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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]

Introduction Despite its overall decline in the United States, trends in cigarette smoking could vary by intersection with demographic characteristics. We explored trends in education-related disparities in current smoking among U.S. adults by race (Black or African American and White), sex, and U.S. census region. Aims and Methods Data were from U.S. civilian non-institutionalized adults (aged ≥18 years) who self-identified as Black or African American and White and participated in the 1995–2019 Tobacco Use Supplement to the Current Population Survey. We estimated average annual percent changes in current cigarette smoking by the intersections of race, sex, census region, and educational attainment. We calculated educated-related prevalence differences in current cigarette smoking by subtracting the prevalence of bachelor's degrees from that of 1995–1996 = 22.8%; PD2018–2019 = 27.2%) and female adults (PD1995–1996 = 12.1%; PD2018–2019 = 16.5%). By region, Black or African American male adults in the Midwest showed the largest increase in education-related current cigarette smoking disparities, followed by Black or African American male and female adults in the South, and White male and female adults in the Midwest. These findings were because of small to no declines in the prevalence of current cigarette smoking among those with

The AIDS data from 1981 - 1996 identified (60+ years old) and their records were linked to data in local cancer registries, finding 1142 cases. The cancer risks profile of elderly persons with AIDS (EPWAs) generally resembled that in younger adults with AIDS, though RRs were lower due to higher background incidence rates.

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 cervical cancer risk overall is elevated among women living with human immunodeficiency virus (HIV; WLH), it is unclear whether risks are similarly elevated across histologic subtypes. Methods Data from the HIV/AIDS Cancer Match Study, a linkage of 12 US HIV and cancer registries during 1996 -2016, were used. Cervical cancers were categorized as adenocarcinoma (AC), squamous cell carcinoma (SCC), or other histologic subtype. Standardized incidence ratios compared rates of AC and SCC in WLH to those in general population. For WLH, risk factors for AC and SCC were evaluated using Poisson regression. Five-year survival was estimated by HIV status and histology. Results Overall, 62 615 cervical cancers were identified, including 609 in WLH. Compared with the general population, incidence of AC was 1.47 times higher (95% confidence interval [CI]: 1.03–2.05) and SCC was 3.62 times higher among WLH (95% CI: 3.31–3.94). Among WLH, there was no difference in AC rates by race/ethnicity or HIV transmission group, although SCC rates were lower among White women (vs Black) and higher among women who inject drugs (vs heterosexual transmission). Among WLH, 5-year overall survival was similar for AC (46.2%) and SCC (43.8%) but notably lower than for women not living with HIV. Conclusions Among WLH, AC rates were modestly elevated, whereas SCC rates were greatly elevated compared with the general population. These findings suggest there may be differences in the impact of immunosuppression and HIV in the development of AC versus SCC, given their common etiology in human papillomavirus infection. [ABSTRACT FROM AUTHOR]