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Perceived mental health (PMH) was reportedly associated with mortality in general populations worldwide. However, little is known about sex differences and pathways potentially linking PMH to mortality. We explored the relationship between PMH and mortality in Italian men and women, and analysed potential explanatory factors. We performed longitudinal analyses on 9045 men and 9467 women (population mean age 53.8 ± 11.2 years) from the Moli-sani Study. Baseline PMH was assessed through a self-administered Short Form 36-item questionnaire. Cox proportional hazard regression was used to estimate hazard ratios (HRs) and 95 % confidence intervals (95%CI) of death across sex-specific quartiles of PMH, controlling for age, chronic health conditions, and perceived physical health. Socioeconomic, behavioural, and physiological factors were examined as potential explanatory factors of the association between PMH and mortality. In women, HRs for the highest (Q4) vs. bottom quartile (Q1) of PMH were 0.75 (95%CI 0.60–0.96) for all-cause mortality and 0.59 (0.40–0.88) for cardiovascular mortality. Part of these associations (25.8 % and 15.7 %, for all-cause and cardiovascular mortality, respectively) was explained by physiological factors. In men, higher PMH was associated with higher survival (HR = 0.82; 0.69–0.98, for Q4 vs. Q1) and reduced hazard of other cause mortality (HR = 0.67; 0.48–0.95). More than half of the association with all-cause mortality was explained by physiological factors. PMH was measured at baseline only. PMH was independently associated with mortality in men and women. Public health policies aimed at reducing the burden of chronic diseases should prioritize perceived mental health assessment along with other interventions. • Perceived mental health (PMH) is associated with all-cause and cardiovascular (CVD) mortality in women. • PMH is associated with all-cause and other cause mortality in men. • Physiological factors explained 25.8% and 15.7% of the association of PMH with all-cause and CVD mortality in women. • In men, the association of PMH with all-cause mortality was largely explained by physiological factors. [ABSTRACT FROM AUTHOR]

• One of the largest cohort studies of asbestos-exposed workers. • Retrospective exposure assessment. • New considerations on latency until death. The time between initial asbestos exposure and asbestos-related disease can span several decades. The Asbestos Surveillance Program aims to detect early asbestos-related diseases in a cohort of 8,565 power industry workers formerly exposed to asbestos. How does asbestos exposure patterns affect cancer mortality and the duration of latency until death? A mortality follow-up was conducted with available vital status for 8,476 participants (99 %) and available death certificates for 89.9 % of deceased participants. Standardised mortality ratios (SMR) were calculated for asbestos-related cancers. The SMR of mesothelioma and lung cancer were stratified by exposure duration, cumulative asbestos exposure and smoking. The effect of age at first exposure, cumulative asbestos exposure and smoking on the duration of latency until death was examined using multiple linear regression analysis. The mortality risk of mesothelioma (n = 104) increased with cumulative asbestos exposure but not with exposure duration; the highest mortality (SMR: 23.20; 95 % CI: 17.62–29.99) was observed in participants who performed activities with short extremely high exposures (steam turbine revisions). Lung cancer mortality (n = 215) was not increased (SMR: 1.03; 95 % CI: 0.89–1.17). Median latency until death was 46 (15–63) years for mesothelioma and 44 (15–70) years for lung cancer and deaths occurred between age 64 and 82 years. Latency until death was not influenced by age at first exposure, cumulative exposure, or smoking. Cumulative dose seems to be more appropriate than exposure duration for estimating the risk of mesothelioma death. Additionally, exposure with high cumulative doses in short time should be considered. Since only lung cancer mortality, not incidence, was recorded in this study, lung cancer risk associated with asbestos exposure could not be assessed and the lung cancer mortality was lower than expected probably due to screening effects and improved treatments. The critical time window of death from asbestos-related cancer is between the seventh and ninth decade of life. Future studies should further explore the concept of latency, especially since large ranges are reported throughout the literature. [ABSTRACT FROM AUTHOR]

Although some studies have found that short-term PM 2.5 exposure is associated with lung cancer deaths, its impact on other cancer sites is unclear. To answer this research question, this time-stratified case-crossover study used individual cancer death data between January 1, 2000, and December 31, 2019, extracted from the Brazilian mortality information system to quantify the associations between short-term PM 2.5 exposure and cancer mortality from 25 common cancer sites. Daily PM 2.5 concentration was aggregated at the municipality level as the key exposure. The study included a total of 34,516,120 individual death records, with the national daily mean PM 2.5 exposure 15.3 (SD 4.3) μg/m3. For every 10-μg/m3 increase in three-day average PM 2.5 exposure, the odds ratio (OR) for all-cancer mortality was 1.04 (95% CI 1.03–1.04). Apart from all-cancer deaths, PM 2.5 exposure may impact cancers of oesophagus (1.04, 1.00–1.08), stomach (1.05, 1.02–1.08), colon-rectum (1.04, 1.01–1.06), lung (1.04, 1.02–1.06), breast (1.03, 1.00–1.06), prostate (1.07, 1.04–1.10), and leukaemia (1.05, 1.01–1.09). During the study period, acute PM 2.5 exposure contributed to an estimated 1,917,994 cancer deaths, ranging from 0 to 6,054 cases in each municipality. Though there has been a consistent downward trend in PM 2.5 -related all-cancer mortality risks from 2000 to 2019, the impact remains significant, indicating the continued importance of cancer patients avoiding PM 2.5 exposure. This nationwide study revealed a notable association between acute PM 2.5 exposure and heightened overall and site-specific cancer mortality for the first time to our best knowledge. The findings suggest the importance of considering strategies to minimize such exposure in cancer care guidelines. The 20-year analysis of nationwide death records in Brazil revealed that heightened short-term exposure to PM 2.5 is associated with increased cancer mortality at various sites, although this association has gradually decreased over time. Despite the declining impact, the research highlights the persistent adverse effects of PM 2.5 on cancer mortality, emphasizing the importance of continued research and preventive measures to address the ongoing public health challenges posed by air pollution. [Display omitted] • First investigation for acute PM2.5 exposure and site-specific cancer mortality. • Significant adverse effects were observed at various cancer sites. • Potential adaptation exists in the PM2.5-cancer association. • Cancer guidelines may include acute PM2.5 exposure avoidance. [ABSTRACT FROM AUTHOR]

Using patient-specific data, the present study aimed to identify organ and effective dose to estimate the lifetime attributable risks (LARs) of cancer incidence and mortality associated with routine CT procedures. A cross-sectional investigation was conducted on 515 patients who underwent CT scan. The effective dose was computed using two methods: first, the ImPACT software and relevant conversion factors. Second, the effective dose was determined using the scanner-derived DLP and AAPM TG 23's conversion factor. Using the biological effects of ionizing radiation (BEIR VII) report, LAR of cancer incidence and mortality were computed. The greatest mean organ doses for abdomen-pelvis, routine chest, chest HRCT, brain, and sinus examinations were 20.64 ± 3.27 mGy (kidneys), 21.55 ± 5.47 mGy (thymus and esophagus), 10.51 ± 1.31 mGy (thymus and esophagus), 22.72 ± 3.01 mGy (lens), and 18.56 ± 1.25 mGy (lens) respectively. Using ImPACT dosimetry software, the mean effective dose for routine chest, abdomen-pelvis, HRCT chest, brain, and sinus examinations was 8.46 mSv, 10.13 mSv, 4.19 mSv, 1 mSv, and 0.68 mSv, respectively. Using the DLP to effective dose conversion factor, the mean effective dose was lower. The mean cancer incidence risks per 100,000 people were 63.33, 54.98, 27.82, 6.31, and 5.22 for abdomen-pelvis, routine chest, HRCT, brain, and sinus examinations, respectively. The mean LAR of cancer mortality for all cancer was 38.22, 33.17, 16.72, 3.87, 2.93 for abdomen-pelvis, routine chest, HRCT, brain, and sinus examinations, respectively, per 100,000 people. Thus, CT scan exams are connected with a non-negligible risk of cancer, and patient radiation dose must be optimized to limit radiation risk. • The effective dose of routine CT examinations was calculated by two methods. • Abdomen-pelvis scans had the highest mean DLP, scan length, and effective dose. • The current study's CTDIvol and DLP were below recognized diagnostic reference levels. • The abdomen-pelvis had the highest mean LAR of all cancers, all solid, and leukemia, respectively, at 63.33, 56.56, and 6.77. [ABSTRACT FROM AUTHOR]

• Elevated SII levels linked to higher frailty and mortality risk. • U-shaped relationship found between SII levels and mortality. • Critical SII thresholds identified for all-cause and cancer-related mortality. • Maintaining low SII levels may reduce frailty and mortality risk. Frailty is a state of heightened vulnerability to stress, whether from within the body or external factors. We aim to assess the prognostic value of the Systemic Immune-Inflammation Index (SII) in middle-aged and older frail adults. We used data from the 2003–2018 National Health and Nutrition Examination Survey (NHANES) linked to the 2019 National Death Index (NDI) to study mortality. Cox proportional hazards model and two-piecewise Cox proportional hazards model were used to elucidate the nonlinear relationship between SII level and mortality. Our study included 7,446 frail patients (mean age 65.6) with 2,524 deaths (726 from cardiovascular disease and 458 from cancer) over 49,565 person-years. Elevated SII levels were associated with an increased risk of all-cause, cardiovascular disease (CVD)-related and cancer-related mortality, even after adjusting for potential confounders (adjusted HR (95 % CI) = 1.35 (1.25, 1.46), 1.42 (1.22, 1.65) and 1.26 (1.05, 1.51), respectively). Moreover, a U-shaped correlation was discerned between SII levels and the risks of all-cause and cancer-related mortality, with respective thresholds identified at 334.96 and 348.28. Our findings reveal SII levels positively correlate with frailty, all-cause mortality, CVD-related mortality, and cancer-related mortality in middle-aged and elderly frail individuals in the U.S. The critical thresholds for SII index were 334.96 for all-cause mortality and 348.28 for cancer-related mortality. This study underscores the potential benefits of maintaining a certain low level of SII to effectively mitigate the incidence of frailty and mortality among frail patients. [ABSTRACT FROM AUTHOR]