinoma (n = 1,998), small cell carcinoma (n = 1,524), undifferentiated carcinoma (n = 559), and other (n = 2,110). Compared with nondrinking, alcohol consumption was associated with a modest nonlinear reduction in total lung carcinoma risk at lower levels of consumption (for 0.5-<1 drink/day, HR = 0.89,95% confidence interval: 0.82,0.96) but a modest increase in risk in the highest category (for ≥7 drinks/day, HR= 1.11, 95% confidence interval: 1.00,1.24). Regarding histological type, alcohol was associated with a nonlinear reduction in squamous cell carcinoma that became attenuated as consumption increased and a modest increase in adenocarcinoma among heavier drinkers. Cubic spline models confirmed these findings. Our data suggest that the relationship between alcohol consumption and lung carcinoma differs by histological subtype. [ABSTRACT FROM AUTHOR]

Concerns about high caffeine intake and coffee as a vehicle for added fat and sugar have raised questions about the net impact of coffee on health. Although inverse associations have been observed for overall mortality, data for cause-specific mortality are sparse. Additionally, few studies have considered exclusively decaffeinated coffee intake or use of coffee additives. Coffee intake was assessed at baseline by self-report in the Prostate, Lung, Colo-rectal and Ovarian Cancer Screening Trial. Hazard ratios were estimated using Cox proportional hazards models. Among 90,317 US adults without cancer at study baseline (1998-2001) or history of cardiovascular disease at study enrollment (1993-2001), 8,718 deaths occurred during 805,644 person-years of follow-up from 1998 through 2009. Following adjustment for smoking and other potential confounders, coffee drinkers, as compared with nondrinkers, had lower hazard ratios for overall mortality (<1 cup/day: hazard ratio (HR) = 0.99 (95% confidence interval (CI): 0.92, 1.07); 1 cup/day: HR = 0.94 (95% CI: 0.87, 1.02); 2-3 cups/day: HR = 0.82 (95% CI: 0.77, 0.88); 4-5 cups/ day: HR = 0.79 (95% CI: 0.72, 0.86); ≥6 cups/day: HR = 0.84 (95% CI: 0.75, 0.95)). Similar findings were observed for decaffeinated coffee and coffee additives. Inverse associations were observed for deaths from heart disease, chronic respiratory diseases, diabetes, pneumonia and influenza, and intentional self-harm, but not cancer. Coffee may reduce mortality risk by favorably affecting inflammation, lung function, insulin sensitivity, and depression. [ABSTRACT FROM AUTHOR]

Sweetened beverages, coffee, and tea are the most consumed non-alcoholic beverages and may have important health consequences. We prospectively evaluated the consumption of various types of beverages assessed in 1995–1996 in relation to self-reported depression diagnosis after 2000 among 263,923 participants of the NIH-AARP Diet and Health Study. Odds ratios (OR) and 95% confidence intervals (CI) were derived from multivariate logistic regressions. The OR (95% CI) comparing ≥4 cans/cups per day with none were 1.30 (95%CI: 1.17–1.44) for soft drinks, 1.38 (1.15–1.65) for fruit drinks, and 0.91 (0.84–0.98) for coffee (all P for trend<0.0001). Null associations were observed for iced-tea and hot tea. In stratified analyses by drinkers of primarily diet versus regular beverages, the ORs were 1.31 (1.16–1.47) for diet versus 1.22 (1.03–1.45) for regular soft drinks, 1.51 (1.18–1.92) for diet versus 1.08 (0.79–1.46) for regular fruit drinks, and 1.25 (1.10–1.41) for diet versus 0.94 (0.83–1.08) for regular sweetened iced-tea. Finally, compared to nondrinkers, drinking coffee or tea without any sweetener was associated with a lower risk for depression, adding artificial sweeteners, but not sugar or honey, was associated with higher risks. Frequent consumption of sweetened beverages, especially diet drinks, may increase depression risk among older adults, whereas coffee consumption may lower the risk. [ABSTRACT FROM AUTHOR]

Gallstones and cholecystectomy may be related to digestive system cancer through inflammation, altered bile flux, and changes in metabolic hormone levels. Although gallstones are recognized causes of gallbladder cancer, associations with other cancers of the digestive system are poorly established. We used the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked database (1992–2005), which includes 17 cancer registries that cover approximately 26% of the US population, to identify first primary cancers (n = 236,850) occurring in persons aged ≥66 years and 100,000 cancer-free population-based controls frequency-matched by calendar year, age, and gender. Odds ratios and 95% confidence intervals were calculated using logistic regression analysis, adjusting for the matching factors. Gallstones and cholecystectomy were associated with increased risk of noncardia gastric cancer (odds ratio (OR) = 1.21 (95% confidence interval (CI): 1.11, 1.32) and OR = 1.26 (95% CI: 1.13, 1.40), respectively), small-intestine carcinoid (OR = 1.27 (95% CI: 1.01, 1.60) and OR = 1.78 (95% CI: 1.41, 2.25)), liver cancer (OR = 2.35 (95% CI: 2.18, 2.54) and OR = 1.26 (95% CI: 1.12, 1.41)), and pancreatic cancer (OR = 1.24 (95% CI: 1.16, 1.31) and OR = 1.23 (95% CI: 1.15, 1.33)). Colorectal cancer risk associated with gallstones and cholecystectomy decreased with increasing distance from the common bile duct (P-trend < 0.001). Hence, gallstones and cholecystectomy are associated with the risk of cancers occurring throughout the digestive tract. [ABSTRACT FROM PUBLISHER]

Background: Head and neck cancer (HNC) is the seventh most common cancer worldwide. Although diet has been proposed to play an important role in HNC, few associations with diet have been convincing other than alcohol intake. Studies of dietary patterns that examine overall diets may provide broader insight than studies of individual foods. Little is known about the association between dietary patterns and risk of HNC. Objective: We prospectively evaluated the association between 2 index-based dietary patterns [ie, the Healthy Eating Index-2005 (HEI-2005) and alternate Mediterranean Diet Score (aMED)] and risk of head and neck squamous cell carcinoma. Design: We included 494,967 participants from the NIH-AARP Diet and Health study (1995-2006). HRs (95% CIs) were estimated by using Cox regression. Scores for the HEI-2005 and aMED were calculated on the basis of diet assessed by using a baseline foodfrequency questionnaire. Higher scores reflected adherence to dietary recommendations for healthy eating. Our main outcome was the incidence of HNC, including cancer of the larynx, oral cavity, and orohypopharynx. Results: A total of 1868 HNC cases were identified during follow-up. Higher HEI-2005 scores were associated with reduced risk of HNC in men [HR: 0.74 (95% CI: 0.61, 0.89) for highest compared with lowest quintiles; P-trend = 0.0008] and women [HR: 0.48; 95% CI: 0.33, 0.70; P-trend < 0.0001]. High aMED scores were also associated with lower HNC risk in men (HR: 0.80; 95% CI: 0.64, 1.01; P-trend = 0.002) and women (HR: 0.42; 95% CI: 0.24, 0.74; P-trend < 0.0001). Associations were similar among subsites. We did not find significant interactions between smoking and alcohol intake and each index on HNC risk. Conclusions: HEI-2005 and aMED scores were associated inversely with risk of HNC. Large interventional studies are required to assess the causality before conveying definite public health messages. [ABSTRACT FROM AUTHOR]

Background: Coffee and tea are widely consumed globally and are rich sources of potential chemopreventive compounds. Epidemiologic data for coffee and tea intakes in relation to colorectal cancer remain unclear. Despite differences in gut physiology, few studies have conducted investigations by anatomic subsites. Objective: We evaluated coffee and tea intakes (caffeinated and decaffeinated) in relation to colon (proximal and distal) and rectal cancers. Design: The NIH-AARP Diet and Health Study included 489,706 men and women who completed a baseline (1995-1996) self-administered questionnaire of demographics, diet, and lifestyle. Over a median of 10.5 y of follow-up, we identified 2863 proximal colon, 1993 distal colon, and 1874 rectal cancers. Multivariable HRs and 95% CIs were estimated by using Cox regression. Results: Approximately 16% of participants drank ≥4 cups coffee/d. Compared with nondrinkers, drinkers of 4-5 cups coffee/d (HR: 0.85; 95% CI: 0.75, 0.96) and ≥6 cups coffee/d (HR: 0.74; 95% CI: 0.61, 0.89; P-trend < 0.001) had a lower risk of colon cancer, particularly of proximal tumors (HR for ≥6 cups/d: 0.62; 95% CI: 0.49, 0.81; P-trend < 0.0001). Results were similar to those overall for drinkers of predominantly caffeinated coffee. Although individual HRs were not significant, there was a significant f-trend for both colon and rectal cancers for people who drank predominantly decaffeinated coffee. No associations were observed for tea. Conclusions: In this large US cohort, coffee was inversely associated with colon cancer, particularly proximal tumors. Additional investigations of coffee intake and its components in the prevention of colorectal cancer by subsites are warranted. The NIH-AARP Diet and Health Study was registered at clinicaltrials.gov as NCT00340015. [ABSTRACT FROM AUTHOR]

The authors prospectively examined whether caffeine intake was associated with lower risk of Parkinson disease (PD) in both men and women among 304,980 participants in the National Institutes of Health-AARP Diet and Health Study and whether smoking affected this relation. Multivariate odds ratios and 95% confidence intervals were derived from logistic regression models. Higher caffeine intake as assessed in 1995–1996 was monotonically associated with lower PD risk (diagnosed in 2000–2006) in both men and women. After adjustment for age, race, and physical activity, the odds ratio comparing the highest quintile of caffeine intake with the lowest was 0.75 (95% confidence interval: 0.60, 0.94; Ptrend = 0.005) for men and 0.60 (95% confidence interval: 0.39, 0.91; Ptrend = 0.005) for women. Further adjustment for duration of smoking and analyses carried out among never smokers showed similar results. A joint analysis with smoking suggested that smoking and caffeine may act independently in relation to PD risk. Finally, the authors conducted a meta-analysis of prospective studies and confirmed that caffeine intake was inversely associated with PD risk in both men and women. These findings suggest no gender difference in the relation between caffeine and PD. [ABSTRACT FROM AUTHOR]

Summary: Background: Whether women are more susceptible than men to lung cancer caused by cigarette smoking has been controversial. To address this question, we aimed to compare incidence rates of lung cancer by stratum of smoking use in men and women of the National Institutes of Health (NIH)-AARP cohort. Methods: Participants in the NIH-AARP Diet and Health study responded to a postal questionnaire between Oct 13, 1995, and May 6, 1996, and were followed up until Dec 31, 2003. The questionnaire asked participants about their past and current smoking status, demographics, alcohol intake, tobacco smoking, physical activity, and included a food-frequency questionnaire of 124 items. Incident lung cancers were identified by linkage to individual state cancer registries. We present age-standardised incidence rates for cancer and multivariate hazard ratios (HRs) adjusted for potential confounders, with 95% CIs. This study conforms to the STROBE guidelines. Findings: 279 214 men and 184 623 women from eight states in the USA aged 50–71 years at study baseline were included in this analysis. During follow-up, lung cancers occurred in 4097 men and 2237 women. Incidence rates were 20·3 (95% CI 16·3–24·3) per 100 000 person-years in men who had never smoked (99 cancers) and 25·3 (21·3–29·3) in women who had never smoked (152 cancers); for this group, the adjusted HR for lung cancer was 1·3 (1·0–1·8) for women compared with men. Smoking was associated with increased risk of lung cancer in men and women. The incidence rate of current smokers who smoked more than two packs per day was 1259·2 (1035·0–1483·3) in men and 1308·9 (924·2–1693·6) in women. In current smokers, in a model adjusted for typical smoking dose, the HR was 0·9 (0·8–0·9) for women compared with men. For former smokers, in a model adjusted for years of cessation and typical smoking dose, the HR was 0·9 (0·9–1·0) for women compared with men. Incidence rates of adenocarcinoma, small-cell carcinoma, and undifferentiated tumours were similar in men and women; incidence rates of squamous tumours in men were about twice that in women. Interpretation: Our findings suggest that women are not more susceptible than men to the carcinogenic effects of cigarette smoking in the lung. In smokers, incidence rates tended to be higher in men than women with comparable smoking histories, but differences were modest; smoking was strongly associated with lung cancer risk in both men and women. Future studies should confirm whether incidence rates are indeed higher in women who have never smoked than in men who have never smoked. Funding: Intramural Research Program of the National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics, Bethesda, MD, USA. [Copyright &y& Elsevier]

The authors convey their response to a feedback about their report on the importance of smoking cessation to public health. Topics mentioned include the association of changes in cigarettes smoked per day (CPD) between ages 25 to 29 and 50 to 59 years with subsequent mortality risk, changes in CPD between 1995-1995 and 2004-2005, and the impact of large changes in CPD over a long duration of time on the total number of cigarettes that people smoke during their lifetime.

Background: Cutaneous melanoma is the fifth most common cancer in the United States. Modifiable risk factors, with the exception of exposure to ultraviolet radiation (UVR), are poorly understood. Coffee contains numerous bioactive compounds and may be associated inversely with melanoma. However, previous epidemiological evidence is limited. Methods: Coffee intake was assessed at baseline with a food frequency questionnaire in the National Institutes of Health–AARP prospective cohort study. Among 447 357 non-Hispanic whites who were cancer-free at baseline, 2904 incident cases of malignant melanoma were identified during 4 329 044 person-years of follow-up, with a median of 10.5 years of follow-up. Multivariable-adjusted Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for coffee intake and subsequent melanoma risk with non–coffee drinkers as the reference group. Statistical tests were two-sided, and P values less than .05 were interpreted as statistically significant. Results: The highest category of coffee intake was inversely associated with malignant melanoma (≥4 cups/day: HR = 0.80, 95% CI = 0.68 to 0.93, Ptrend = .01). This association was statistically significant for caffeinated (≥4 cups/day: HR = 0.75, 95% CI = 0.64 to 0.89, Ptrend = .01) but not for decaffeinated coffee (Ptrend = .55). Conclusions: Higher coffee intake was associated with a modest decrease in risk of melanoma in this large US cohort study. Additional investigations of coffee intake and its constituents, particularly caffeine, with melanoma are warranted. [ABSTRACT FROM PUBLISHER]

INTRODUCTION: To help target preventive strategies, we estimated US population attributable risks (PARs) of demographic and potentially modifiable risk factors for esophageal squamous cell carcinoma (ESCC), esophageal adenocarcinoma (EAC), gastric cardia adenocarcinoma (GCA), and gastric noncardia adenocarcinoma (GNCA). METHODS: We prospectively examined the associations for risk factors and these cancers in 490,605 people in the National Institutes of Health-the American Association of Retired PersonsDiet andHealth cohort Diet and Health Study cohort from 1995 to 2011. Exposures were obtained from the baseline questionnaire. Diagnoses of gastroesophageal reflux disease were extracted for a subset of eligible National Institutes of Health-the American Association of Retired Persons Diet and Health cohort subjects through linkage to Medicare and then multiply imputed for non-Medicare-eligible subjects. Hazard ratios were calculated usingmultivariable-adjusted Cox proportional hazards regression. Adjusted population attributable risks were calculated for the US population aged 50-71 years by combining the hazard ratios with the estimated joint distribution of risk factor prevalence from the 2015 National Health Interview Survey. RESULTS: Smoking remained themost important risk factor for ESCC andwas estimated to cause more than 1/3 of EAC and GCA and 1/10 of GNCA. Obesity and gastroesophageal reflux diseasewere associated with more than 1/2 of EACand1/3 of GCA. Compared with eachlowest-risk level category, commonrisk factorswere estimated to be associated with 73.7% of ESCC (95% confidence interval [CI]: 62.1%-85.4%), 70.3% of EAC (95% CI: 64.4%-76.2%), 69.3% of GCA (95%CI: 61.0%-77.7%), and 33.6% of GNCA (95% CI: 21.7%-45.5%). DISCUSSION: These factors accounted for a large proportion of esophageal and gastric cancers in the United States, highlighting opportunities for education and intervention to reduce the burden of these highly fatal cancers. [ABSTRACT FROM AUTHOR]

Background: Reduction of premature mortality is a UN Sustainable Development Goal. Unlike other high-income countries, age-adjusted mortality in the USA plateaued in 2010 and increased slightly in 2015, possibly because of rising premature mortality. We aimed to analyse trends in mortality in the USA between 1999 and 2014 in people aged 25-64 years by age group, sex, and race and ethnicity, and to identify specific causes of death underlying the temporal trends.Methods: For this analysis, we used cause-of-death and demographic data from death certificates from the US National Center for Health Statistics, and population estimates from the US Census Bureau. We estimated annual percentage changes in mortality using age-period-cohort models. Age-standardised excess deaths were estimated for 2000 to 2014 as observed deaths minus expected deaths (estimated from 1999 mortality rates).Findings: Between 1999 and 2014, premature mortality increased in white individuals and in American Indians and Alaska Natives. Increases were highest in women and those aged 25-30 years. Among 30-year-olds, annual mortality increases were 2·3% (95% CI 2·1-2·4) for white women, 0·6% (0·5-0·7) for white men, and 4·3% (3·5-5·0) and 1·9% (1·3-2·5), respectively, for American Indian and Alaska Native women and men. These increases were mainly attributable to accidental deaths (primarily drug poisonings), chronic liver disease and cirrhosis, and suicide. Among individuals aged 25-49 years, an estimated 111 000 excess premature deaths occurred in white individuals and 6600 in American Indians and Alaska Natives during 2000-14. By contrast, premature mortality decreased substantially across all age groups in Hispanic individuals (up to 3·2% per year), black individuals (up to 3·9% per year), and Asians and Pacific Islanders (up to 2·6% per year), mainly because of declines in HIV, cancer, and heart disease deaths, resulting in an estimated 112 000 fewer deaths in Hispanic individuals, 311 000 fewer deaths in black individuals, and 34 000 fewer deaths in Asians and Pacific Islanders aged 25-64 years. During 2011-14, American Indians and Alaska Natives had the highest premature mortality, followed by black individuals.Interpretation: Important public health successes, including HIV treatment and smoking cessation, have contributed to declining premature mortality in Hispanic individuals, black individuals, and Asians and Pacific Islanders. However, this progress has largely been negated in young and middle-aged (25-49 years) white individuals, and American Indians and Alaska Natives, primarily because of potentially avoidable causes such as drug poisonings, suicide, and chronic liver disease and cirrhosis. The magnitude of annual mortality increases in the USA is extremely unusual in high-income countries, and a rapid public health response is needed to avert further premature deaths.Funding: US National Cancer Institute Intramural Research Program. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: Hepatocellular carcinoma (HCC) incidence rates continue to increase in the United States. Geographic variation in rates suggests a potential contribution of area-based factors, such as neighborhood socioeconomic deprivation, retail alcohol availability, and access to health care. Methods: Using the National Institutes of Health-American Association of Retired Persons Diet and Health Study, we prospectively examined area socioeconomic variations in HCC incidence (n = 434 cases) and chronic liver disease (CLD) mortality (n = 805 deaths) and assessed contribution of alcohol outlet density, health care infrastructure, diabetes, obesity, and health behaviors. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from hierarchical Cox regression models. Results: Area socioeconomic deprivation was associated with increased risk of HCC incidence and CLD mortality (HR, 1.48; 95% CI, 1.03–2.14 and HR, 2.36; 95% CI, 1.79–3.11, respectively) after accounting for age, sex, and race. After additionally accounting for educational attainment and health risk factors, associations for HCC incidence were no longer significant; associations for CLD mortality remained significant (HR, 1.78; 95% CI, 1.34–2.36). Socioeconomic status differences in alcohol outlet density and health behaviors explained the largest proportion of socioeconomic status-CLD mortality association, 10% and 29%, respectively. No associations with health care infrastructure were observed. Conclusions: Our results suggest a greater effect of area-based factors for CLD than HCC. Personal risk factors accounted for the largest proportion of variance for HCC but not for CLD mortality. [Copyright &y& Elsevier]

This article presents a study on temporal trends in smoking-related mortality in the U.S. from 1959 to 2010. Mortality risks were compared according to sex and self-reported smoking status in two cohort studies and five pooled contemporary cohort studies. The study concludes that risk of smoking-related mortality continues to increase among women and the increased risks are nearly identical for men and women.

Introduction: Smoking is known to be a major cause of death among middle-aged adults, but evidence on its impact and the benefits of smoking cessation among older adults has remained limited. Therefore, we aimed to estimate the influence of smoking and smoking cessation on all-cause mortality in people aged ≥60 years.Methods: Relative mortality and mortality rate advancement periods (RAPs) were estimated by Cox proportional hazards models for the population-based prospective cohort studies from Europe and the U.S. (CHANCES [Consortium on Health and Ageing: Network of Cohorts in Europe and the U.S.]), and subsequently pooled by individual participant meta-analysis. Statistical analyses were performed from June 2013 to March 2014.Results: A total of 489,056 participants aged ≥60 years at baseline from 22 population-based cohort studies were included. Overall, 99,298 deaths were recorded. Current smokers had 2-fold and former smokers had 1.3-fold increased mortality compared with never smokers. These increases in mortality translated to RAPs of 6.4 (95% CI=4.8, 7.9) and 2.4 (95% CI=1.5, 3.4) years, respectively. A clear positive dose-response relationship was observed between number of currently smoked cigarettes and mortality. For former smokers, excess mortality and RAPs decreased with time since cessation, with RAPs of 3.9 (95% CI=3.0, 4.7), 2.7 (95% CI=1.8, 3.6), and 0.7 (95% CI=0.2, 1.1) for those who had quit <10, 10 to 19, and ≥20 years ago, respectively.Conclusions: Smoking remains as a strong risk factor for premature mortality in older individuals and cessation remains beneficial even at advanced ages. Efforts to support smoking abstinence at all ages should be a public health priority. [ABSTRACT FROM AUTHOR]

Purpose The proportion of cancer deaths in the contemporary United States caused by cigarette smoking (the population attributable fraction [PAF]) is not well documented. Methods The PAF of all cancer deaths due to active cigarette smoking among adults 35 years and older in the United States in 2010 was calculated using age- and sex-specific smoking prevalence from the National Health Interview Survey (NHIS) and age- and sex-specific relative risks from the Cancer Prevention Study-II (for ages 35–54 years) and from the Pooled Contemporary Cohort data set (for ages 55 years and older). Results The PAF for active cigarette smoking was 28.7% when estimated conservatively, including only deaths from the 12 cancers currently formally established as caused by smoking by the US Surgeon General. The PAF was 31.7% when estimated more comprehensively, including excess deaths from all cancers. These estimates do not include additional potential cancer deaths from environmental tobacco smoke or other type of tobacco use such as cigars, pipes, or smokeless tobacco. Conclusions Cigarette smoking causes a large proportion of cancer deaths in the contemporary United States. Reducing smoking prevalence as rapidly as possible should be a top priority for the US public health efforts to prevent cancer deaths. [ABSTRACT FROM AUTHOR]

Importance: There are consistent data demonstrating that socioeconomic disadvantage is associated with risk of premature mortality, but research on the relationship between neighborhood socioeconomic factors and premature mortality is limited. Most studies evaluating the association between neighborhood socioeconomic status (SES) and mortality have used a single assessment of SES during middle to older adulthood, thereby not considering the contribution of early life neighborhood SES., Objective: To investigate the association of life course neighborhood SES and premature mortality., Design, Setting, and Participants: This cohort study included Black and White participants of the multicenter Atherosclerosis Risk in Communities Study, a multicenter study conducted in 4 US communities: Washington County, Maryland; Forsyth County, North Carolina; Jackson, Mississippi; and the northwestern suburbs of Minneapolis, Minnesota. Participants were followed up for a mean (SD) of 18.8 (5.7) years (1996-2020). Statistical analysis was performed from March 2023 through May 2024., Exposure: Participants' residential addresses during childhood, young adulthood, and middle adulthood were linked with US Census-based socioeconomic indicators to create summary neighborhood SES scores for each of these life epochs. Neighborhood SES scores were categorized into distribution-based tertiles., Main Outcomes and Measures: Premature death was defined as all-cause mortality occurring before age 75 years. Multivariable-adjusted Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% CIs., Results: Among 12 610 study participants, the mean (SD) age at baseline was 62.6 (5.6) years; 3181 (25.2%) were Black and 9429 (74.8%) were White; and 7222 (57.3%) were women. The lowest, compared with the highest tertile, of neighborhood SES score in middle adulthood was associated with higher risk of premature mortality (HR, 1.28; 95% CI, 1.07-1.54). Similar associations were observed for neighborhood SES in young adulthood among women (HR, 1.25; 95% CI, 1.00-1.56) and neighborhood SES in childhood among White participants (HR, 1.25; 95% CI, 1.01-1.56). Participants whose neighborhood SES remained low from young to middle adulthood had an increased premature mortality risk compared with those whose neighborhood SES remained high (HR, 1.25; 95% CI, 1.05-1.49)., Conclusions and Relevance: In this study, low neighborhood SES was associated with premature mortality. The risk of premature mortality was greatest among individuals experiencing persistently low neighborhood SES from young to middle adulthood. Place-based interventions that target neighborhood social determinants of health should be designed from a life course perspective that accounts for early-life socioeconomic inequality.

Background: It is important to understand the impact of the COVID-19 pandemic on cancer death rates in 2020 in the US. We estimated whether there were larger-than-expected changes in cancer mortality rates from March to December 2020 after accounting for temporal and seasonal patterns using data from January 2011 to February 2020 by cancer type and age., Methods: We obtained death counts and underlying causes of death by cancer type, month/year (2011-2020), and age group from the National Center for Health Statistics and population estimates from the US Census Bureau. Poisson regression was used to test for significant changes in cancer death rates from March to December 2020 compared with prior years., Results: After accounting for temporal trends and seasonal patterns, total cancer death rates were significantly lower than expected during March to December 2020 among 55- to 64-year-olds and ≥75-year-olds, but not in other age groups. Cancer death rates were 2% lower than expected from March to June among 55- to 64-year-olds and 2% to 3% lower from March to July and December among ≥75-year-olds. Among ≥75-year-olds, colorectal cancer death rates were lower from March to June [rate ratios (RR) = 0.94-0.96; P < 0.05]; however, lung cancer death rates were 5% lower across each month (all RRs = 0.95; P < 0.05)., Conclusions: In the US, cancer death rates based on the underlying cause of death were broadly similar to expected rates from March to December 2020. However, cancer death rates were lower than expected among 55- to 64-year-olds and ≥75-year-olds, likely due to COVID-19 as a competing cause of death., Impact: Cancer mortality rates from 2020 should be interpreted with caution., (©2024 American Association for Cancer Research.)

Importance: One in 3 US adults uses multivitamins (MV), with a primary motivation being disease prevention. In 2022, the US Preventive Services Task Force reviewed data on MV supplementation and mortality from randomized clinical trials and found insufficient evidence for determining benefits or harms owing, in part, to limited follow-up time and external validity., Objective: To estimate the association of MV use with mortality risk, accounting for confounding by healthy lifestyle and reverse causation whereby individuals in poor health initiate MV use., Design, Setting, and Participants: This cohort study used data from 3 prospective cohort studies in the US, each with baseline MV use (assessed from 1993 to 2001), and follow-up MV use (assessed from 1998 to 2004), extended duration of follow-up up to 27 years, and extensive characterization of potential confounders. Participants were adults, without a history of cancer or other chronic diseases, who participated in National Institutes of Health-AARP Diet and Health Study (327 732 participants); Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (42 732 participants); or Agricultural Health Study (19 660 participants). Data were analyzed from June 2022 to April 2024., Exposure: Self-reported MV use., Main Outcomes and Measures: The main outcome was mortality. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% CIs., Results: Among 390 124 participants (median [IQR] age, 61.5 [56.7-66.0] years; 216 202 [55.4%] male), 164 762 deaths occurred during follow-up; 159 692 participants (40.9%) were never smokers, and 157 319 participants (40.3%) were college educated. Among daily MV users, 49.3% and 42.0% were female and college educated, compared with 39.3% and 37.9% among nonusers, respectively. In contrast, 11.0% of daily users, compared with 13.0% of nonusers, were current smokers. MV use was not associated with lower all-cause mortality risk in the first (multivariable-adjusted HR, 1.04; 95% CI, 1.02-1.07) or second (multivariable-adjusted HR, 1.04; 95% CI, 0.99-1.08) halves of follow-up. HRs were similar for major causes of death and time-varying analyses., Conclusions and Relevance: In this cohort study of US adults, MV use was not associated with a mortality benefit. Still, many US adults report using MV to maintain or improve health.

Background: In the United States, lung cancer death rates have been declining for decades, primarily as a result of pronounced decreases in cigarette smoking. It is unclear, however, whether there have been similar declines in mortality rates of lung cancer unrelated to smoking. We estimated trends in US lung cancer death rates attributable and not attributable to smoking from 1991 to 2018., Methods: The study included 30- to 79-year-olds in the National Health Interview Survey who were linked to the National Death Index, 1991-2014. Adjusted hazard ratios for smoking status and lung cancer death were estimated, and age-specific population attributable fractions were calculated. Annual population attributable fractions were multiplied by annual US national lung cancer mortality, partitioning rates into smoking-attributable and smoking-unrelated lung cancer deaths. All statistical tests were 2-sided., Results: During 1991-2018, the proportion of never smokers increased among both men (35.1%-54.6%) and women (54.0%-65.4%). Compared with those who had ever smoked, those who had never smoked had 86% lower risk (hazard ratio = 0.14; 95% confidence interval [CI] = 0.12 to 0.16) of lung cancer death. The fraction of lung cancer deaths attributable to smoking decreased from 81.4% (95% CI = 78.9 to 81.4) to 74.7% (95% CI = 78.1 to 71.4). Smoking-attributable lung cancer death rates declined 2.7% per year (95% CI = ‒2.9% to ‒2.5%) and smoking-unrelated lung cancer death rates declined 1.8% per year (95% CI = ‒2.0% to ‒1.5%); these declines have accelerated in recent years., Conclusions: An increasing proportion of lung cancer deaths are unrelated to smoking based on declines in smoking prevalence. Smoking-unrelated lung cancer death rates have declined, however, perhaps because of decreases in secondhand smoke and air pollution exposure as well as treatment improvements., (Published by Oxford University Press 2023.)

Unaffordable housing has been associated with poor health. We investigated the relationship between severe housing cost burden and premature cancer mortality (death before 65 years of age) overall and by Medicaid expansion status. County-level severe housing cost burden was measured by the percentage of households that spend 50% or more of their income on housing. States were classified on the basis of Medicaid expansion status (expanded, late-expanded, nonexpanded). Mortality-adjusted rate ratios were estimated by cancer type across severe housing cost burden quintiles. Compared with the lowest quintile of severe housing cost burden, counties in the highest quintile had a 5% greater cancer mortality rate (mortality-adjusted rate ratio = 1.05, 95% confidence interval = 1.01 to 1.08). Within each severe housing cost burden quintile, cancer mortality rates were greater in states that did not expand Medicaid, though this association was significant only in the fourth quintile (mortality-adjusted rate ratio = 1.08, 95% confidence interval = 1.03 to 1.13). Our findings demonstrate that counties with greater severe housing cost burden had higher premature cancer death rates, and rates are potentially greater in non-Medicaid-expanded states than Medicaid-expanded states., (Published by Oxford University Press 2024.)

Despite decades of declining mortality rates, lung cancer remains the leading cause of cancer death in the United States. This article examines lung cancer incidence, stage at diagnosis, survival, and mortality using population-based data from the National Cancer Institute, the Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries. Over the past 5 years, declines in lung cancer mortality became considerably greater than declines in incidence among men (5.0% vs. 2.6% annually) and women (4.3% vs. 1.1% annually), reflecting absolute gains in 2-year relative survival of 1.4% annually. Improved outcomes likely reflect advances in treatment, increased access to care through the Patient Protection and Affordable Care Act, and earlier stage diagnosis; for example, compared with a 4.6% annual decrease for distant-stage disease incidence during 2013-2019, the rate for localized-stage disease rose by 3.6% annually. Localized disease incidence increased more steeply in states with the highest lung cancer screening prevalence (by 3%-5% annually) than in those with the lowest (by 1%-2% annually). Despite progress, disparities remain. For example, Native Americans have the highest incidence and the slowest decline (less than 1% annually among men and stagnant rates among women) of any group. In addition, mortality rates in Mississippi and Kentucky are two to three times higher than in most western states, largely because of elevated historic smoking prevalence that remains. Racial and geographic inequalities highlight longstanding opportunities for more concerted tobacco-control efforts targeted at high-risk populations, including improved access to smoking-cessation treatments and lung cancer screening, as well as state-of-the-art treatment., (© 2024 American Cancer Society.)

Background: Starting in 2018, national death certificates included a new racial classification system that accounts for multiple-race decedents and separates Native Hawaiian and Pacific Islander (NHPI) individuals from Asian individuals. We estimated cancer death rates across updated racial and ethnic categories, sex, and age., Methods: Age-standardized US cancer mortality rates and rate ratios from 2018 to 2020 among individuals aged 20 years and older were estimated with national death certificate data by race and ethnicity, sex, age, and cancer site., Results: In 2018, there were approximately 597 000 cancer deaths, 598 000 in 2019, and 601 000 in 2020. Among men, cancer death rates were highest in Black men (298.2 per 100 000; n = 105 632), followed by White (250.8; n = 736 319), American Indian/Alaska Native (AI/AN; 249.2; n = 3376), NHPI (205.6; n = 1080), Latino (177.2; n = 66 167), and Asian (147.9; n = 26 591) men. Among women, Black women had the highest cancer death rates (206.5 per 100 000; n = 104 437), followed by NHPI (192.1; n = 1141), AI/AN (189.9; n = 3239), White (183.0; n = 646 865), Latina (128.4; n = 61 579), and Asian (111.4; n = 26 396) women. The highest death rates by age group occurred among NHPI individuals aged 20-49 years and Black individuals aged 50-69 and 70 years and older. Asian individuals had the lowest cancer death rates across age groups. Compared with Asian individuals, total cancer death rates were 39% higher in NHPI men and 73% higher in NHPI women., Conclusions: There were striking racial and ethnic disparities in cancer death rates during 2018-2020. Separating NHPI and Asian individuals revealed large differences in cancer mortality between 2 groups that were previously combined in vital statistics data., (© The Author(s) 2023. Published by Oxford University Press.)

Introduction: The impact of cigarette smoking on mortality is well studied, with estimates of the relative mortality risks for the overall population widely available. However, age-specific mortality estimates for different sociodemographic groups in the U.S. are lacking., Methods: Using the 1987-2018 National Health Interview Survey Linked Mortality Files through 2019, all-cause mortality relative risks (RRs) were estimated for current smokers or recent quitters and long-term quitters compared with those for never smokers. Stratified Cox proportional hazards regression models were used to estimate RRs by age, gender, race/ethnicity, and educational attainment. RRs were also assessed for current smokers or recent quitters by smoking intensity and for long-term quitters by years since quitting. The analysis was conducted in 2021-2022., Results: All-cause mortality RRs among current smokers or recent quitters were generally highest for non-Hispanic White individuals than for never smokers, followed by non-Hispanic Black individuals, and were lowest for Hispanic individuals. RRs varied greatly by educational attainment; generally, higher-education groups had greater RRs associated with smoking than lower-education groups. Conversely, the RRs by years since quitting among long-term quitters did not show clear differences across race/ethnicity and education groups. Age-specific RR patterns varied greatly across racial/ethnic and education groups as well as by gender., Conclusions: Age-specific all-cause mortality rates associated with smoking vary considerably by sociodemographic factors. Among high-education groups, lower underlying mortality rates for never smokers result in correspondingly high RR estimates for current smoking. These estimates can be incorporated in modeling analyses to assess tobacco control interventions' impact on smoking-related health disparities between different sociodemographic groups., (Copyright © 2022 American Journal of Preventive Medicine. All rights reserved.)

Competing Interests: We declare no competing interests. We thank Gail Ackermann, Amnon Amir, James Gaffney, Grant Gogul, Greg Humphrey, Jody McLean, Tara Schwartz, and Weihong Xiao for their role in project management and data production. We also thank the research contributions of the Cancer Genomics Research Laboratory for their expertise, execution, and support of this research in the area of bioinformatics analysis of generated data. This work was supported by a grant from the US Food and Drug Administration's Center for Tobacco Products and the Intramural programme of the National Institutes of Health.

The human oral microbiome is associated with chronic diseases including cancer. However, our understanding of its relationship with diet is limited. We assessed the associations between carbohydrate and glycemic index (GI) with oral microbiome composition in 834 non-diabetic subjects from the NCI-PLCO and ACS-CPSII cohorts. The oral microbiome was characterized using 16Sv3-4 rRNA-sequencing from oral mouthwash samples. Daily carbohydrate and GI were assessed from food frequency questionnaires. We used linear regression, permutational MANOVA, and negative binomial Generalized Linear Models (GLM) to test associations of diet with α- and β-diversity and taxon abundance (adjusting for age, sex, cohort, BMI, smoking, caloric intake, and alcohol). A q-value (FDR-adjusted P-value) of <0.05 was considered significant. Oral bacterial α-diversity trended higher in participants in the highest quintiles of carbohydrate intake, with marginally increased richness and Shannon diversity (p-trend=0.06 and 0.07). Greater carbohydrate intake was associated with greater abundance of class Fusobacteriia (q=0.02) and genus Leptotrichia (q=0.01) and with lesser abundance of an Actinomyces OTU (q=4.7E-04). Higher GI was significantly related to greater abundance of genus Gemella (q=0.001). This large, nationwide study provides evidence that diets high in carbohydrates and GI may influence the oral microbiome., Competing Interests: Competing interests: The authors declare no competing financial interests

Background: Lung cancer is a common cancer in people living with HIV, but the risk of cancer in this group has not been investigated for over a decade. We investigated trends in relative and absolute risk of lung cancer among people living with HIV of various age groups in the USA., Methods: In this population-based registry linkage study, we used 2001-16 data from the HIV/AIDS Cancer Match study, which links data from HIV and cancer registries from 13 regions in the USA. We included non-Hispanic White, non-Hispanic Black, and Hispanic individuals living with HIV aged 20-89 years in our study population. Average annual percentage changes in lung cancer rates were estimated with multivariable Poisson regression, and standardised incidence ratios (SIRs) and excess absolute risks were estimated comparing people living with HIV with the general US population. We used non-parametric cumulative incidence curves to estimate the 5-year cumulative incidence of lung cancer and two AIDS-defining cancers (non-Hodgkin lymphoma and Kaposi sarcoma)., Findings: There were 3426 lung cancers in 4 310 304 person-years of follow-up in our study population. Age-standardised lung cancer incidence rates in people living with HIV declined by 6% per year (95% CI -7 to -5) during 2001-16, with greater declines in the 20-29 age group (-11%, -16 to 6) than in the older age groups (eg, -3% [-6 to 1] in those aged 70-89 years). During 2013-16, the SIR of lung cancer in people living with HIV was 2·01 (95% CI 1·52 to 2·61) in those aged 40-49 years, and 1·31 (1·12 to 1·52) in those aged 60-69 years, whereas the excess absolute risk among people living with HIV was 11·87 (3·95 to 21·89) per 100 000 person-years for those aged 40-49 years and 48·23 (6·88 to 95·47) per 100 000 person-years for those aged 60-69 years. Beginning in 2011, the 5-year cumulative incidence for lung cancer (1·36%, 95% CI 1·17 to 1·53) surpassed that of Kaposi sarcoma (0·12%, 0·06 to 0·17) and non-Hodgkin lymphoma (0·45%, 0·35 to 0·56) for people living with HIV aged 60-69 years., Interpretation: Between 2001 and 2016, the risk of lung cancer decreased for people living with HIV aged 20-69 years, but remained substantially elevated compared with the general population, probably due to a combination of smoking and immunosuppression. For people living with HIV aged 60 years and older, the risk of lung cancer exceeds that of two of the most common AIDS-defining cancers, highlighting the importance of lung cancer among the growing older population of people living with HIV., Funding: Intramural Research Program of the US National Cancer Institute., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Motivation: The Division of Cancer Epidemiology and Genetics (DCEG) and the Division of Cancer Prevention (DCP) at the National Cancer Institute (NCI) have recently generated genome-wide association study (GWAS) data for multiple traits in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Genomic Atlas project. The GWAS included 110 000 participants. The dissemination of the genetic association data through a data portal called GWAS Explorer, in a manner that addresses the modern expectations of FAIR reusability by data scientists and engineers, is the main motivation for the development of the open-source JavaScript software development kit (SDK) reported here., Results: The PLCO GWAS Explorer resource relies on a public stateless HTTP application programming interface (API) deployed as the sole backend service for both the landing page's web application and third-party analytical workflows. The core PLCOjs SDK is mapped to each of the API methods, and also to each of the reference graphic visualizations in the GWAS Explorer. A few additional visualization methods extend it. As is the norm with web SDKs, no download or installation is needed and modularization supports targeted code injection for web applications, reactive notebooks (Observable) and node-based web services., Availability and Implementation: code at https://github.com/episphere/plco; project page at https://episphere.github.io/plco., (Published by Oxford University Press 2022.)

In 1988, Blot and colleagues reported results from a U.S. case-control study of oral cavity or pharyngeal (oropharyngeal and hypopharyngeal) cancers, with results showing independent associations of smoking and alcohol with increased risk, multiplicative interaction effects between smoking and alcohol, and that nearly three-quarters of these cancers are attributable to smoking and alcohol. The report by Blot and colleagues represents a landmark in oropharyngeal cancer epidemiology. This study, the largest at the time, introduced several novel concepts in oropharyngeal cancer epidemiology that remain relevant today-etiologic heterogeneity, statistical interaction effects, adjusted attributable fractions, and disparities by sex and race/ethnicity. Perhaps the most significant recognition in the field since 1988 is the etiologic association of human papillomavirus (HPV, primarily HPV16) with cancers arising in the oropharynx. Today, more than 80% of oropharyngeal cancers in the United States are caused by HPV while only approximately 3% of oral cavity cancers are caused by HPV. This etiologic heterogeneity across head and cancer subsites revealed by HPV is manifest at the genetic/genomic, epidemiologic, and clinical levels. Tobacco and alcohol remain the major etiologic factors for oral cavity cancers while HPV is the major cause of oropharyngeal cancers. Thus, tobacco and alcohol control and prophylactic HPV vaccination remain the most promising prevention tools for oral cavity and oropharyngeal cancers at this time. Importantly, the ever-emerging alternative tobacco products, such as smokeless tobacco/snus, hookah and water pipes, e-cigarettes, flavored cigars and cigarillos, and oral dissolvable products, represent a key public health concern and the carcinogenic effects of these products remains an active area of investigation. See related article by Blot and colleagues, Cancer Res 1988;48:3282-7., (©2022 American Association for Cancer Research.)

Importance: Cancer is the second leading cause of mortality in the US. Despite national decreases in cancer mortality, Black individuals continue to have the highest cancer death rates., Objective: To examine national trends in cancer mortality from 1999 to 2019 among Black individuals by demographic characteristics and to compare cancer death rates in 2019 among Black individuals with rates in other racial and ethnic groups., Design, Setting, and Participants: This serial cross-sectional study used US national death certificate data obtained from the National Center for Health Statistics and included all cancer deaths among individuals aged 20 years or older from January 1999 to December 2019. Data were analyzed from June 2021 to January 2022., Exposures: Age, sex, and race and ethnicity., Main Outcomes and Measures: Trends in age-standardized mortality rates and average annual percent change (AAPC) in rates were estimated by cancer type, age, sex, and race and ethnicity., Results: From 1999 to 2019, 1 361 663 million deaths from cancer occurred among Black individuals. The overall cancer death rate significantly decreased among Black men (AAPC, -2.6%; 95% CI, -2.6% to -2.6%) and women (AAPC, -1.5%; 95% CI, -1.7% to -1.3%). Death rates decreased for most cancer types, with the greatest decreases observed for lung cancer among men (AAPC, -3.8%; 95% CI, -4.0% to -3.6%) and stomach cancer among women (AAPC, -3.4%; 95% CI, -3.6% to -3.2%). Lung cancer mortality also had the largest absolute decreases among men (-78.5 per 100 000 population) and women (-19.5 per 100 000 population). We observed a significant increase in deaths from liver cancer among men (AAPC, 3.8%; 95% CI, 3.0%-4.6%) and women (AAPC, 1.8%; 95% CI, 1.2%-2.3%) aged 65 to 79 years. There was also an increasing trend in uterus cancer mortality among women aged 35 to 49 years (2.9%; 95% CI, 2.3% to 2.6%), 50 to 64 years (2.3%; 95% CI, 2.0% to 2.6%), and 65 to 79 years (1.6%; 95% CI, 1.2% to 2.0%). In 2019, Black men and women had the highest cancer mortality rates compared with non-Hispanic American Indian/Alaska Native, Asian or Pacific Islander, and White individuals and Hispanic/Latino individuals., Conclusions and Relevance: In this cross-sectional study, there were substantial decreases in cancer death rates among Black individuals from 1999 to 2019, but higher cancer death rates among Black men and women compared with other racial and ethnic groups persisted in 2019. Targeted interventions appear to be needed to eliminate social inequalities that contribute to Black individuals having higher cancer mortality.

Background: In response to the US opioid epidemic, the Centers for Disease Control and Prevention updated their guideline on prescription opioids for chronic pain management in March 2016. The aim of this study was to provide detailed analysis of trends in opioid claims among cancer patients in the United States during 2013-2018., Methods: We analyzed pharmaceutical dispensing data from Symphony Health's Integrated Dataverse database, which covers approximately 80% of the US population. We examined annual trends in dispensed opioids in cancer patients during 2013-2018. We examined quarterly trends of the prevalence, mean number of days, and dose (stated as morphine milligram equivalents) of opioid dispensing in cancer patients., Results: Dispensing records of an average of over 3.7 million cancer patients contributed to the study annually in 2013-2018. The annual prevalence of opioid dispensing claims declined from 40.2% in 2013 to 34.5% in 2018. Annual declines occurred across cancer sites, and particularly among patients with metastatic cancer (decline of 19.8%), breast cancer (18.2%), and lung cancer (13.8%). By quarter, the prevalence of opioid claims declined statistically significantly from 26.6% in Q1 2013 to 21.2% in Q4 2018; this decline was more pronounced after Q3 2016 (2-sided P  =   .004). Both quarterly trends in mean days and morphine milligram equivalents of opioids supplied showed a gradual decline from 2013 to 2018, with a slightly larger decline after 2016., Conclusions: We observed a decline in opioid use among cancer patients, particularly after 2016, coinciding with the publication of the Centers for Disease Control and Prevention's guideline on prescription opioids for chronic pain management., (Published by Oxford University Press 2021. This work is written by US Government employees and is in the public domain in the US.)

Introduction: To help target preventive strategies, we estimated US population attributable risks (PARs) of demographic and potentially modifiable risk factors for esophageal squamous cell carcinoma (ESCC), esophageal adenocarcinoma (EAC), gastric cardia adenocarcinoma (GCA), and gastric noncardia adenocarcinoma (GNCA)., Methods: We prospectively examined the associations for risk factors and these cancers in 490,605 people in the National Institutes of Health-the American Association of Retired Persons Diet and Health cohort Diet and Health Study cohort from 1995 to 2011. Exposures were obtained from the baseline questionnaire. Diagnoses of gastroesophageal reflux disease were extracted for a subset of eligible National Institutes of Health-the American Association of Retired Persons Diet and Health cohort subjects through linkage to Medicare and then multiply imputed for non-Medicare-eligible subjects. Hazard ratios were calculated using multivariable-adjusted Cox proportional hazards regression. Adjusted population attributable risks were calculated for the US population aged 50-71 years by combining the hazard ratios with the estimated joint distribution of risk factor prevalence from the 2015 National Health Interview Survey., Results: Smoking remained the most important risk factor for ESCC and was estimated to cause more than 1/3 of EAC and GCA and 1/10 of GNCA. Obesity and gastroesophageal reflux disease were associated with more than 1/2 of EAC and 1/3 of GCA. Compared with each lowest-risk level category, common risk factors were estimated to be associated with 73.7% of ESCC (95% confidence interval [CI]: 62.1%-85.4%), 70.3% of EAC (95% CI: 64.4%-76.2%), 69.3% of GCA (95% CI: 61.0%-77.7%), and 33.6% of GNCA (95% CI: 21.7%-45.5%)., Discussion: These factors accounted for a large proportion of esophageal and gastric cancers in the United States, highlighting opportunities for education and intervention to reduce the burden of these highly fatal cancers., (Copyright © 2021 by The American College of Gastroenterology.)