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Background: There is broad consensus regarding the health impact of tobacco use and secondhand smoke exposure, yet considerable ambiguity exists about the nature and consequences of thirdhand smoke (THS). Objectives: We introduce definitions of THS and THS exposure and review recent findings about constituents, indoor sorption—desorption dynamics, and transformations of THS; distribution and persistence of THS in residential settings; implications for pathways of exposure; potential clinical significance and health effects; and behavioral and policy issues that affect and are affected by THS. Discussion: Physical and chemical transformations of tobacco smoke pollutants take place over time scales ranging from seconds to months and include the creation of secondary pollutants that in some cases are more toxic (e.g., tobacco-specific nitrosamines). THS persists in real-world residential settings in the air, dust, and surfaces and is associated with elevated levels of nicotine on hands and cotinine in urine of nonsmokers residing in homes previously occupied by smokers. Much still needs to be learned about the chemistry, exposure, toxicology, health risks, and policy implications of THS. Conclusion: The existing evidence on THS provides strong support for pursuing a programmatic research agenda to close gaps in our current understanding of the chemistry, exposure, toxicology, and health effects of THS, as well as its behavioral, economic, and sociocultural considerations and consequences. Such a research agenda is necessary to illuminate the role of THS in existing and future tobacco control efforts to decrease smoking initiation and smoking levels, to increase cessation attempts and sustained cessation, and to reduce the cumulative effects of tobacco use on morbidity and mortality.

Central nervous system is sensitive and vulnerable to microwave radiation. Numerous studies have reported that microwave could damage cognitive functions, such as impairment of learning and memory ability. However, the biological effects and mechanisms of accumulative microwave radiation on cognitive functions were remained unexplored. In this study, we analyzed differential expressed proteins in rat models of microwave-induced cognitive impairment by iTRAQ high-resolution proteomic method. Rats were exposed to 2.856 GHz microwave (S band), followed by 1.5 GHz microwave exposure (L band) both at an average power density of 10 mW/cm 2 (SL10 group). Sham-exposed (control group), 2.856 GHz microwave-exposed (S10 group), or 1.5 GHz microwave-exposed (L10 group) rats were used as controls. Hippocampus was isolated, and total proteins were extracted at 7 days after exposure, for screening differential expressed proteins. We found that accumulative microwave exposure induced 391 differential expressed proteins, including 9 downregulated and 382 upregulated proteins. The results of GO analysis suggested that the biological processes of these proteins were related to the adhesion, translation, brain development, learning and memory, neurogenesis, and so on. The cellular components mainly focused on the extracellular exosome, membrane, and mitochondria. The molecular function contained the protein complex binding, protein binding, and ubiquitin-protein transferase activity. And, the KEGG pathways mainly included the synaptic vesicle cycle, long-term potentiation, long-term depression, glutamatergic synapse, and calcium signaling pathways. Importantly, accumulative exposure (SL10 group) caused more differential expressed proteins than single exposure (S10 group or L10 group). In conclusion, 10 mW/cm 2 S or L band microwave induced numerous differential expressed proteins in the hippocampus, while accumulative exposure evoked strongest responses. These proteins were closely associated with cognitive functions and were sensitive to microwave.

The historic debate of nature vs. nurture has emerged as a central yin-yang of contemporary health and disease research. The Human Genome Project provided the capability to define the nature of an individual by one's genetic sequence. But tools are not available to sequence lifelong exposures (i.e., the nurture of an individual). Many believe that nurture has an even greater role than genetics in determining lifelong success, health, and well-being. In contemporary terminology, the cumulative measure of environmental influences and associated biological responses throughout the life span is termed the exposome. This includes all external exposures from the environment, diet, behavior, societal influences and infections, and also cumulative biological responses to exposures and endogenous processes. Pursuit of a “Human Exposome Project” is a vision worthy of our youth: development of strategies and tools will require the brightest and most imaginative. Incorporation of the exposome into education curricula will foster discussion, development of interest, improvement of skills, and promotion of critical thinking to prepare students for civically engaged lives, ongoing study, and future career opportunities. The longterm vision is that sequencing the exposome will support better understanding of healthful and harmful lifelong exposures and lead to improved opportunity for the health and prosperity of all.

Background Hyperglycaemia and dyslipidaemia are well-known risk factors for coronary artery disease (CAD) in type 1 diabetes. The impact of long-term cumulative exposure to these risk factors is less explored. We investigated the relationship between cumulative glycaemic and lipid exposure and CAD in individuals with type 1 diabetes. Methods This longitudinal study included 3495 adults with type 1 diabetes from the FinnDiane cohort, without end-stage kidney disease and no history of CAD or stroke at the study baseline. Total cumulative glycaemic exposure (CGE tot ) and cumulative hyperglycaemic exposure (CGE hg ), accounting only for time spent above an HbA 1c of 53 mmol/mol (7%), were calculated from diabetes diagnosis. Results During a median follow-up of 19.38 years, 534 participants had their first-ever CAD event. CGE hg (odds ratio 1.03 [95% CI 1.02–1.05], p < 0.001) and cumulative exposure to LDL cholesterol, triglycerides, and non-HDL cholesterol all significantly increased the odds for incident CAD. The highest tertile of CGE hg associated with a twofold odds increase for incident CAD. CGE tot was not significantly associated with CAD after adjusting for cumulative lipid exposure. Conclusions Both hyperglycaemia and dyslipidaemia are independently associated with CAD in type 1 diabetes. These findings emphasize the importance of reaching an HbA 1c below 53 mmol/mol (7%) and minimizing lipid exposure, as well as calling on health care professionals to not settle for suboptimal care, but to continue their support and encouragement towards better management of diabetes. Graphical Abstract

This review updates the scientific literature concerning asbestos and lung cancer, emphasizing cumulative exposure and synergism between asbestos exposure and tobacco smoke, and proposes an evidence-based and equitable approach to compensation for asbestos-related lung cancer cases. This update is based on several earlier reviews written by the second and third authors on asbestos and lung cancer since 1995. We reevaluated the peer-reviewed epidemiologic studies. In addition, selected in vivo and in vitro animal studies and molecular and cellular studies in humans were included. We conclude that the mechanism of lung cancer causation induced by the interdependent coaction of asbestos fibers and tobacco smoke at a biological level is a multistage stochastic process with both agents acting conjointly at all times. The new knowledge gained through this review provides the evidence for synergism between asbestos exposure and tobacco smoke in lung cancer causation at a biological level. The evaluated statistical data conform best to a multiplicative model for the interaction effects of asbestos and smoking on the lung cancer risk, with no requirement for asbestosis. Any asbestos exposure, even in a heavy smoker, contributes to causation. Based on this information, we propose criteria for the attribution of lung cancer to asbestos in smokers and non-smokers.

Background Atherogenic index of plasma (AIP) has been demonstrated as a surrogate marker for ischemic stroke, but there is limited evidence for the effect of long-term elevation of AIP on ischemic stroke. Therefore, we aimed to characterize the relationship between cumulative exposure to AIP and the risk of ischemic stroke. Methods A total of 54,123 participants in the Kailuan Study who attended consecutive health examinations in 2006, 2008, and 2010 and had no history of ischemic stroke or cancer were included. The time-weighted cumulative AIP (cumAIP) was calculated as a weighted sum of the mean AIP values for each time interval and then normalized to the total duration of exposure (2006–2010). Participants were divided into four groups according to quartile of cumAIP: the Q1 group, ≤−0.50; Q2 group, − 0.50 to − 0.12; Q3 group, − 0.12 to 0.28; and Q4 group, ≥ 0.28. Cox proportional hazard models were used to evaluate the relationship between cumAIP and ischemic stroke by calculating hazard ratios (HRs) and 95% confidence intervals (95% CIs). Results After a median follow-up of 11.03 years, a total of 2,742 new ischemic stroke events occurred. The risk of ischemic stroke increased with increasing quartile of cumAIP. After adjustment for potential confounders, Cox regression models showed that participants in the Q2, Q3, and Q4 groups had significantly higher risks of ischemic stroke than those in the Q1 group. The HRs (95% CIs) for ischemic stroke in the Q2, Q3, and Q4 groups were 1.17 (1.03, 1.32), 1.33 (1.18, 1.50), and 1.45 (1.28, 1.64), respectively. The longer duration of high AIP exposure was significantly associated with increased ischemic stroke risk. Conclusions High cumulative AIP is associated with a higher risk of ischemic stroke, which implies that the long-term monitoring and maintenance of an appropriate AIP may help prevent such events.

OBJECTIVES: This discussion paper aims to provide recommendations for the development of occupational exposure limits (OEL) for psychosocial hazards. By comparing the characteristics of non-psychosocial and psychosocial hazards at work as well as approaches to derive occupational limit values for both types of hazards, the paper summarizes conceptual requirements and methodological perspectives for OEL in psychosocial risk assessment. METHODS: An interdisciplinary working group comprised of academics, active practitioners in company occupational health management and members of national committees advising policymakers conducted regular face-to-face and online meetings between October 2022 and August 2024 to draft a narrative review and discussion of the current state of research on OEL for psychosocial hazards within the fields of psychology, sociology and medicine. RESULTS: The current field of research is in its early stages, indicated by individual efforts and a lack of joint decision-making. Existing approaches towards OEL focus on disease-level outcomes (eg, burnout, depression), which limits their effectiveness for primary prevention and identifying early warning signs of harm. CONCLUSION: Based on the limited existing literature, we recommend (i) the use of outcome variables that enable detection of early stages of adverse effects aligned with the no-observed adverse effect level (NOAEL) and the lowest-observed-adverse effect level (LOAEL), (ii) standardization and harmonization of hitherto independent assessments of identical hazards, and (iii) policy-level actions to foster collaborative decision-making based on the full spectrum of scientific evidence.

Background Previous studies has shown a significant relationship between baseline triglyceride-glucose (TyG) index and cardiovascular disease (CVD). However, the long-term effect of TyG index and incident CVD remains uncertain. This study aimed to investigate the association between cumulative TyG index and the risk of CVD. Method In this study, we recruited individuals participating in Kailuan Study from 2006 to 2013 without stroke, myocardial infarction, and cancer in the four consecutive examinations. Cumulative TyG index was calculated by multiplying the average TyG index and the time between the two consecutive examinations. Cumulative TyG index levels were categorized into four quartile groups: Q1 group, ≤ 50.65 (as reference group), Q2 group, 50.65–53.86, Q3 group, 53.86–57.44, Q4 group, > 57.44. The association between cumulative TyG index and the risk of CVD was estimated by multivariable Cox proportional hazard models. Result A total of 44,064 individuals participated in the final analysis. After a mean follow-up of 6.52 ± 1.14 years, incident CVD, MI and stroke occurred in 2057, 395 and 1695, respectively. The risk of developing CVD increased with the quartile of cumulative in TyG index, after adjustment for multiple potential confounders, the HR for CVD events were 1.25 (1.08–1.44) in Q2, 1.22 (1.05–1.40) in Q3 and 1.39 (1.21–1.61) in Q4, compared to Q1 group. The longer duration of higher TyG index exposure was significantly associated with increased CVD risk. Similar results were obtained in the subgroup and sensitivity analysis. Conclusion Cumulative TyG index was associated with increased risk of CVD. Maintaining an appropriate level of TG and FBG within the desirable range and better control of cumulative TyG index are important for prevention of CVD.

Background Atherogenic index of plasma (AIP) has been confirmed as a novel marker for myocardial infarction (MI), but few evidence on the long-term AIP and MI risk in general populations. We thus aimed to evaluate the relationships of cumulative exposure to AIP and its accumulation time course with the risk of MI. Methods A total of 54,440 participants were enrolled in the Kailuan study. Time-weighted cumulative AIP was calculated as the weighted sum of the mean AIP value for each time interval, then normalized by total exposure duration, the exposure duration was from 2006 to 2010. Duration of high AIP exposure was defined as the duration with high AIP and ranged from 0 to 6 years. The time course of AIP accumulation was categorized by the combination of time-weighted cumulative AIP < or ≥ median (− 0.12) and AIP slope. Results After 11.05 years of follow-up, 766 incident MI cases were documented. After adjustment for potential confounders, higher risk of MI was observed in participants with the highest time-weighted cumulative AIP quartile (HR, 1.89; 95% CI 1.47–2.43), the longest exposure duration of high AIP (HR, 1.52; 95% CI 1.18–1.95), and those with high time-weighted cumulative AIP and negative slope (HR, 1.42; 95% CI 1.13–1.79). Conclusions Long-term cumulative exposure to AIP and the time course of AIP accumulation increased the risk of MI. High AIP earlier resulted in a greater risk increase than later in life with the same time-weighted cumulative AIP, emphasizing the importance of controlling atherogenic dyslipidemia early in life.

Background A single measurement of the triglyceride-glucose (TyG) index, a simple and reliable surrogate marker of insulin resistance, is associated with ischemic stroke. However, evidence for an effect of a long-term elevation in TyG index on ischemic stroke is limited. Therefore, we evaluated the relationship between cumulative TyG index exposure and the risk of ischemic stroke. Methods A total of 54,098 participants in the Kailuan study who had not experienced ischemic stroke underwent three measurements of fasting blood glucose and triglycerides during 2006–2007, 2008–2009, and 2010–2011. Cumulative exposure to TyG index was calculated as the weighted sum of the mean TyG index value for each time interval (value × time). Participants were placed into four groups according to the quartile of the weighted mean: Q1 group, < 32.01; Q2 group, 32.01–34.45; Q3 group, 34.45–37.47; and Q4 group, ≥ 37.47. Cox proportional hazard models were used to assess the relationships of the cumulative TyG index with incident ischemic stroke by calculating hazard ratios (HRs) and 95% confidence intervals (95% CIs). Results There were 2083 incident ischemic stroke events over the 9 years of follow-up. The risk of ischemic stroke increased with the quartile of cumulative TyG index. After adjustment for multiple potential confounders, participants in groups Q4, Q3, and Q2 had significantly higher risks of ischemic stroke, with HRs (95% CIs) of 1.30 (1.12–1.52), 1.26 (1.09–1.45), and 1.09 (0.94–1.27), respectively ( P trend  < 0.05), compared with the Q1 group. The longer duration of high TyG index exposure was significantly associated with increased ischemic stroke. Conclusions High cumulative TyG index is associated with a higher risk of ischemic stroke. This finding implies that monitoring and the maintenance of an appropriate TyG index may be useful for the prevention of ischemic stroke.